NUP210 and MicroRNA-22 Modulate Fas to Elicit HeLa Cell Cycle Arrest.

Abstract:

PURPOSE:Cervical cancer is one of the most fatal diseases among women in under-developed countries. To improve cervical cancer treatment, discovery of new targets is needed. In this study, we investigated the expression of NUP210, miR-22, and Fas in cervical cancer tissues and their functions in cell cycle regulation. MATERIALS AND METHODS:We detected and compared the expression levels of NUP210, miR-22, and Fas in cervical cancer tissues with paired normal tissues using immunohistochemistry, Western blot, and real-time quantitative polymerase chain reaction. NUP210 was knocked down in HeLa cells via lentivirus, followed by cell cycle and proliferation analysis. Using a luciferase reporter assay, we explored the link between miR-22 and NUP210. We overexpressed miR-22 in HeLa cells and analyzed cell cycle and proliferation function. We then overexpressed miR-22 in NUP210 knockdown cells to explore the connection between Fas and miR-22-NUP210 signaling. RESULTS:We found that NUP210 was overexpressed in cervical cancer patients. Knocking down NUP210 restored cell apoptosis and proliferation. We confirmed miR-22 as a regulator of NUP210 and verified that miR-22 was inhibited in cervical cancer development. We also found that restoring miR-22 expression could induce cell apoptosis. Finally, we found that miR-22-regulated expression of NUP210 could alter Fas expression and, in turn, elicit cell cycle arrest and proliferation. CONCLUSION:miR-22 in cervical cancer is downregulated, resulting in NUP210 overexpression and inhibition of Fas-induced cell apoptosis.

journal_name

Yonsei Med J

journal_title

Yonsei medical journal

authors

Gu Q,Hou W,Liu H,Shi L,Zhu Z,Ye W,Ni X

doi

10.3349/ymj.2020.61.5.371

subject

Has Abstract

pub_date

2020-05-01 00:00:00

pages

371-381

issue

5

eissn

0513-5796

issn

1976-2437

pii

61.371

journal_volume

61

pub_type

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