Endogenous Metabolite; Microbial Metabolite

Under bile acid stress, sodium deoxycholate hydrate (DCA) (100 μM) promotes the survival and proliferation of the gastric cancer cell line MGC803, which is resistant to acidified bile acids [2]. Drug-resistant cells produced by sodium deoxycholate hydrate (DCA) at a concentration of 100 μM showed morphological alterations, a considerable increase in telomerase activity, improved cell survival, and decreased apoptosis in comparison to normal MGC803 cells [2].

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Generation of MGC803 cells resistant to acidified bile acids [2]
To simulate chronic local recurrent disease in vitro, the gastric cancer cell line MGC803 was exposed to acidified medium (pH 5.5) containing 100 μmol/L DCA and CDCA. An untreated log‐growth MGC803 cell line was generated to be used as a control in normal pH media. After daily 10‐min exposure to the acidified bile acids for 60 weeks, MGC803‐resistant cells were able to survive and proliferate after 120‐min exposure.

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Bile acids (BAs), well-defined signaling molecules with diverse metabolic functions, play important roles in cellular processes associated with many cancers. As one of the most common BAs, Deoxycholic Acid (DCA) is originally synthesized in the liver, stored in the gallbladder, and processed in the gut. Deoxycholic Acid (DCA) plays crucial roles in various tumors; however, functions and molecular mechanisms of DCA in gallbladder cancer (GBC) still remain poorly characterized. Here, we analyzed human GBC samples and found that DCA was significantly downregulated in GBC, and reduced levels of DCA was associated with poor clinical outcome in patients with GBC. DCA treatment impeded tumor progression by halting cell proliferation. DCA decreased miR-92b-3p expression in an m6A-dependent posttranscriptional modification manner by facilitating dissociation of METTL3 from METTL3–METTL14–WTAP complex, which increased the protein level of the phosphatase and tensin homolog, a newly identified target of miR-92b-3p, and subsequently inactivated the PI3K/AKT signaling pathway. Our findings revealed that DCA might function as a tumor suppressive factor in GBC at least by interfering with miR-92b-3p maturation, and suggested that DCA treatment could provide a new therapeutic strategy for GBC[3].

Klb–/– mice show a modified BA composition. [1]
Given the key role of FGF21/FGFR1c/β-klotho signaling in fat oxidation, glucose uptake, and energy homeostasis, the resistance of Klb–/– mice to DIO was an unexpected observation. Further, these findings raised the question of the underlying mechanism(s). Since β-klotho is known to participate in a negative feedback loop that represses hepatic BA synthesis, we investigated whether Klb deficiency could also qualitatively impact BA homeostasis. Cyp7a1, the rate-limiting enzyme in BA synthesis, was highly overexpressed in the liver of Klb–/– mice (Figure 3A), as previously reported. Cyp8b1 (encoding sterol 12-α-hydroxylase) was also upregulated, while Cyp7b1 and Cyp27a1 (driving the alternative [acidic] BA synthesis) were underexpressed compared with WT mice (Figure 3B). This specific transcriptional pattern of BA enzymes led us to investigate differences in hepatic primary BA production and the circulating BA composition. Primary BAs are directly synthesized by the liver and converted into secondary BAs by bacterial action in the colon. In the liver, tauro-β-muricholic acid (T-βMCA) levels were decreased in Klb–/– mice (Figure 3C), confirming the downregulation of the alternative pathway. Plasma levels of both primary taurocholic acid (T-CA) and its secondary derivative deoxycholic acid (conjugated [T-DCA] and unconjugated [Deoxycholic Acid (DCA)] forms) were dramatically increased in Klb–/– mice (Figure 3, D and E). The global composition of circulating BAs was substantially modified between genotypes, with a predominance of T-CA and T-DCA in Klb–/– mice (Figure 3F).

