MicroRNA‚Ä?14 promotes proliferation and inhibits apoptosis via targeting Bax in nasopharyngeal carcinoma cells
Authors: Yongquan Tian
Yaoyun Tang
Jian He
Journal: Molecular Medicine Reports (2015)
Discipline: CLINICAL MEDICINE
Keywords: miR-214; nasopharyngeal carcinoma; proliferation; apoptosis; Bax
Affiliations: Department of Otorhinolaryngology Head and Neck Surgery, Xiangya Hospital of Central South University, Changsha, Hunan 410008, P.R. China.

Abstract:  The deregulation of microRNAs (miRNAs) is involved in the development and progression of various types of human malignancy. Previously, it has been suggested that miR‚Ä?14 has an oncogenic role in nasopharyngeal carcinoma. However, the detailed molecular mechanisms remain to be elucidated. In the present study, reverse transcription‚Äëquantitative polymerase chain reaction and western blot analysis were conducted to determine the relative mRNA and protein levels, respectively. The MTT assay was performed to examine cell proliferation. Flow cytometry was conducted to determine cell apoptosis level. In the present study, the expression of miR‚Ä?14 was found to be notably upregulated in nasopharyngeal carcinoma tissues and cell lines. Further investigation demonstrated that inhibition of miR‚Ä?14 inhibited proliferation and promoted apoptosis in nasopharyngeal carcinoma cells. By contrast, overexpression of miR‚Ä?14 promoted nasopharyngeal carcinoma cell proliferation and inhibited cell apoptosis. Bcl‚Ä?‚Äëassociated X protein (Bax) was then identified as a novel target of miR‚Ä?14. miR‚Ä?14 negatively regulated the protein expression of Bax in nasopharyngeal carcinoma cells. siRNA‚Äëinduced Bax inhibition attenuated the promoting effect of miR‚Ä?14 downregulation on nasopharyngeal carcinoma cell apoptosis, suggesting that Bax acts as a downstream effector in miR‚Ä?14‚Äëmediated nasopharyngeal carcinoma cell proliferation and apoptosis. Finally, the present study demonstrated that the expression level of Bax was downregulated in nasopharyngeal carcinoma tissues. In conclusion, the present study suggests that miR‚Ä?14 may be a potential target for the treatment of nasopharyngeal carcinoma. 

Retracted: Yes

PubPeer comments:
 Figs 2C; 4B  A cell apoptosis assay was performed to examine the cell proliferation of CNE1 cells transfected with miR-214 mimics or the miR-214 inhibitor ;  A cell apoptosis assay was performed to determine the apoptotic rate of CNE1 cells transfected with the miR-214 inhibitor or co-transfected with the miR-214 inhibitor and Bax siRNA .  *[above]* Fig 4A from [Peng et al (2013)] .  Flow cytometry was used to determine the apoptotic rate of U87 and CHG-5 cells after forced downregulation of RACK1.  *[below[* Fig 4B from [Lai, Chen Li (2015)] .  ... a Transwell assay were performed to examine the cell proliferation of AGS cells transfected with miR-133a mimics, miR-133a inhibitor, or co-transfected with miR-133a mimics and FSCN1 plasmid. Control: AGS cells without any transfection.  Figs 1C, 4D from [Zhao et al (2015)] .  Overexpression of miR-148a promoted paclitaxel-induced cell apoptosis, whereas inhibition of miR-148a suppressed paclitaxel-induced cell apoptosis, compared with the control group ;  Overexpression of PDIA3 inhibited paclitaxel-induced cell apoptosis, whereas inhibition of PDIA3 promoted paclitaxel-induced cell apoptosis, compared with the control .  Surprisingly similar hockey-sticks. , 
 Retracted [2 August 2021] . ------------------------------- Following the publication of this paper, it was drawn to the Editorsu2019 attention by a concerned reader that certain of the cell apoptotic assay data shown in Figs. 2C and 4B 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. ,