Inhibition of microRNA-181a may suppress proliferation and invasion and promote apoptosis of cervical cancer cells through the PTEN/Akt/FOXO1 pathway
Authors: Hua Song
Jihong Zhu
Yiyang Li
Hongmei Xu
Cong Hu
Journal: Journal of Physiology and Biochemistry (2016)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Apoptosis; Cervical cancer; Invasion; MicroRNA-181a; PTEN/Akt/FOXO1 signaling pathway.
Affiliations: Department of Obstetrics, the First Hospital of Jilin University, Changchun, 130021, China., Section I, Department of General Gynecology, the First Hospital of Jilin University, No. 71, Xinmin Street, Changchun, 130021, China., Reproductive Center, the First Hospital of Jilin University, Changchun, 130021, China., Department of Gynecology and Obstetrics, Qianwei Hospital of Jilin Province, Changchun, 130012, China., Section I, Department of General Gynecology, the First Hospital of Jilin University, No. 71, Xinmin Street, Changchun, 130021, China. .

Abstract:  MicroRNAs (miRNAs) are endogenous, non-coding, small RNAs, which play a critical role in regulating varieties of the biological and pathologic processes. miR-181a has been reported to participate in tumorigenic progression. However, the roles of miR-181a in cervical cancer (CC) are still unknown. The aim of this research was to explore the effects and molecular mechanism of miR-181a in CC cells. In this paper, the levels of miR-181a in CC cell lines were determined by real-time PCR. We found that the levels of miR-181a were evidently enhanced in CC cell lines compared with normal cervical epithelium cells. Then, the miR-181a inhibitor was transiently transfected into HeLa and CaSKi cells using Lipofectamine 2000 reagent. Subsequently, the Cell Counting Kit-8 (CCK-8) and BrdU-ELISA results showed that down-regulation of miR-181a inhibited the cell viability and proliferation. Our data also demonstrated that miR-181a inhibitor arrested cell cycle progression of HeLa and CaSKi cells by up-regulation of p21 and p27 expressions. In addition, inhibition of miR-181a promoted apoptosis of HeLa and CaSKi cells due to increasing Bax expression and decreasing Bcl-2 expression. Ultimately, the effect of miR-181a inhibitor on the PTEN/Akt/FOXO1 signaling pathway was investigated by Western blot. From our results, down-regulation of miR-181a increased the expression of PTEN and decreased phosphorylation of Akt and FOXO1. Altogether, miR-181a might be an oncogene in CC cells. The potential mechanism was that inhibition of miR-181a might suppress proliferation and invasion and promote apoptosis of HeLa and CaSKi cells by modulating the PTEN/Akt/FOXO1 signaling pathway. 

Retracted: No

PubPeer comments:
  Fig. 5 Down-regulation of miR-181a suppressed invasion of CC cells. HeLa and CaSKi cells were transfected with anti-miR-181a or anti-miR-NC, and then seeded in the top chamber ![file] Transfected HeLa and CaSKi cells are more similar than one might expect. , 
 Figs 5(D)  STAT3, p-STAT3, CyclinD1, and Bcl-2 protein expression levels were determined by western blot in RA-FLS cells transfected with miR-29a mimic or miR-NC. GAPDH was used as an internal control *[at right]* and 7(A)  STAT3 protein expression was measured by western blot in RA-FLS transfected with miR-29a miR-NC and with without STAT3 overexpression plasmid *[at left]*. ![file] Bands have been duplicated (with a 180-deg rotation). ,