miR-22 inhibits proliferation and invasion in estrogen receptor α-positive endometrial endometrioid carcinomas cells
Authors: Fang Guo
Xiaoli Li
Shaoru Li
Chuanhong Wang
Shijin Wang
Ruili Hu
Journal: Molecular Medicine Reports (2014)
Discipline: CLINICAL MEDICINE
Keywords: Endometrial endometrioid carcinomas; EEC; estrogen receptor; ERα; MicroRNA-22
Affiliations: Department of Gynecology and Obstetrics, The First Affiliated Hospital of Xinxiang Medical University, Weihui, Henan 453100, P.R. China., Department of Gynecology and Obstetrics, Maternal and Child Health Hospital of Zhengzhou City, Zhengzhou, Henan 450012, P.R. China., Department of Gynecology and Obstetrics, Maternal and Child Health Hospital of Fangcheng County, Nanyang, Henan 473200, P.R. China.

Abstract:  Endometrial endometrioid carcinomas (EECs) account for &gt;80% of endometrial carcinomas (ECs). Continuous stimulation of the endometrium by estrogen is a risk factor for the tumorigenesis of estrogen receptor (ER) α-positive EEC. MicroRNA-22 (miR-22) has been reported to be implicated in the regulation of various types of cancer and directly targets ERα. However, an exact regulatory mechanism between miR-22 and ERα in EEC has yet to be investigated. To the best of our knowledge, the present study demonstrated for the first time that the expression of miR-22 was significantly downregulated in ERα-positive EEC tissues and cell lines, RL95-2 and Ishikawa, when compared with that in normal endometrium and ERα-negative EEC samples. This indicated that miR-22 may be important in ERα-positive EEC, possibly through an estrogen-dependent mechanism. miR-22 mimics were then transfected into RL95-2 and Ishikawa cells, respectively, and revealed that the introduction of miR-22 markedly downregulated the mRNA and protein levels of ERα. Further investigation demonstrated that miR-22 was able to effectively reverse 17β-estradiol (E2)‑induced cell proliferation, cell cycle progression and invasion of ERα-positive RL95-2 and Ishikawa cells, at least partially through inhibiting the expression of Cyclin D1 as well as the secretion of matrix metalloproteinase (MMP)-2 and MMP-9. In conclusion, the present study, to the best of our knowledge, was the first to reveal an inhibitory role of miR-22 in ERα-positive EEC tissues and cells, indicating that miR-22 may be a novel candidate for the endocrine therapy of ERα-positive EEC. 

Retracted: Yes

PubPeer comments:
 Fig 5A.  Transwell assay was performed to determine the effect of miR-22 on E2-induced cell invasion in RL95-2 and Ishikawa cells . ![file] Colored rectangles refer to Fig 6 from [Chen et al (2014)] .  PLD2 overexpression abrogated the suppressive effect of miR-203 on U251 cell invasion. Cell invasion assay was performed to determine the effects of miR-203 and PLD2 on U251 cell invasion . Many other appearances of the same panel are linked in that thread. ![file] Fig 3A from [Dai et al (2015)] .  A Transwell assay was performed to determine the effect of Res on cell invasion of JJ012 chondrosarcoma cells . ![file] Figs 4B and 5B from [Lei et al (2015)] .  Cell invasion assay was performed on MG63 cells with or without transfection with galectin-3-specific siRNA ;  Transwell assay was performed to examine the invasive capacity of MG63 cells transfected with galectin-3 siRNA, with or without pre-treatment of curcumin . ![file] , 
 Fig 4A.  miR-22 inhibited E2-induced cell cycle progression in RL95-2 and Ishikawa cells. (A) Cell cycle assay was performed to investigate the effect of miR-22 on E2-induced cell cycle progression in RL95-2 and Ishikawa cells. ![file] Fig 4A from [Meng et al (2015)] .  A cell-cycle assay was used to examine the cell-cycle distribution of MCF-7 cells following transfection with the microRNA-335 (miR-335) mimic or inhibitor, or co-transfection with the miR-335 inhibitor and the paired box 6 (PAX6) small interfering RNA (siRNA). Control, non-transfected MCF-7 cells. ![file] Fig 3 of [Liu et al (2016)] . ![file] How to explain the shared panels? UPDATE. Three more panels are shared with Fig 3 of [Chen et al (2016)] .  B16 and A375 cells were transfected with miR-NC or miR-18b mimic, respectively. (A and B) Cell cycle distribution was determined using flow cytometry . ![file] And bright blue panel, shared with Fig 3 of [Zhou et al (2017)] .  Cell cycle analysis was performed to examine the cell cycle distribution in each group. Non-transfected EPCs were used as a control. ![file] The earliest sighting so far is Fig 3 from [Wang et al (2013)] .  Effects of miR-138 RhoC on cell viability and cell cycle distribution. The cholangiocarcinoma cells were transfected with miR-138 mimics, miR-138 inhibtor (inhibitor) or negative control (NC) of miR-138 . ![file] , 
 Retracted [9 July 2021] . ------------------------------------------ Following the publication of this paper, it was drawn to the Editors attention by a concerned reader that certain of the cellu2011cycle data shown in Fig. 4A and Transwell cell migration data shown in Fig. 5A were strikingly similar to data appearing in different form in other articles by different authors. Owing to the fact that the contentious data in the above article had already been published elsewhere, or were already under consideration for publication, prior to its submission to *Molecular Medicine Reports*, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive any reply. The Editor apologizes to the readership for any inconvenience caused ,