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Resistance of Klb–/– mice to DIO is Deoxycholic Acid (DCA) driven and microbiota dependent. [1]
The massive increase of Deoxycholic Acid (DCA) and T-DCA levels in Klb–/– mice led us to investigate the specific contribution of this secondary BA to the increase in energy expenditure on HFD. To this end, we treated orally (0.5 g/l in drinking water) both Klb–/– and WT mice with vancomycin (VCM) 1 week before initiation and during the entire period of HFD consumption. VCM is a poorly absorbed antibiotic preferentially targeting Gram-positive bacteria, including Clostridium species classically described as responsible for the conversion of primary BAs into secondary BAs (such as 7α-dehydroxylation of CA into Deoxycholic Acid (DCA)). VCM treatment similarly reshapes the gut microbiota of Klb–/– and WT mice, massively decreasing both intestinal Bacteroidetes and Firmicutes content in both genotypes on HFD (Figure 7A). In contrast, Proteobacteria content was not impacted by VCM in WT and showed an increasing trend in Klb–/– mice (Figure 7A). Notably, the reshaped microbiota presents drastically reduced 7α-dehydroxylation activity, leading to residual circulating levels of DCA and T-DCA (Figure 7, B and C). Instead, the circulating BA pool is mainly composed of T-βMCA and T-CA in WT mice and of T-CA in Klb–/– mice on HFD+VCM (Figure 7D). The specific pattern of primary BA synthesis due to Klb deficiency was not affected by VCM treatment, since HFD-fed Klb–/– mice presented again higher levels of Cyp7a1 and Cyp8b1 and lower levels of Cyp7b1 compared with HFD-fed WT mice (Supplemental Figure 2A). Importantly, following VCM administration, Klb–/– mice lose their resistance to DIO. Indeed, they gain similar weight (Figure 7E) and exhibit similar fat proportion and content to that of WT (Figure 7F and Supplemental Figure 2B), despite a still lighter eWAT (Figure 7G); no major change was observed in adipose-targeted gene expression (Supplemental Figure 2, C and D), glucose tolerance (Figure 7H), or stool energy content (Figure 7I). Consistently, BAT weight (Figure 8A) and morphology (Figure 8B) were indistinguishable between Klb–/– and WT mice on HFD+VCM. VO2 (Figure 8, C and D), VCO2 (Supplemental Figure 2, E and F), and RER (Figure 8E) were also similar between Klb–/– and WT mice on HFD+VCM. Gene expression analysis in this tissue confirmed the abrogation of thermogenesis induction in Klb–/– mice on HFD+VCM, with a trend towards lower Ucp1, Dio2, and Elovl3 expression levels and significantly lower Pgc1a and Cidea expression levels (Figure 8F). We also observed a massive increase in liver weight (Figure 8G), indicating a preferential storage of fat in the liver rather than in the WAT of Klb–/– mice in the absence of Deoxycholic Acid (DCA)-driven BAT overactivity (Figure 8, H and I). This observation is also corroborated by increased hepatic expression of the scavenger receptor (fatty acid translocase, Cd36) involved in lipid accumulation under excessive fat supply (Figure 8J). Finally, hepatic gene expression of cholesterogenesis enzymes (Figure 8K) and proinflammatory cytokines (Figure 8L) remained elevated in Klb–/– mice on HFD+VCM.

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Deoxycholic Acid (DCA) suppresses GBC tumor growth by downregulating miR-92b-3p expression [3]
To further explore the critical role of miR-92b-3p in GBC, we subcutaneously inoculated ectopically expressed miR-92b-3p or the empty vector as a control in NOZ cells into nude mice, which were then fed food containing Deoxycholic Acid (DCA) or equal amount of vehicle. Compared with the empty vector, overexpression of miR-92b-3p significantly increased the cell proliferation, whereas DCA treatment could significantly attenuated miR-92b-3p-mediated tumor growth (Fig. 7a). Consistently, the tumors excised from mice with miR-92b-3p-overexpressing cells increased weights compared with those excised from mice inoculated with the empty vector, even when treated with DCA (Fig. 7b, c). Similarly, immunohistochemical measurement of Ki-67 as well as p-AKT (Ser473), p-70S6K (Thr389), and p-eIF4EBP1 (phospho T37) showed remarkably lower proliferation rates coupled with significantly decreased levels of AKT signaling pathway after treatment with DCA; miR-92b-3p overexpression partially rescued the DCA-induced growth inhibition by targeting PTEN in GBC tumors (Fig. 7d).

