<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Su Y</submitter><funding>National Natural Science Foundation of Shanghai</funding><funding>National Natural Science Foundation of China</funding><pagination>326</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10685607</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>42(1)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>As a small G protein of Ras family, Ras-like-without-CAAX-1 (RIT1) plays a critical role in various tumors. Our previous study has demonstrated the involvement of RIT1 in promoting malignant progression of hepatocellular carcinoma (HCC). However, its underlying mechanism remains unclear.&lt;h4>Methods&lt;/h4>Gene set enrichment analysis (GSEA) was conducted in the TCGA LIHC cohort to investigate the underlying biological mechanism of RIT1. Live cell imaging, immunofluorescence (IF) and flow cytometry assays were used to verify biological function of RIT1 in HCC mitosis. Subcutaneous xenografting of human HCC cells in BALB/c nude mice was utilized to assess tumor proliferation in vivo. RNA-seq, co-immunoprecipitation (Co-IP), mass spectrometry analyses, western blot and IF assa</pubmed_abstract><journal>Journal of experimental &amp; clinical cancer research : CR</journal><pubmed_title>RIT1 regulates mitosis and promotes proliferation by interacting with SMC3 and PDS5 in hepatocellular carcinoma.</pubmed_title><pmcid>PMC10685607</pmcid><funding_grant_id>20ZR1454000</funding_grant_id><funding_grant_id>82172904</funding_grant_id><pubmed_authors>Ge C</pubmed_authors><pubmed_authors>Li H</pubmed_authors><pubmed_authors>Jin W</pubmed_authors><pubmed_authors>Geng Q</pubmed_authors><pubmed_authors>Li J</pubmed_authors><pubmed_authors>Jiang S</pubmed_authors><pubmed_authors>Yu J</pubmed_authors><pubmed_authors>Liu T</pubmed_authors><pubmed_authors>Zhang S</pubmed_authors><pubmed_authors>Mao L</pubmed_authors><pubmed_authors>Zhou X</pubmed_authors><pubmed_authors>Cui Y</pubmed_authors><pubmed_authors>Lin H</pubmed_authors><pubmed_authors>Zhao F</pubmed_authors><pubmed_authors>Su Y</pubmed_authors><pubmed_authors>Hou H</pubmed_authors><pubmed_authors>Wu Y</pubmed_authors><pubmed_authors>Chen T</pubmed_authors></additional><is_claimable>false</is_claimable><name>RIT1 regulates mitosis and promotes proliferation by interacting with SMC3 and PDS5 in hepatocellular carcinoma.</name><description>&lt;h4>Background&lt;/h4>As a small G protein of Ras family, Ras-like-without-CAAX-1 (RIT1) plays a critical role in various tumors. Our previous study has demonstrated the involvement of RIT1 in promoting malignant progression of hepatocellular carcinoma (HCC). However, its underlying mechanism remains unclear.&lt;h4>Methods&lt;/h4>Gene set enrichment analysis (GSEA) was conducted in the TCGA LIHC cohort to investigate the underlying biological mechanism of RIT1. Live cell imaging, immunofluorescence (IF) and flow cytometry assays were used to verify biological function of RIT1 in HCC mitosis. Subcutaneous xenografting of human HCC cells in BALB/c nude mice was utilized to assess tumor proliferation in vivo. RNA-seq, co-immunoprecipitation (Co-IP), mass spectrometry analyses, western blot and IF assa</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Nov</publication><modification>2025-04-04T19:00:11.369Z</modification><creation>2025-02-19T04:43:58.735Z</creation></dates><accession>S-EPMC10685607</accession><cross_references><pubmed>38017479</pubmed><doi>10.1186/s13046-023-02892-x</doi></cross_references></HashMap>