Àá½Ã¸¸ ±â´Ù·Á ÁÖ¼¼¿ä. ·ÎµùÁßÀÔ´Ï´Ù.
KMID : 0311120200610050371
Yonsei Medical Journal
2020 Volume.61 No. 5 p.371 ~ p.381
NUP210 and MicroRNA-22 Modulate Fas to Elicit HeLa Cell Cycle Arrest
Gu Qiao

Hou Wenjie
Liu Huan
Shi Lijuan
Zhu Zonghao
Ye Wenfeng
Ni Xiaoyuan
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.
KEYWORD
Cervical cancer, apoptosis, cell cycle arrest, Fas, miR-22, NUP210
FullTexts / Linksout information
  
Listed journal information
SCI(E) MEDLINE ÇмúÁøÈïÀç´Ü(KCI) KoreaMed