Drug affinity responsive targets stability (DARTS) [3]
DARTS was performed to determine the potential targets of Deoxycholic Acid (DCA). Briefly, 50 × 106 cells were lysed with M-PER supplemented with protease/phosphatase inhibitor cocktail. TNC buffer (50 mM Tris-HCL pH8.0, 50 mM NaCl, and 10 mM CaCl2) was added to the lysates. The supernatants were incubated with increasing concentration of Deoxycholic Acid (DCA) or EtOH (vehicle) for 1 h at room temperature following digestion with Pronase (1:3000) for 30 min. The digestion was terminated with protease inhibitor cocktail following ice incubation immediately. The immunoblotting signals were detected by the ECL Kit. The experiments were performed with three biological replicates.

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Cellular thermal shift assay (CETSA) [3]
Cells were pretreated with 50 μM Deoxycholic Acid (DCA) for 24 h prior to subject to the CETSA protocol. Cells were washed with PBS containing protease inhibitor cocktail and transferred into PCR tubes. The cells were subjected to heat shocked with indicated temperature for 5 min to denature proteins, then were immediately cooled down at room temperature for 5 min. All the samples were next undergone three freeze-thaw cycles to lyse cells. The supernatant was subjected to immunoblotting and the band density was detected. The experiments were performed with three biological replicates.

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miRNA expression analysis (NGS) [3]
For miRNAs-seq, total RNA of two pairs NOZ cells treated with vehicle or Deoxycholic Acid (DCA) were extracted using the miRNeasy Micro Kit. RNA-seq libraries were obtained by using the NEBnext Multiplex Small RNA Library Prep Set, following the manufacturer’s instructions. Sequencing was performed on Illumina Hi-Seq4000 platform with 50 bp single end reads using Illumina reagents according to the manufacturer’s instructions.

Cell lines and cell culture conditions [2]
MGC803 cells were cultured in Roswell Park Memorial Institute media supplemented with 10% fetal calf serum and 100 U/mL penicillin and 100 mg/mL streptomycin. To generate MGC803‐resistant cells, we adjusted the pH value of the MGC803 culture medium to the experimental conditions using the hydrochloric acid (A). The bile acids GCDA and Deoxycholic Acid (DCA) were diluted to optimal working concentrations of 100 μmol/L (B) with culture medium, and the overall pH (A + B) was adjusted to pH 5.5, simulating the gastric environment. Initially, MGC803 cells were chronically exposed to acidified medium with bile acids (A + B) for 10 min every 24 h. The experimental time and conditions were optimized in our preliminary experiments, which showed that 10 min was enough and did not result in cell damage. This procedure was repeated and it took 60 weeks for the MGC803 cells to survive and proliferate under the exposure of A + B for 120 min 12, 13. Control untreated cells were cultured in neutral RPMI medium at pH 7.4 in parallel to the resistant cells for 60 weeks. The morphological changes in MGC803 cells exposed to acidified bile acids (A+B) were documented at 30 and 60 weeks.

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Cell proliferation assays [3]
Cells were seeded in 96-well plates (2000 cells per well) treated with indicated concentration of Deoxycholic Acid (DCA) (50 μM) or vehicle and after a certain time of culturation, cell growth rate was measured using CCK-8 assays, followed by detection of the absorbance at 450 nm through Synergy 2 microplate reader.. Each experiment with three replicates was repeated three times.

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Cytotoxic assays in vitro [3]
Cells were seeded in 96-well plates (2000 cells per well) then treated with increasing concentrations of Deoxycholic Acid (DCA) for indicated times. Cell viability was assessed by the Cell Counting Kit-8 assay. The absorbance at 450 nm was measured thorough a Synergy 2 microplate reader. Each experiment with three replicates was repeated three times.

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Colony formation assay [3]
Cells were seeded in 6-well plates (1000 cells per well) for 10 days until colonies were visible, and then treated with 50 μM Deoxycholic Acid (DCA) or vehicle for 48 h. The colonies were fixed with 4% paraformaldehyde and followed by staining with 0.1% crystal violet.

