Lithocholic acid inhibits the expression of HLA class I genes in colon adenocarcinoma cells. differential effect on HLA-A, -B and -C LOCI

Arvind, Padma; Papavassiliou, Efstathios; Tsioulias, George J.; Duceman, Barry W.; Lovelace, Christopher I.P.; Geng, Wenjing; Staiano‐Coico, Lisa; Rigas, Basil

doi:10.1016/0161-5890(94)90168-6

Cited by 21 publications

(11 citation statements)

References 18 publications

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“…Loss of HLA antigen expression helps tumor cells to escapes immune surveillance. Therefore, this is considered to be one of the mechanisms whereby BAs promote tumor development[ 66 ] (Figure 4 ).…”

Section: Molecular Mechanism Of Bile Acids In Colon Carcinogenesismentioning

confidence: 99%

Role of bile acids in colon carcinogenesis

Nguyen

Ung

Kim

et al. 2018

WJCC

118

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Bile acids (BAs) are cholesterol derivatives synthesized in the liver and then secreted into the intestine for lipid absorption. There are numerous scientific reports describing BAs, especially secondary BAs, as strong carcinogens or promoters of colon cancers. Firstly, BAs act as strong stimulators of colorectal cancer (CRC) initiation by damaging colonic epithelial cells, and inducing reactive oxygen species production, genomic destabilization, apoptosis resistance, and cancer stem cells-like formation. Consequently, BAs promote CRC progression via multiple mechanisms, including inhibiting apoptosis, enhancing cancer cell proliferation, invasion, and angiogenesis. There are diverse signals involved in the carcinogenesis mechanism of BAs, with a major role of epidermal growth factor receptor, and its down-stream signaling, involving mitogen-activated protein kinase, phosphoinositide 3-kinase/Akt, and nuclear factor kappa-light-chain-enhancer of activated B cells. BAs regulate numerous genes including the human leukocyte antigen class I gene, p53, matrix metalloprotease, urokinase plasminogen activator receptor, Cyclin D1, cyclooxygenase-2, interleukin-8, and miRNAs of CRC cells, leading to CRC promotion. These evidence suggests that targeting BAs is an efficacious strategies for CRC prevention and treatment.

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Section: Molecular Mechanism Of Bile Acids In Colon Carcinogenesismentioning

confidence: 99%

Role of bile acids in colon carcinogenesis

Nguyen

Ung

Kim

et al. 2018

WJCC

118

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“…LCA was found to reduce the expression of HLA class I antigens on the surface of colon cells by 42% [42]. This dose-dependent reduction was specific for both the target genes and the chemical structure of LCA.…”

Section: Reviewmentioning

confidence: 99%

Secondary bile acids: an underrecognized cause of colon cancer

2014

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Bile acids were first proposed as carcinogens in 1939. Since then, accumulated evidence has linked exposure of cells of the gastrointestinal tract to repeated high physiologic levels of bile acids as an important risk factor for gastrointestinal cancers. High exposure to bile acids may occur in a number of settings, but most importantly, is prevalent among individuals who have a high dietary fat intake.A rapid effect on cells of high bile acid exposure is the generation of reactive oxygen species and reactive nitrogen species, disruption of the cell membrane and mitochondria, induction of DNA damage, mutation and apoptosis, and development of reduced apoptosis capability upon chronic exposure. Here, we review the substantial evidence of the mechanism of secondary bile acids and their role in colon cancer.

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“…Since epidemiological evidence indicated the pivotal role of bile acids in CRC metastasis [Flynn et al, ; Bernstein et al, ; Ou et al, ], studies on the molecular mechanisms of bile acid‐driven CRC have been eventful. High physiological concentrations of bile acids have been thought to influence CRC development through oxidative/nitrosative stress [Payne et al, ], DNA damage [Suzuki and Bruce, ], induction of cell proliferation [Simanowski et al, ], activation of protein kinase C [Pongracz et al, ], and suppression of HLA gene expression [Arvind et al, ]. Bile acids were initially shown to control the expression of the first and rate‐limiting enzyme in the bile acid biosynthetic pathway, cholesterol 7 alpha‐hydroxylase, through protein kinase C dependent‐mechanism [Stravitz et al, ].…”

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confidence: 99%

Lithocholic Acid Stimulates IL-8 Expression in Human Colorectal Cancer Cells Via Activation of Erk1/2 MAPK and Suppression of STAT3 Activity

et al. 2017

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The secondary bile acid lithocholic acid (LCA), an established tumor promoter, has been implicated in colorectal cancer (CRC) metastasis. Overexpression of interleukin-8 (IL-8) has been detected in CRC, and it contributes to poor prognosis. However, the effect of LCA on IL-8 expression is still undefined. In this study, we observed that LCA treatment induced IL-8 expression in CRC HCT116 cells. Pharmacological inhibition and mutagenesis studies indicated that Erk1/2 is critical for LCA-induced IL-8 expression. Furthermore, LCA reduced the phosphorylation of STAT3, and the STAT3 inhibitor Stattic, accelerated LCA-induced IL-8 expression, suggesting that STAT3 is involved in LCA-induced IL-8 expression. Activation of Erk1/2 functioned as an upstream signal of the STAT3 suppression induced by LCA. In conclusion, LCA activated Erk1/2 and in turn, suppressed STAT3 phosphorylation to induce IL-8 expression in HCT116 cells, thus stimulating endothelial cell proliferation and tube like formation. J. Cell. Biochem. 118: 2958-2967, 2017. © 2017 Wiley Periodicals, Inc.

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Lithocholic acid inhibits the expression of HLA class I genes in colon adenocarcinoma cells. differential effect on HLA-A, -B and -C LOCI

Cited by 21 publications

References 18 publications

Role of bile acids in colon carcinogenesis

Role of bile acids in colon carcinogenesis

Secondary bile acids: an underrecognized cause of colon cancer

Lithocholic Acid Stimulates IL-8 Expression in Human Colorectal Cancer Cells Via Activation of Erk1/2 MAPK and Suppression of STAT3 Activity

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