scholarly journals MicroRNA-135b, a HSF1 target, promotes tumor invasion and metastasis by regulating RECK and EVI5 in hepatocellular carcinoma

Oncotarget ◽  
2014 ◽  
Vol 6 (4) ◽  
pp. 2421-2433 ◽  
Author(s):  
Yan Li ◽  
Dan Xu ◽  
Chunyang Bao ◽  
Yuannv Zhang ◽  
Di Chen ◽  
...  
2016 ◽  
Vol 375 (1) ◽  
pp. 73-83 ◽  
Author(s):  
Jing-Song Chen ◽  
Hua-Shu Li ◽  
Jiong-Qiang Huang ◽  
Shi-Hao Dong ◽  
Zhi-Jie Huang ◽  
...  

Hepatology ◽  
2010 ◽  
pp. NA-NA ◽  
Author(s):  
Jian Yao ◽  
Linhui Liang ◽  
Shenglin Huang ◽  
Jie Ding ◽  
Ning Tan ◽  
...  

2021 ◽  
Vol 2021 ◽  
pp. 1-9 ◽  
Author(s):  
Shuqiao Zhang ◽  
Zhuomao Mo ◽  
Shijun Zhang ◽  
Xinyu Li

Objective. To investigate the potential active ingredients and underlying mechanisms of Artemisia annua (AA) on the treatment of hepatocellular carcinoma (HCC) based on network pharmacology. Methods. In the present study, we used a network pharmacological method to predict its underlying complex mechanism of treating HCC. First, we obtained relative compounds of AA based on the traditional Chinese medicine systems pharmacology (TCMSP) database and collected potential targets of these compounds by target fishing. Then, we built HCC-related targets target by the oncogenomic database of hepatocellular carcinoma (OncoDB.HCC) and biopharmacological network (PharmDB-K) database. Based on the matching results between AA potential targets and HCC targets, we built a protein-protein interaction (PPI) network to analyze the interactions among these targets and screen the hub targets by topology. Furthermore, the function annotation and signaling pathways of key targets were performed by Gene Oncology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis using DAVID tools. Finally, the binding capacity between active ingredients and key targets was validated by molecular docking. Results. A total of 19 main active ingredients of AA were screened as target prediction; then, 25 HCC-related common targets were seeked out via multiple HCC databases. The areas of nodes and corresponding degree values of EGFR, ESR1, CCND1, MYC, EGF, and PTGS2 were larger and could be easily found in the PPI network. Furthermore, GO and KEGG enrichment analysis showed that these key targets were significantly involved in multiple biological processes and pathways which participated in tumor cell proliferation, apoptosis, angiogenesis, tumor invasion, and metastasis to accomplish the anti-HCC activity. The molecular docking analysis showed that quercetin could stably bind to the active pocket of EGFR protein 4RJ5 via LibDock. Conclusion. The anticancer effects of AA on HCC were predicted to be associated with regulating tumor cell proliferation, apoptosis, angiogenesis, tumor invasion, and metastasis via various pathways such as the EGFR signaling pathway, ESR1 signaling pathway, and CCND1 signaling pathway. It is suggested that AA might be developed as a broad-spectrum antitumor drug based on its characteristics of multicomponent, multipath, and multitarget.


Hepatology ◽  
2008 ◽  
Vol 49 (2) ◽  
pp. 460-470 ◽  
Author(s):  
Dou-Sheng Bai ◽  
Zhi Dai ◽  
Jian Zhou ◽  
Yin-Kun Liu ◽  
Shuang-Jian Qiu ◽  
...  

Author(s):  
Fan Pan ◽  
Xin-Rong Lin ◽  
Li-Ping Hao ◽  
Xiao-Yuan Chu ◽  
Hai-Jun Wan ◽  
...  

Hepatocellular carcinoma (HCC) is the 6th most prevalent cancer and the 4th leading cause of cancer-related death worldwide. Mechanisms explaining the carcinogenesis of HCC are not clear yet. In recent years, rapid development of N6-methyladenosine (m6A) modification provides a fresh approach to disclosing this mystery. As the most prevalent mRNA modification in eukaryotes, m6A modification is capable to post-transcriptionally affect RNA splicing, stability, and translation, thus participating in a variety of biological and pathological processes including cell proliferation, apoptosis, tumor invasion and metastasis. METTL3 has been recognized as a pivotal methyltransferase and essential to the performance of m6A modification. METTL3 can regulate RNA expression in a m6A-dependent manner and contribute to the carcinogenesis, tumor progression, and drug resistance of HCC. In the present review, we are going to make a clear summary of the known roles of METTL3 in HCC, and explicitly narrate the potential mechanisms for these roles.


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