For xenograft tumor model experiments, 2 × 106 cells GBC-SD or NOZ cells were resuspended with 100 μl of 1 × PBS and subcutaneously into the flanks of BALB/c nude mice (male, 4–6-week old). Six days after injection, mice were randomly allocated to control and treatment groups. All mice were sacrificed and tumors were embedded in paraffin for tissue staining. [3]

Absorption, Distribution and Excretion
Following subcutaneous injection, deoxycholic acid is rapidly absorbed. After the maximum recommended single therapeutic dose of 100 mg, post-treatment plasma concentrations return to endogenous levels within 24 hours. Accumulation is not expected with the recommended treatment regimen. Exogenous deoxycholic acid enters the enterohepatic circulation and is excreted unchanged in feces along with endogenous deoxycholic acid. The liver normally secretes approximately 24 grams of bile acids within 24 hours, dissolved in 700 to 1000 ml of bile. Most bile acids are reabsorbed in the lower small intestine and reused for secretion. The bile acid pool is approximately 2 to 5 grams. /Bile Acids/

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Metabolism/Metabolites Under normal circumstances, deoxycholic acid is not significantly metabolized.

Protein Binding
98% Interaction ... The competition between deoxycholic acid and bromosulfonphthalein for extravascular binding sites may explain the reduced distribution volume of bromosulfonphthalein in the presence of bile acids. Compounds (including deoxycholic acid) enhanced the anticoccal activity of gentamicin, monomycin, kanamycin, and neomycin. Deoxycholic acid was tested alone and as a promoter of N-nitrosobis(2-hydroxypropyl)amine-induced carcinogenesis in hamsters. This study used three groups of 5- to 6-week-old male Syrian hamsters (SYR)/NI, 10 hamsters per group, who were subcutaneously injected with 0.9% sodium chloride solution once a week for 5 weeks. Group 1 received no other treatment; Groups 2 and 3 were supplemented with 0.1% and 0.5% dichloroacetic acid (DCA), respectively, in their diet for 30 weeks. Animals were dissected at week 35. There was no significant difference in body weight between groups 1 and 2, while group 3 showed a significant decrease in body weight (P<0.005). None of the animals in these three groups exhibited liver tumors, bile duct hyperplasia, gallbladder lesions or polyps, pancreatic lesions, or pancreatic duct hyperplasia. In the promoter study, hamsters aged 5–6 weeks in all three groups (number not specified) were subcutaneously injected weekly with 500 mg/kg body weight of N-nitrosobis(2-hydroxypropyl)amine for 5 weeks. Group 4 received no further treatment, while groups 5 and 6 received 0.1% DCA (group 5) or 0.5% DCA (group 6) in their diet, respectively, for 30 weeks. Compared to group 4, both groups 5 and 6 showed a significant decrease in body weight (P<0.005). DCA significantly increased the incidence of cholangiocarcinoma. In group 5, 10 out of 19 hamsters developed cholangiocarcinoma (P<0.006), in group 6, 9 out of 25 hamsters developed cholangiocarcinoma (P<0.05), while only 1 hamster in group 4 developed cholangiocarcinoma (out of 1 out of 15 hamsters in group 4). The incidence of pancreatic cancer was significantly increased in group 5 (14/19, P<0.03). Therefore, under the conditions of this experiment, DCA alone is not carcinogenic, but it can effectively promote the development of N-nitrosobis(2-hydroxypropyl)amine-induced liver and pancreatic cancer in hamsters.

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222528 Oral LD50 in rats 1 gm/kg Behavior: Food intake (animals) Nara Medical Journal, 33(71), 1982
222528 Oral LD50 in mice 1 gm/kg Nara Medical Journal, 33(71), 1982
222528 Intravenous LD50 in mice 130 mg/kg Arzneimittel-Forschung. Drug Research., 20(323), 1970 [PMID:5467505]
222528 Intravenous LD50 in rabbits 2 gm/kg Zeitschrift fuer die Gesamte Experimentelle Medizin., 52(779), 1926

[1]. β-Klotho deficiency protects against obesity through a crosstalk between liver, microbiota, and brown adipose tissue. JCI Insight. 2017 Apr 20;2(8). pii: 91809.

[2]. Acidified bile acids enhance tumor progression and telomerase activity of gastric cancer in micedependent on c-Myc expression. Cancer Med. 2017 Apr;6(4):788-797.

[3]. Deoxycholic acid modulates the progression of gallbladder cancer through N6-methyladenosine-dependent microRNA maturation. Oncogene. 2020 Jun 8;39(26):4983–5000.

