NOL6 promotes the proliferation and migration of endometrial cancer cells by regulating TWIST1 expression

Aim: To investigate the role and function of NOL6, a protein related to ribosome biogenesis, in endometrial cancer. Methods: Methyl thiazolyl tetrazolium assay, colony formation assay, flow cytometry apoptosis assay, transwell and wound healing assays were carried out for evaluating cell proliferation, migration and apoptosis. Immunohistochemistry, western blot and tumor xenograft assays were carried out for detecting the level of protein expression and tumor formation. Results: We demonstrated that NOL6 is overexpressed in endometrial cancer and promotes cell proliferation and migration while reducing apoptosis. NOL6 regulates the expression of TWIST1, which can restore the changes in cells caused by NOL6 knockdown. Conclusions: NOL6 can promote the proliferation and migration of endometrial cancer cells by regulating TWIST1 expression.

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Human Umbilical Cord Mesenchymal Stem Cell-Derived Extracellular Vesicles Inhibit Endometrial Cancer Cell Proliferation and Migration through Delivery of Exogenous miR-302a

Stem Cells International ◽

10.1155/2019/8108576 ◽

2019 ◽

Vol 2019 ◽

pp. 1-11 ◽

Cited By ~ 9

Author(s):

Xin Li ◽

Li li Liu ◽

Ju lei Yao ◽

Kai Wang ◽

Hao Ai

Keyword(s):

Cell Proliferation ◽

Endometrial Cancer ◽

Cancer Cells ◽

Umbilical Cord ◽

Extracellular Vesicles ◽

Target Cells ◽

Human Umbilical Cord ◽

Cell Proliferation And Migration ◽

And Migration ◽

Proliferation And Migration

MicroRNAs (miRNAs) are potential therapeutic targets in endometrial cancer, but the difficulties associated with their delivery to tumor target cells have hampered their applications. Human umbilical cord mesenchymal stem cells (hUCMSCs) have a well-recognized tumor-homing ability, emphasizing the capacity of tumor-targeted delivery of extracellular vesicles. hUCMSCs release extracellular vesicles rich in miRNAs, which play a vital role in intercellular communication. The purpose of this study was to verify a potential tumor suppressor microRNA, miR-302a, and engineered hUCMSC extracellular vesicles enriched with miR-302a for therapy of endometrial cancer. Here, we observed that miR-302a was significantly downregulated in endometrial cancer tissues when compared with adjacent tissues. Overexpression of miR-302a in endometrial cancer cells robustly suppressed cell proliferation and migration. Meanwhile, the proliferation and migration were significantly inhibited in endometrial cancer cells when cultured with miR-302a-loaded extracellular vesicles derived from hUCMSCs. Importantly, our data showed that engineered extracellular vesicles rich in miR-302 significantly inhibited the expression of cyclin D1 and suppressed AKT signaling pathway in endometrial cancer cells. These results suggested that exogenous miR-302a delivered by hUCMSC-derived extracellular vesicles has exciting potential as an effective anticancer therapy.

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