Dataset Information

Protein expression profile of miR-33b overexpressing ES-2 cells upon OCM treatment

ABSTRACT: Omentum conditioned medium (OCM) is known to enhance ovarian cancer oncogenesis. In this study, miR-33b exerts tumor suppressive effects on ovarian cancer cells in response to omentum conditioned medium (OCM) treatment. To identify the molecular mechanism and main biological pathways involved in the tumor inhibiting activity by miR-33b in the ovarian cancer metastasis. To achieve this, miR-33b was stably overexpressed in ovarian cancer cell line ES-2, and the protein expression profile of miR-33b overexpressing ES-2 cells upon OCM treatment was determined.

INSTRUMENT(S): Orbitrap Fusion Lumos

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Ovarian Surface Epithelial Cell Line, Ovarian Surface Epithelial Cell

DISEASE(S): Malignant Neoplasm Of Ovary

SUBMITTER: Xueyu WANG

LAB HEAD: Dr CHAN, David Wai

PROVIDER: PXD026901 | Pride | 2022-02-17

REPOSITORIES: Pride

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Publications

Epigenetic Silencing of miR-33b Promotes Peritoneal Metastases of Ovarian Cancer by Modulating the TAK1/FASN/CPT1A/NF-κB Axis.

Wang Xueyu X Yung Mingo M H MMH Sharma Rakesh R Chen Fushun F Poon Ying-Tung YT Lam Wai-Yip WY Li Benjamin B Ngan Hextan Y S HYS Chan Karen K L KKL Chan David W DW

Cancers 20210924 19

Peritoneal metastases are frequently found in high-grade serous carcinoma (HGSOC) patients and are commonly associated with a poor prognosis. The tumor microenvironment (TME) is a complex milieu that plays a critical role in epigenetic alterations driving tumor development and metastatic progression. However, the impact of epigenetic alterations on metastatic ovarian cancer cells in the harsh peritoneal microenvironment remains incompletely understood. Here, we identified that miR-33b is frequen ...[more]

PMID: 34638280

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Project description:Background & Aims: Extracellular vesicles (EVs) play a pivotal role in connecting tumor cells and their local and distant microenvironment. Here, we aimed to understand the role and molecular basis of patient-derived EVs in modulating cancer stemness and tumorigenesis in the context of hepatocellular carcinoma (HCC). Methods: EVs were isolated, quantified and characterized from patients’ sera. EVs were tested vigorously, both in vitro and in vivo, by various functional assays. Proteomic analysis was performed to identify the functional components of EVs. The expression level of polymeric immunoglobulin receptor (pIgR) in circulating EVs, tumor and non-tumorous tissues of HCC patients was determined by ELISA, immunoblotting, immunohistochemistry and quantitative PCR. The functional role and underlying mechanism of EVs with an enhanced pIgR expression was elucidated. Blockage of EV-pIgR with neutralizing antibody was performed in nude mice implanted with patient-derived tumor xenograft (PDTX). Results: Circulating EVs of late-stage HCC (L-HCC) patient had significantly elevated pIgR expression when compared to the EVs released by control individuals. The augmenting effect of L-HCC patient in cancer stemness and tumorigenesis was hindered by anti-pIgR antibody. EVs enriched with pIgR consistently promoted cancer stemness and cancerous phenotypes in the recipient cells. Mechanistically, EV-pIgR-induced cancer aggressiveness was abrogated by Akt and β-catenin inhibitors, ascertaining the role of EV-pIgR through the activation of PDK1/Akt/GSK3β/β-catenin signaling axis. Furthermore, anti-pIgR neutralizing antibody attenuated the tumor growth in mice implanted with PDTX. Conclusion: The study illustrates an unrevealed role of EV-pIgR in regulating cancer stemness and aggressiveness, in which EV-pIgR activates PDK1/Akt/GSK3β/β-catenin signaling cascades. The blockage of intercellular communications mediated by EV-pIgR in the tumor microenvironment may provide a new therapeutic strategy for cancer patients.

Dataset Information

Protein expression profile of miR-33b overexpressing ES-2 cells upon OCM treatment

Publications

Epigenetic Silencing of miR-33b Promotes Peritoneal Metastases of Ovarian Cancer by Modulating the TAK1/FASN/CPT1A/NF-κB Axis.

Similar Datasets

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