Therapeutic Uses
Cholagogues and choleretic agents; cleansers. The beneficial effects of exogenous bile acids stem from their ability to lower cholesterol levels in bile and promote the dissolution of cholesterol gallstones. /Bile Acids/ Veterinary Uses: Increases bile volume without significantly altering its composition. The most effective bile acid, aiding in the absorption of fats and fat-soluble vitamins.

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Deoxycholic acid is a bile acid, a 5β-cholan-24-acid with hydroxyl groups at positions 3 and 12. It is a human serum metabolite. It is a bile acid, dihydroxy-5β-cholanic acid, and C24 sterol. It is the conjugate acid of deoxycholic acid.
Deoxycholic acid is a bile acid capable of emulsifying and dissolving dietary fats in the intestines. After subcutaneous injection, it disrupts the cell membranes of adipocytes, thereby destroying adipocytes in the tissue. In April 2015, the U.S. Food and Drug Administration (FDA) approved deoxycholic acid for the treatment of submental fat to improve facial appearance and reduce facial fullness or prominence. Marketed by Kythera Biopharma under the brand name Kybella, it was the first drug approved for reducing submental fat and is considered a safer, less invasive alternative to surgery. ATX-101 (medical use), sodium deoxycholate for subcutaneous injection, is currently being evaluated as a treatment for reducing localized fat deposits. This includes treating superficial lipomas (benign soft tissue tumors composed of mature fat cells), fat deposits in the submental region of the face/neck, and localized fat deposits in other parts of the body. Deoxycholic acid is a naturally occurring bile acid produced by the liver and is one of several end products of cholesterol metabolism. As a natural component of the human body, deoxycholate is considered a "biocompatible" detergent capable of dissolving fat in the small intestine. ATX-101 is relatively selective for adipose tissue than for other tissues. Deoxycholic acid is a metabolite found or produced in Escherichia coli (K12 strain, MG1655 strain). According to the E. coli Metabolomics Database (ECMDB), deoxycholic acid is a cell-lysing agent. Its physiological effects are achieved by reducing cell membrane integrity. Deoxycholic acid has been reported in both humans and Pseudomonas syringae, and relevant data are available. LOTUS—a database of natural products—is also available. Deoxycholic acid is a steroidal acid, belonging to the secondary bile acid family, and possesses cell-lysing activity. Subcutaneous injection of deoxycholic acid can lead to the dissolution of adipocytes, improving the feeling of fullness caused by submental fat accumulation. Furthermore, it may reduce fat in other subcutaneous adipose tissues. Deoxycholic acid is naturally produced by intestinal bacteria metabolizing bile acids and participates in the emulsification of dietary fats in the intestine. Deoxycholic acid is a small molecule drug that has completed the most Phase IV clinical trials (covering all indications), was first approved in 2015, and has four investigational indications. Deoxycholic acid is a bile acid formed from bile salts by bacterial action. It is usually bound to glycine or taurine. As a surfactant, deoxycholic acid dissolves fats to facilitate intestinal absorption and is itself reabsorbed, thus serving as a choleretic and surfactant. Bile acids are steroidal acids primarily found in the bile of mammals. The differences between various bile acids are very subtle, depending solely on the presence of hydroxyl groups at positions 3, 7, and 12. Bile acids are physiological detergents that promote the excretion, absorption, and transport of fats and sterols in the intestine and liver. Bile acids are also steroidal amphiphilic molecules produced from cholesterol catabolism. They regulate bile flow and lipid secretion, are crucial for the absorption of dietary fats and vitamins, and participate in regulating all key enzymes related to cholesterol homeostasis. Bile acids circulate between the liver, bile ducts, small intestine, and portal vein, forming the enterohepatic circulation. At physiological pH, they exist in anionic form and therefore require carriers for transport across the enterohepatic tissue membrane. Bile acids possess unique detergency properties, which are crucial for the digestion and intestinal absorption of hydrophobic nutrients. Bile acids are potent toxicities (e.g., disrupting cell membranes), and multiple mechanisms exist to limit their accumulation in the blood and tissues (A3407, A3408, A3409, A3410). A3407: St-Pierre MV, Kullak-Ublick GA, Hagenbuch B, Meier PJ: Transport of bile acids in liver and non-liver tissues. J Exp Biol. 2001 May; 204(Pt 10):1673-86. PMID: 11316487. A3408: Claudel T, Staels B, Kuipers F: Farnesol X receptor: Molecular links between bile acids and lipid and glucose metabolism. Arterioscler Thromb Vasc Biol. 2005 Oct; 25(10):2020-30. Published online on July 21, 2005. PMID: 16037564A3409: Chiang JY: Regulation of liver physiology by bile acids: III. Bile acids and nuclear receptors. American Journal of Physiology: Gastrointestinal and Liver Physiology. March 2003; 284(3): G349-56. PMID: 12576301A3410: Davis RA, Miyake JH, Hui TY, Spann NJ: Regulation of cholesterol-7α-hydroxylase: almost absence of SHP. Journal of Lipid Research. April 2002; 43(4): 533-43. PMID: 11907135
