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Control of PD-L1 expression by miR-140/142/340/383 and oncogenic activation of the OCT4–miR-18a pathway in cervical cancer
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Control of PD-L1 expression by miR-140/142/340/383 and oncogenic activation of the OCT4–miR-18a pathway in cervical cancer
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Control of PD-L1 expression by miR-140/142/340/383 and oncogenic activation of the OCT4–miR-18a pathway in cervical cancer
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Journal Article
Control of PD-L1 expression by miR-140/142/340/383 and oncogenic activation of the OCT4–miR-18a pathway in cervical cancer
2018
Overview
PD-L1, a key inhibitory immune receptor, has crucial functions in cancer immune evasion, but whether PD-L1 promotes the malignant properties of cervical cancer (CC) cells and the mechanism by which PD-L1 is regulated in CC remains unclear. We report that PD-L1 is overexpressed in CC, and shRNA-mediated PD-L1 depletion suppresses the proliferation, invasion, and tumorigenesis of CC cells. Loss of miR-140/142/340/383 contributes to PD-L1 upregulation. miR-18a enhances PD-L1 levels by targeting
PTEN
,
WNK2
(ERK1/2 pathway inhibitor), and
SOX6
(Wnt/β-catenin pathway inhibitor and p53 pathway activator) to activate the PI3K/AKT, MEK/ERK, and Wnt/β-catenin pathways and inhibit the p53 pathway, and miR-18a also directly suppresses the expression of the tumor suppressors BTG3 and RBSP3 (CTDSPL). miR-18a overexpression in CC cells is triggered by OCT4 overexpression. Our data implicate PD-L1 as a novel oncoprotein and indicate that miR-140/142/340/383 and miR-18a are key upstream regulators of PD-L1 and potential targets for CC treatment.
Publisher
Nature Publishing Group UK,Nature Publishing Group
Subject
1-Phosphatidylinositol 3-kinase
/ 13/1
/ 13/44
/ 13/89
/ 38/39
/ 38/70
/ 82/51
/ 82/80
/ Animals
/ B7-H1 Antigen - biosynthesis
/ Cell Proliferation - physiology
/ Cell Transformation, Neoplastic - genetics
/ Cell Transformation, Neoplastic - metabolism
/ Cell Transformation, Neoplastic - pathology
/ Cervix
/ Extracellular signal-regulated kinase
/ Female
/ Gene Expression Regulation, Neoplastic - genetics
/ Humans
/ Medicine
/ Mice
/ MicroRNA
/ Octamer Transcription Factor-3 - genetics
/ Octamer Transcription Factor-3 - metabolism
/ Oncology
/ Tumors
/ Uterine Cervical Neoplasms - genetics
/ Uterine Cervical Neoplasms - metabolism
