miRNA-217 inhibits proliferation of hepatocellular carcinoma cells by regulating KLF5
Authors: F Wang
Y-X Lu
W Gao
H-Y Wu
J-X Bian
J Sun
Journal: European review for medical and pharmacological sciences (2019)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: microRNA-217; hepatocellular carcinoma; KLF5; proliferation; expression
Affiliations: School of Nursing, Jiangsu Vocational College of Medicine, Yancheng, China. .

Abstract:  Objective: The aim of this study was to figure out the effect of microRNA-217 on the proliferation of hepatocellular carcinoma (HCC) cells, and to explore its influence on KLF5 expression and the underlying regulatory mechanisms. Patients and methods: Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was used to detect the expression of microRNA-217 in tumor tissues and paracancerous tissues of 60 patients with HCC. Meanwhile, the relationship between microRNA-217 expression and HCC pathological parameters was analyzed. In HCC cell lines, including HepG2 and Bel-7402, negative control group (NC) and microRNA-217 overexpression group were set up, and qRT-PCR was performed to further verify their transfection efficiency. In addition, Cell Counting Kit-8 (CCK-8), 5-Ethynyl-2'-deoxyuridine (EdU) assay were performed to analyze the effect of microRNA-217 on the biological function of HCC cells. Finally, the potential mechanism of KLF5, the downstream gene of microRNA-217, was explored using bioinformatics analysis and cell recovery experiments. Results: QRT-PCR results showed that microRNA-217 level in tumor tissues of HCC patients was conspicuously lower than that in adjacent tissues, and the difference was statistically significant. Compared with patients with high expression of microRNA-217, the pathological stage was higher and the overall survival rate was lower in patients with low expression. Compared with the NC group, the cell proliferation ability of the microRNA-217 mimics group was conspicuously decreased. Subsequently, in the HCC cell line and tissue verification, the expression of KLF5 was found remarkably increased, and microRNA-217 exhibited a negative correlation with KLF5 level. In addition, the overexpression of microRNA-217 conspicuously reduced the protein expression of CD31, Ki-67, c-Myc, MMP-2, and MMP-9. In cell recovery experiment, it was found that the overexpression of KLF5 could counteract the effect of microRNA-217 mimics on the cell proliferation of HCC, thereby inhibiting the malignant progression of this disease. Conclusions: The above studies demonstrated that microRNA-217 was markedly associated with the pathological stage and poor prognosis of HCC, and could inhibit the malignant progression of this disease. In addition, our investigation has showed that microRNA-217 might be capable of inhibiting cell proliferation of HCC via regulating KLF5. 

Retracted: No

PubPeer comments:
 From left to right: - Fig 1 from [Zang et al (2020)] - Fig 1 from [Li et al (2020)] - Fig 1, and Fig 4D, from [Cui et al (2019)] - **Fig 1D from [Gao et al (2019)] **. ![file] It appears that **any** combination of a cancer type, and the undesirable half of a non-coding RNA dichotomy, results in 100% mortality at 75 months. More examples: *[left]* Figure 1C from [Wu et al (2020)] . *[right]* Fig 3E from [Wu et al (2019)] . ![file] , 
 *[left]* Fig 3C from [Gao et al (2019)] .  miR-217 in hepatocellular carcinoma tissues was markedly negatively correlated with the expression level of KLF5 . *[right]* Fig 3E from [Xu et al (2019)] .  MiR-424-5p was significantly negatively correlated with the expression level of ITGB1 in NSCLC tissues. All 16 points from 3C are also present in 3E. It is rather depressing how little effort goes into this entire genre of research . ![file] , 
  Our research was approved by the Ethics Oversight Committee. Authors are spread across three institutions: Jiangsu Vocational College of Medicine, China Pharmaceutical University, and Nanjing University of Chinese Medicine Hanlin College. Evasiveness about (a) specific recruitment of the purported patients and (b) the source of ethics approval does not foster confidence in the existence of those patients. ,