<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Wu Y</submitter><funding>Changsha Science and Technology Bureau Guiding Science and Technology Plan project</funding><funding>Science and Education (2023) 4, Nanshan District Health Commission, Shenzhen</funding><pagination>30</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11520121</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>12(1)</volume><pubmed_abstract>&lt;h4>Objective&lt;/h4>Chondrosarcoma (CHS) is resistant to conventional chemotherapy and radiotherapy and currently lacks effective treatment options when in advanced stages. Accordingly, this research investigated the mechanism of RNF2/CBX7 in CHS to drive the development of molecularly targeted drugs for CHS.&lt;h4>Methods&lt;/h4>RNF2 and CBX7 levels were detected in CHS cells and tissues. RNF2 and CBX7 expression was modulated through cell transfection to examine their effects on cell proliferation, apoptosis, migration, and angiogenesis. The correlation between RNF2 and CBX7 levels was determined, and the ubiquitination level of CBX7 was tested. Protein synthesis was blocked in RNF2-knockdown/overexpressing cells with CHX to assess the effect of RNF2 on CBX7 stability. JJ012 cells transfected wi</pubmed_abstract><journal>Cancer &amp; metabolism</journal><pubmed_title>RNF2 promotes chondrosarcoma progression by regulating ubiquitination and degradation of CBX7.</pubmed_title><pmcid>PMC11520121</pmcid><funding_grant_id>(NS202304)</funding_grant_id><funding_grant_id>(kzd22066)</funding_grant_id><pubmed_authors>Luo P</pubmed_authors><pubmed_authors>Li J</pubmed_authors><pubmed_authors>Huang Z</pubmed_authors><pubmed_authors>Chen Z</pubmed_authors><pubmed_authors>Xiang Z</pubmed_authors><pubmed_authors>Zhang M</pubmed_authors><pubmed_authors>Zhou Y</pubmed_authors><pubmed_authors>Wu Y</pubmed_authors></additional><is_claimable>false</is_claimable><name>RNF2 promotes chondrosarcoma progression by regulating ubiquitination and degradation of CBX7.</name><description>&lt;h4>Objective&lt;/h4>Chondrosarcoma (CHS) is resistant to conventional chemotherapy and radiotherapy and currently lacks effective treatment options when in advanced stages. Accordingly, this research investigated the mechanism of RNF2/CBX7 in CHS to drive the development of molecularly targeted drugs for CHS.&lt;h4>Methods&lt;/h4>RNF2 and CBX7 levels were detected in CHS cells and tissues. RNF2 and CBX7 expression was modulated through cell transfection to examine their effects on cell proliferation, apoptosis, migration, and angiogenesis. The correlation between RNF2 and CBX7 levels was determined, and the ubiquitination level of CBX7 was tested. Protein synthesis was blocked in RNF2-knockdown/overexpressing cells with CHX to assess the effect of RNF2 on CBX7 stability. JJ012 cells transfected wi</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Oct</publication><modification>2026-07-15T14:42:42.843Z</modification><creation>2025-04-06T15:24:53.387Z</creation></dates><accession>S-EPMC11520121</accession><cross_references><pubmed>39456039</pubmed><doi>10.1186/s40170-024-00359-x</doi></cross_references></HashMap>