MicroRNA-21 promotes the proliferation and inhibits apoptosis in Eca109 via activating ERK1/2/MAPK pathway
Authors: Wenya Liu
Xiuling Li
Qing Liu
Meng Liang
Shutao Zheng
Fengxia Liu
Xiaomei Lu
Ilyar Sheyhidin
Tao Liu
Journal: Molecular and cellular biochemistry (2013)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: miR-21; proliferation; apoptosis; esophageal squamous cell carcinoma (ESCC); Eca109 cells
Affiliations: State Key Lab Breeding Base of Xinjiang Major Diseases Research, First Affiliated Hospital of Xinjiang Medical University, Urumqi, Xinjiang Uygur Autonomous Region, People's Republic of China.

Abstract:  The aim of this study was to investigate how miR-21 promotes proliferation and inhibits apoptosis in esophageal squamous cell carcinoma (ESCC). MTT, wound healing assay and cell cycle showed that proliferation and migration of ESCC cell line Eca109 cells were increased in miR-21 mimics group, and decreased in anti-miR-21 Oligonucleotide (AMO) group after transfection into Eca109 cells with miR-21 mimics, AMO and scramble sequence, respectively. Cell apoptosis assay indicated that cell apoptosis can be obviously inhibited by overexpression of miR-21 and promoted by downregulation of miR-21. Meanwhile, western-blot results showed that p-ERK1/2 expression was elevated in miR-21 mimics group, whereas decreased in AMO group. Furthermore, the ERK1/2, a key component of MAPK signaling pathway, was knocked down, and overexpressed successfully using shRNA-ERK1/2 and overexpressing plasmids containing full length cDNA of ERK1/2, respectively. It was observed that shRNA-ERK1/2 can significantly decreased the level of miR-21 expression, while overexpression of ERK1/2 can up-regulate expression of miR-21. As further confirmation, Eca109 cells were treated with gradient concentration of U0126, a kind of MEK inhibitor, and expression of miR-21 was subsequently examined. It was found that U0126 can significantly decreased endogenous expression of miR-21. In parallel, U0126 decreased cell proliferation, migration and increased the apoptosis in Eca109 cells, with the expression of miR-21 being reduced significantly in U0126 group as compared with control groups. Our findings indicated that miR-21 promoted the proliferation, migration and inhibited apoptosis of Eca109 cells through activating ERK1/2/MAPK pathway, and that targeting miR-21 could be a promising therapeutic strategy in ESCC. 

Retracted: No

PubPeer comments:
 Figure 1C and 4B. * Some panels displaying different experiments appear to overlap. Partially reported (minus yellow boxes) to the journal in October 2015, with a friendly reminder in 2017, but no response as of today. I would love to hear from the authors if the journal ever contacted them in the past five years. ![file] , 
 #1 Dear Elisabeth Thank you so much for pointing out the error we had inadvertently made in this paper. We have been aware of the error and now going to try to apply for Erratum Correction from editor as soon as we can. This error will not affect the overall conclusions. The answer to the question you have to us is that, by now, we actually have never heard from any email from the Editor of this journal requiring us to respond on the matter we talk of. Anyway, we will actively contact the Editor as soon as possible on this matter. At last, we apologize for the inconvenience brought about by this error we had inadvertently made. Best regards Xiaomei Lu. , 
 #2 Is there an update on this correction? There are multiple papers with similar issues with at least one overlapping author: https: pubpeer.com search?q=+Ilyar+Sheyhidin, suggestive of a systemic problem. , 
 @Actinopolyspora Biskrensis, thank you for your concern for our paper. actually, we had ever tried to repeatedly reach out to the Editor by email after our paper being pointed out by peers. disappointingly, editors from this journal seems to neglect our request for up-dating. therefore, we end up failing to up-date the paper with correction. hope it explains. ,