Repressing phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit gamma by microRNA-142-3p restrains the progression of hepatocellular carcinoma
Authors: Airong Hu
Chuanli Zeng
Yina Meng
Donghui Wang
Gang Yuan
Xiaojun Shi
Jialin Lu
Dedong Zhu
Yaoren Hu
Journal: Bioengineered (2022)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Mir-142-3p; apoptosis; hepatocellular carcinoma; pik3cg.
Affiliations: Department of Severe Liver Disease, Ningbo HuaMei Hospital, University of Chinese Academy of Science, Ningbo, Zhejiang, China, Department of Acute Infection, Ningbo Huamei Hospital, University of Chinese Academy of Science, Ningbo, Zhejiang, China, Department of Hepatology, Ningbo Huamei Hospital, University of Chinese Academy of Science, Ningbo, Zhejiang, China, Institute of Liver Disease, Ningbo Huamei Hospital, University of Chinese Academy of Sciences, Ningbo, Zhejiang, China, Medical School of Ningbo University, Ningbo, Zhejiang, China

Abstract:  This paper probes the mechanisms underlying miR-142-3p's modulation of hepatocellular carcinoma (HCC) invasion and apoptosis. Quantitative real-time PCR and Western blot monitored the miR-142-3p profile in HCC tissues and non-tumor tissues. The correlation between miR-142-3p expression and HCC patients' clinicopathological indicators was analyzed. miR-142-3p overexpression and knockdown models were established in HCC cell lines. Cell proliferation was gauged by the colony formation assay and BrdU staining. For measuring apoptosis, flow cytometry and Western blot were implemented. Transwell assay tested cell migration and invasion. miR-142-3p mimics or inhibitors were transfected in Huh7 and HCCLM3 cells. The targeting association between miR-142-3p and PIK3CG was predicted through bioinformatics and further verified by related experiments. The influence of PIK3CG overexpression on miR-142-3p's role in HCC was assayed. A xenografted tumor model was built in mice to validate miR-142-3p knockdown's influence on HCC in vivo. As a result, miR-142-3p exhibited a decreased profile in HCC tissues and cells. Overexpressing miR-142-3p accelerated apoptosis and suppressed the PI3K/AKT/HIF-1α signal. Knocking down miR-142-3p presented opposite effects. PIK3CG overexpression dampened the anti-tumor effect of miR-142-3p. miR-142-3p repressed HCC invasion and intensified apoptosis to restrain HCC by abating the PIK3CG-mediated PI3K/AKT/HIF-1α pathway. 

Retracted: No

PubPeer comments:
 Can I ask the authors to please provide the details for the use of patient materials in this study (approval number)? Furthermore, I have some concerns regarding this paper: Two PCR primers listed in Materials and Methods appear to be incorrect (NCBI blastn human G+T standard databases was used; only forward primers were checked). Details regarding methods are not provided. Eg. for the Western immunoblotting, the instrument for reading the ECL signal is not provided. There is a reference to another study (Ref. 24), but in the cited paper (also a Bioengineered paper) there is no further information). When looking at the Reference list, a total of five Bioengineered paper are listed. Four are from 2021, one from 2020. They are listed successively and they seem to not bring any further information, indicating that they are included just to pump up the journal impact factor. The methodical details regarding the xenograft experiments show a mismatch between what is presented in the Materials and Methods and in the Results section Figure 4 legend. ![file] ![file] ,