Bile acids are formed by the action of bacteria on bile acids. It is usually bound to glycine or taurine. Deoxycholic acid, as a detergent, can dissolve fat to promote intestinal absorption. It is also reabsorbed and plays a choleretic and detergent role. β-Klotho (encoded by the Klb gene) is an essential co-receptor mediating FGF21 and FGF15/19 signaling. Klb-/- mice are unresponsive to the beneficial effects of FGF21 therapy, including stimulation of glucose utilization and thermogenesis. This study aimed to investigate energy homeostasis in Klb-/- mice under a high-fat diet to better understand the consequences of blocking endogenous FGF15/19 and FGF21 signaling during caloric overload. Surprisingly, Klb-/- mice were resistant to diet-induced obesity (DIO) due to increased energy expenditure and brown adipose tissue (BAT) activity. Klb-/- mice not only exhibited elevated bile acid (BA) levels but also altered bile acid composition, showing activation of the classical (neutral) BA synthesis pathway and inhibition of the alternative (acidic) pathway. Excessive hepatic bile acid (CA) production led to an overproduction of deoxycholic acid (DCA) from gut microbiota. DCA can activate the TGR5 receptor, thereby stimulating thermogenic activity in brown adipose tissue (BAT). In fact, the combined knockout of the Klb and Tgr5 genes, or the use of antibiotics to block the conversion of CA to DCA by bacteria, eliminated the diet-induced obesity (DIO) resistance in Klb-/- mice. These results suggest that the DIO resistance in Klb-/- mice is caused by high levels of DCA signaling via the TGR5 receptor. These data also suggest that the gut microbiota can regulate host thermogenesis by converting primary bile acids to secondary bile acids. Drugs or nutritional approaches that selectively modulate bile acid (BA) composition may be a promising target for the treatment of metabolic disorders. [1] c-Myc overexpression is associated with a variety of malignancies, including gastric cancer. This study reports that acidified bile acids can promote tumor progression and telomerase activity in gastric cancer in vitro and in vivo by activating c-Myc. We used quantitative real-time polymerase chain reaction (qRT-PCR) and Western blotting to detect the expression levels of c-Myc mRNA and protein in 10 primary gastric cancer and 5 locally recurrent gastric cancer samples. To construct the MGC803 drug-resistant cell line, we exposed the gastric cancer cell line MGC803 to bile salts (100 μmol/L glycocholic acid and deoxycholic acid) in acidic medium (pH 5.5) for 10 minutes daily for 60 weeks. As a control, we cultured MGC803 cells in a medium without acid or bile salts for 60 weeks. After 60 weeks, we analyzed the cell morphology, proliferation, colony formation, and apoptosis of the MGC803 drug-resistant cells. To determine the role of c-Myc in tumor progression and telomere aging in MGC803 drug-resistant cells, we constructed a xenograft tumor model in nude mice and measured the volume of the xenograft tumor and in vivo telomerase activity. The levels of c-Myc and hTERT protein and mRNA in locally recurrent gastric cancer samples were significantly higher than those in primary gastric cancer samples. Under normal growth conditions, MGC803 drug-resistant cells exhibited significant phenotypic changes, with increased cell clusters and acinar numbers, enhanced cell viability and colony formation ability in vitro, and reduced apoptosis. Using the c-Myc inhibitor 10058-F4, these phenotypic changes were found to be dependent on c-Myc activation. MGC803 resistant cells also showed c-Myc-dependent xenograft growth and enhanced telomerase activity in vivo. In summary, these observations support the hypothesis that acidification of bile acids promotes tumor progression and telomerase activity in gastric cancer, and that these effects are dependent on c-Myc activity. These findings suggest that acidification of bile acids plays an important role in the malignant progression of locally recurrent gastric cancer. [2]

