<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>19(1)</volume><submitter>Cheng B</submitter><pubmed_abstract>&lt;h4>Background&lt;/h4>Hepatitis B virus can induce hepatocellular carcinoma (HCC) by inducing a host immune response against infected hepatocytes. C-terminally truncated middle surface protein (MHBSt) has been reported to contribute to HCC through transcriptional activation in epidemiology studies, while the underlying mechanism of MHBSt-induced HCC is unknown.&lt;h4>Methods&lt;/h4>In this study, a premature stop at codon 167 in MHBS (MHBSt&lt;sup>167&lt;/sup>) was investigated into eukaryotic expression plasmid pcDNA3.1(-). MHBSt&lt;sup>167&lt;/sup> expressed plasmid was transfected into the L02 cell line, cell proliferation was analyzed by CCK-8 and high-content screening assays, the cell cycle was analyzed by flow cytometry, and epithelial-to-mesenchymal transition and autophagy were analyzed by immunoblott</pubmed_abstract><journal>Virology journal</journal><pagination>110</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9235077</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>MHBSt&lt;sup>167&lt;/sup> induced autophagy promote cell proliferation and EMT by activating the immune response in L02 cells.</pubmed_title><pmcid>PMC9235077</pmcid><pubmed_authors>Zeng S</pubmed_authors><pubmed_authors>Wang Q</pubmed_authors><pubmed_authors>He Y</pubmed_authors><pubmed_authors>Cheng B</pubmed_authors><pubmed_authors>Li R</pubmed_authors><pubmed_authors>Wei Z</pubmed_authors><pubmed_authors>Meng Z</pubmed_authors><pubmed_authors>Liu G</pubmed_authors></additional><is_claimable>false</is_claimable><name>MHBSt&lt;sup>167&lt;/sup> induced autophagy promote cell proliferation and EMT by activating the immune response in L02 cells.</name><description>&lt;h4>Background&lt;/h4>Hepatitis B virus can induce hepatocellular carcinoma (HCC) by inducing a host immune response against infected hepatocytes. C-terminally truncated middle surface protein (MHBSt) has been reported to contribute to HCC through transcriptional activation in epidemiology studies, while the underlying mechanism of MHBSt-induced HCC is unknown.&lt;h4>Methods&lt;/h4>In this study, a premature stop at codon 167 in MHBS (MHBSt&lt;sup>167&lt;/sup>) was investigated into eukaryotic expression plasmid pcDNA3.1(-). MHBSt&lt;sup>167&lt;/sup> expressed plasmid was transfected into the L02 cell line, cell proliferation was analyzed by CCK-8 and high-content screening assays, the cell cycle was analyzed by flow cytometry, and epithelial-to-mesenchymal transition and autophagy were analyzed by immunoblott</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Jun</publication><modification>2025-04-22T11:49:50.535Z</modification><creation>2025-04-06T00:08:35.709Z</creation></dates><accession>S-EPMC9235077</accession><cross_references><pubmed>35761331</pubmed><doi>10.1186/s12985-022-01840-z</doi></cross_references></HashMap>