PD-L1 regulates tumorigenesis and autophagy of ovarian cancer by activating mTORC signaling

PD-L1 is a well-known immune co-stimulatory molecule that regulates tumour cell escape from immunity by suppressing the immune response. However, the clinical significance of PD-L1 in the progression of ovarian cancer is unclear. Our study demonstrated that PD-L1 is up-regulated in ovarian tumour ti...

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Bibliographic Details
Published in:Bioscience reports 2019-12, Vol.39 (12)
Main Authors: Gao, Hongmin, Zhang, Juan, Ren, Xiaohong
Format: Article
Language:English
Subjects:
Autophagy - genetics
B7-H1 Antigen - genetics
Cancer
Carcinogenesis - genetics
Cell Cycle, Growth & Proliferation
Cell Homeostasis & Autophagy
Cell Line, Tumor
Cell Proliferation - genetics
Disease Progression
Female
Gene Expression Regulation, Neoplastic - genetics
Humans
Interferon-gamma - genetics
Mechanistic Target of Rapamycin Complex 1 - genetics
Ovarian Neoplasms - genetics
Ribosomal Protein S6 Kinases, 70-kDa - genetics
Signal Transduction - genetics
Signaling
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Summary:PD-L1 is a well-known immune co-stimulatory molecule that regulates tumour cell escape from immunity by suppressing the immune response. However, the clinical significance of PD-L1 in the progression of ovarian cancer is unclear. Our study demonstrated that PD-L1 is up-regulated in ovarian tumour tissue compared with its expression level in adjacent normal tissue. Furthermore, we confirmed that PD-L1 increases the proliferation of cancer cells by activating the AKT-mTORC signalling pathway, which is also enhanced by the expression of S6K, the substrate of mTORC. In addition, PD-L1 promotes the autophagy of ovarian cancer cells by up-regulating the expression of BECN1, a crucial molecule involved in the regulation of autophagy. In conclusion, PD-L1 may provide a target for the development of a novel strategy for the treatment of ovarian cancer.
ISSN:0144-8463
1573-4935
DOI:10.1042/BSR20191041