Back to Search Start Over

Loss of hsa_circ_0118530 inhibits human granulosa-like tumor cell line KGN cell injury by sponging miR-136.

Authors :
Jia, Chanwei
Wang, Shuyu
Yin, Chenghong
Liu, Lingyan
Zhou, Liying
Ma, Yanmin
Source :
Gene. Jun2020, Vol. 744, pN.PAG-N.PAG. 1p.
Publication Year :
2020

Abstract

• hsa_circ_0118530 was elevated in EC. • hsa_circ_0118530 induced EC cell progression. • hsa_circ_0118530 acted as a sponge of miR-136. Polycystic ovary syndrome (PCOS) is a kind of endocrine disease among women across the global. Recently, many researches have reported circular RNAs can act as significant molecular biomarkers for diseases, especially in tumors. Several Circular RNAs are reported to be aberrantly expressed in PCOS patients. Here, we investigated the biological effects of hsa_circ_0118530 on human granulosa cells, KGN. We observed that hsa_circ_0118530 was greatly elevated in PCOS patients and granulosa cells (including KGN and COV434 cells) compared to normal IOSE80 cells. hsa_circ_0118530 siRNA was transfected into KGN cells. We found that KGN cell viability was repressed, cell apoptosis was induced while cell migration was greatly inhibited. TGF-β1 was utilized to induce EMT process. As shown, loss of hsa_circ_0118530 significantly enhanced E-cadherin mRNA and protein levels while depressed N-cadherin expression. Furthermore, we indicated that decrease of hsa_circ_0118530 was able to inhibit ROS accumulation, MDA levels while induced SOD activity. Next, it was demonstrated that releases of inflammatory cytokine were suppressed by hsa_circ_0118530 down-regulation. Additionally, miR-136 was predicted and confirmed as the target of hsa_circ_0118530. For another, the functions of hsa_circ_0118530 on KGN cell progression, oxidative stress and inflammation releases were obviously reversed by miR-136 suppression. In conclusion, knockdown of hsa_circ_0118530 repressed PCOS progression via sponging miR-136. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
03781119
Volume :
744
Database :
Academic Search Index
Journal :
Gene
Publication Type :
Academic Journal
Accession number :
143172366
Full Text :
https://doi.org/10.1016/j.gene.2020.144591