Data from SMG5 Inhibition Restrains Hepatocellular Carcinoma Growth and Enhances Sorafenib Sensitivity

• DOI: 10.1158/1535-7163.c.7380214.v1
• Publication Date: 2024-08-01T15:59:31Z
• Authors: Nan Fang; Bing Liu; Qiuzhong Pan; Tingting Gong; Meixiao Zhan; Jingjing Zhao; Qijing Wang; Yan Tang; Yongqiang Li; Jia He; Tong Xiang; Fengze Sun; Ligong Lu; Jianchuan Xia
• Keywords: Pathogenesis; Methionine Adenosyltransferase; Liver Cancer

<div>Abstract<p>Hepatocellular carcinoma (HCC) has a pathogenesis that remains elusive with restricted therapeutic strategies and efficacy. This study aimed to investigate the role of <i>SMG5</i>, crucial component in nonsense-mediated mRNA decay (NMD) degrades containing premature termination codon, HCC resistance. We demonstrated an elevated expression <i>SMG5</i> scrutinized its potential as target. Our findings revealed knockdown not only inhibited migration, invasion, proliferation cells but also influenced sorafenib Differential gene analysis between control groups showed upregulation <i>methionine adenosyltransferase 1A</i> latter. High 1A</i>, catalyst for S-adenosylmethionine (SAM) production, suggested by The Cancer Genome Atlas data, was indicative better prognosis HCC. Further, ELISA higher concentration SAM cell supernatants. Furthermore, we found exogenous supplementation enhanced sensitivity alongside changes Bax Bcl-2, apoptosis-related proteins. underscore important development involvement resistance, highlighting it target treatment.</p></div>