C24H39O4-.NA+.H2O

432.56914

432.285

145224-92-6

Deoxycholic acid;83-44-3;Deoxycholic acid sodium salt;302-95-4;Deoxycholic acid-d4;112076-61-6;Deoxycholic acid-d5;52840-14-9;Deoxycholic acid-13C;52886-37-0;Deoxycholic acid-d6

23679071

Typically exists as solid at room temperature

581.5ºC at 760mmHg

>300ºC

319.5ºC

3.078

3

5

4

30

612

10

C[C@H](CCC(=O)[O-])[C@H]1CC[C@H]2[C@@H]3CC[C@@H]4C[C@@H](CC[C@]4(C)[C@H]3C[C@@H]([C@]12C)O)O.[Na+].O

FHHPUSMSKHSNKW-SMOYURAASA-M

InChI=1S/C24H40O4.Na/c1-14(4-9-22(27)28)18-7-8-19-17-6-5-15-12-16(25)10-11-23(15,2)20(17)13-21(26)24(18,19)3;/h14-21,25-26H,4-13H2,1-3H3,(H,27,28);/q;+1/p-1/t14-,15-,16-,17+,18-,19+,20+,21+,23+,24-;/m1./s1

sodium;(4R)-4-[(3R,5R,8R,9S,10S,12S,13R,14S,17R)-3,12-dihydroxy-10,13-dimethyl-2,3,4,5,6,7,8,9,11,12,14,15,16,17-tetradecahydro-1H-cyclopenta[a]phenanthren-17-yl]pentanoate

Sodium deoxycholate monohydrate; 145224-92-6; Deoxycholic acid (sodium hydrate); DTXSID00635553; Deoxycholic acid sodium salt monohydrate; Desoxycholic acid sodium salt; 7-Deoxycholic acid sodium salt; sodium;(4R)-4-[(3R,5R,8R,9S,10S,12S,13R,14S,17R)-3,12-dihydroxy-10,13-dimethyl-2,3,4,5,6,7,8,9,11,12,14,15,16,17-tetradecahydro-1H-cyclopenta[a]phenanthren-17-yl]pentanoate;hydrate;

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

May dissolve in DMSO (in most cases), if not, try other solvents such as H2O, Ethanol, or DMF with a minute amount of products to avoid loss of samples

Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.

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Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)
*Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution.
Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)
Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil)
Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals).

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Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)]
*Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.
Injection Formulation 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (i.e. 500 μL 2-Hydroxypropyl-β-cyclodextrin → 500 μL Saline)
Injection Formulation 6: DMSO : PEG300 : castor oil : Saline = 5 : 10 : 20 : 65 (i.e. 50 μL DMSO → 100 μLPEG300 → 200 μL castor oil → 650 μL Saline)
Injection Formulation 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (i.e. 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline)
Injection Formulation 8: Dissolve in Cremophor/Ethanol (50 : 50), then diluted by Saline
Injection Formulation 9: EtOH : Corn oil = 10 : 90 (i.e. 100 μL EtOH → 900 μL Corn oil)
Injection Formulation 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL EtOH → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)

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Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium)
Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose
Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals).

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Oral Formulation 3: Dissolved in PEG400
Oral Formulation 4: Suspend in 0.2% Carboxymethyl cellulose
Oral Formulation 5: Dissolve in 0.25% Tween 80 and 0.5% Carboxymethyl cellulose
Oral Formulation 6: Mixing with food powders

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Note: Please be aware that the above formulations are for reference only. InvivoChem strongly recommends customers to read literature methods/protocols carefully before determining which formulation you should use for in vivo studies, as different compounds have different solubility properties and have to be formulated differently.

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 (Please use freshly prepared in vivo formulations for optimal results.)