LncRNA LINC01305 silencing inhibits cell epithelial‚Äêmesenchymal transition in cervical cancer by inhibiting TNXB‚Äêmediated PI3K/Akt signalling pathway
Authors: Hai-Feng Qiu
Ya Xie
Wen-Cai Li
Dan-Xia Chu
Chun-Fang Wang
Shu-Ping Yan
Rui-Xia Guo
Jian-Ying Zhang
Journal: Journal of Cellular and Molecular Medicine (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: PI3K/Akt signalling pathway; TNXB; cervical cancer; epithelial-mesenchymal transition; invasion
Affiliations: Department of Pathology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan Province, P.R. China., Department of Pathology, School of Basic Medicine, Zhengzhou University, Zhengzhou, Henan Province, P.R. China., Henan Key Laboratory for Tumor Pathology, Zhengzhou, Henan Province, P.R. China., Department of Gynecology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan Province, P.R. China., Institute of Medical and Pharmaceutical Sciences, Zhengzhou University, Zhengzhou, Henan Province, P.R. China.

Abstract:  Cervical cancer (CC) remains one of the leading malignancies afflicting females worldwide, with its aetiology associated with long-term papillomavirus infection. Recent studies have shifted their focus and research attention to the relationship between long non-coding RNAs (lncRNAs) and CC therapeutic. Thus, the aim of the current study was to investigate the underlying mechanism of lncRNA LINC01305 on the cell invasion, migration and epithelial-mesenchymal transition (EMT) of CC cells via modulation of the PI3K/Akt signalling pathway by targeting tenascin-X B (TNXB). The expressions of LINC01305, TNXB, MMP2, MMP9, E-cadherin, vimentin, PI3K, Akt, p-PI3K, p-Akt and TNXB were detected in this study. After which, the cell invasion and migration abilities of the CC cells were determined respectively. Bioinformatics and the application of a dual luciferase reporter gene assay provided verification indicating that TNXB is the target gene of lncRNA LINC01305. Reverse transcription quantitative polymerase chain reaction (RT-qPCR) and western blot analysis methods revealed that the expressions of MMP2, MMP9, vimentin, PI3K, Akt, p-PI3K and p-Akt were decreased following the down-regulation of LncRNA LINC01305 or overexpression of TNXB. LncRNA LINC01305 silencing or TNXB overexpression was noted to decrease the migration and invasion of SiHa cells. Taken together, the key findings of the current study present evidence suggesting that lncRNA LINC01305 silencing suppresses EMT, invasion and migration via repressing the PI3K/Akt signalling pathway by means of targeting TNXB in CC cells, which ultimately provides novel insight and identification of potential therapeutic targets for CC. 

Retracted: Yes

PubPeer comments:
 Fig 7A,  LncRNA LINC01305 silencing reduces cell invasion in SiHa cells. A, The images of transwell invasion of SiHa cells in each group .  Shares a panel in common with Fig 9B from [Wu et al (2018)] ,  Cell invasion conditions after transfection among the eight groups, as confirmed by the Transwell assay .  No obvious connection among the teams of researchers. , 
 Fig 5B:  The electrophoresis bands of MMP2, MMP9, Eu2010cadherin, vimentin, PI3K, Akt, pu2010PI3K, pu2010Akt and TNXB proteins in SiHa cells .  Two other occurrences of the same loading band: Fig 9A from [Wu et al (2018a)] and 5C from [Wu et al (2018b)] . More examples in those threads.  , 
 #1 More going on in Fig 7A than I originally noticed.  , 
 Retracted [1 October 2021] . ------------------- The above article from *Journal of Cellular and Molecular Medicine*, published online on 29 January 2020 on Wiley Online Library , has been retracted by agreement between the journal Editor-in-Chief and John Wiley Sons Ltd. The retraction has been agreed following an investigation based on allegations raised by a third party. A detailed investigation revealed that several image elements of the experimental data were published elsewhere in a different scientific context, while duplications were found in two images in the paper. Based on the findings, the editors consider the conclusions invalid. Despite several attempts of contact with all authors of the paper, a response was not received. ,