Research on Mechanism of miRNA-22 Related with Hepatocellular Carcinoma Metastasis for Regulating Process of Tumor Protein P53

2021 ◽  
Vol 11 (11) ◽  
pp. 2115-2119
Author(s):  
Gang Pan ◽  
Min Xiao

The action of miRNA-22 related with HCC metastasis was analyzed in our study and the mechanism of miRNA-22 related with HCC metastasis was discussed. The HCC hep2 cell was transfected with miRNA-22 mimics and miRNA-22 NC instantaneously followed by analysis of cell migration by Transwell assay, cell viability by MTT and clone formation and cell apoptosis by flow cytometry. The action of miRNA-22 mimics and miRNA-22 on the expression of P53 mRNA in HCC Hep2 cell was detected by RT-PCR. The cell activity in miRNA-22 mimics group was significantly elevated compared with miRNA-22 NC group (P < 0.01). Meanwhile, the apoptotic rate, migrated and invaded capacity of HCC cell was significantly elevated (P < 0.01). The expression level of P53 mRNA was reduced (P < 0.01). In conclusion, overexpression of miRNA-22 could restrain the apoptosis of HCC hep2 cell and down-regulated the expression of P53 so as to prompt cell invasion capacity.

2020 ◽  
Author(s):  
Lirui Tu ◽  
Jing Liu ◽  
Wei Li ◽  
Xiuguang Song ◽  
Hongwei Xu

Abstract Background Hepatocellular carcinoma (HCC) is a common malignant cancer worldwide. miR-577 have a role in inhibiting cell viability, metastasis in many tumors. This research was to explore the great role of miR-577 in hepatocellular carcinoma. Methods RT-qPCR and western blot were performed to evaluate the the miR-577 and genes mRNA and protein levels. Transwell assay and CCK-8 were applied to measure the viable and invasive abilities. Meanwhile, Kaplan-Meier method was used to assess the survival of HCC patients. Results miR-577 was downregulated in HCC tissues, which predicted a worse overall survival in HCC. miR-577 targeted to CXCL5 and mediated its expression in HCC. miR-577 suppressed cell invasion and EMT in HuH-7 cells. miR-577 inhibited cell viability via NF-κB pathway. In addition, miR-577 overxpression impaired the xenograft growth of HuH-7 cells. Conclusion miR-577 inhibited cell invasion, EMT and viability via NF-κB pathway by targeting to CXCL5 in HCC. The newly identified miR-577/CXCL5 axis provides novel insight into the pathogenesis of hepatocellular carcinoma.


2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Xiao-Peng Chen ◽  
Jun-Sheng Luo ◽  
Ye Tian ◽  
Chen-Lin Nie ◽  
Wei Cui ◽  
...  

Objective.Heparanase (HPSE) is high-expressed in most malignant tumors including hepatocellular carcinoma (HCC) and promotes cancer cell invasion and migration. The aim of the study is to explore whether HPSE enhances adhesion in metastasis of HCC cells.Methods. HPSE expressions in human HCC cells were measured with real-time RT-PCR and Western blot analysis. Four recombinant miRNA vectors pcDNATM6.2-GW/EmGFP-miR-HPSE (pmiR-HPSE) were transfected into HCCLM3 cell. HPSE expression in transfected cell was measured. The cell invasion, migration, and adhesion abilities were detected, respectively.Results. Both HPSE mRNA and protein relative expression levels were higher in HepG2, BEL-7402, and HCCLM3 cells than those in normal hepatocyte (P<0.05). HPSE showed highest expression level in HCCLM3 cell (P<0.05). Transfection efficiencies of four miRNA vectors were 75%–85%. The recombinant vectors significantly decreased HPSE expression in transfected HCCLM3 cells (P<0.01), and pmiR-HPSE-1 showed best interference effect (P<0.05). pmiR-HPSE-1 significantly decreased the penetrated and migrating cells numbers and adherence rate of HCCLM3 cells (P<0.05).Conclusion. HPSE is a potentiator of cell adhesion in metastasis of HCC.


Oncogene ◽  
2021 ◽  
Author(s):  
Yang-Hsiang Lin ◽  
Meng-Han Wu ◽  
Yi-Chung Liu ◽  
Ping-Chiang Lyu ◽  
Chau-Ting Yeh ◽  
...  

2021 ◽  
Vol 53 (4) ◽  
pp. 474-485
Author(s):  
Yang Yang ◽  
Feifei Mao ◽  
Lei Guo ◽  
Jie Shi ◽  
Mengchao Wu ◽  
...  

Microbiology ◽  
2003 ◽  
Vol 149 (10) ◽  
pp. 2809-2817 ◽  
Author(s):  
Shu-ichi Nakayama ◽  
Akira Kushiro ◽  
Takashi Asahara ◽  
Ryu-ichiro Tanaka ◽  
Lan Hu ◽  
...  

A two-component regulatory system, cpxR–cpxA, plays an important role in the pH-dependent regulation of virF, a global activator for virulence determinants including invasion genes, in Shigella sonnei. The authors examined whether the cpxR–cpxA homologues have some function in the expression of Salmonella enterica serovar Typhimurium invasion genes via the regulation of hilA, an activator for these genes. In a Salmonella cpxA mutant, the hilA expression level was reduced to less than 10 % of that in the parent strain at pH 6·0. This mutant strain also showed undetectable synthesis of an invasion gene product, SipC, at pH 6·0 and reduced cell invasion capacity – as low as 20 % of that of the parent. In this mutant, the reduction in hilA expression was much less marked at pH 8·0 than at pH 6·0 – no less than 50 % of that in the parent, and no significant reduction was observed in either SipC synthesis or cell invasion rate, compared to the parent. Unexpectedly, a Salmonella cpxR mutant strain and the parent showed no apparent difference in all three characteristics described above at either pH. These results indicate that in Salmonella, the sensor kinase CpxA activates hilA, and consequently, invasion genes and cell invasion capacity at pH 6·0. At pH 8·0, however, CpxA does not seem to have a large role in activation of these factors. Further, the results show that this CpxA-mediated activation does not require its putative cognate response regulator, CpxR. This suggests that CpxA may interact with regulator(s) other than CpxR to achieve activation at low pH.


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