Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0019204 (hepatocellular carcinoma)
 71,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Long non-coding (lnc) RNAs are involved in almost every stage of tumor initiation and progression. Here, we have identified an antisense lncRNA, LINC00624, that arises from the antisense strand of CHD1L, located on chr1q21.1, with significant copy number gain and transcriptional activation of CHD1L and BCL9, in hepatocellular carcinoma (HCC). Overexpression of LINC00624 enhances tumor growth and metastasis in vitro and in vivo. Mechanistically, higher levels of LINC00624, strengthen the interaction between HDAC6 and TRIM28, which accelerates HDAC6 ubiquitination and degradation. Moreover, LINC00624 binds to the RBCC domain of TRIM28, inhibits trimer formation, and weakens the interaction between TRIM28 and ZNF354C. Thus, LINC00624 overexpression disrupts the formation of the HDAC6-TRIM28-ZNF354C transcriptional corepressor complex, resulting in the dissociation of the complex from the promoter of CHD1L and BCL9, thereby removing transcription inhibition. Conclusions: our findings suggest that LINC00624 acts as a molecular decoy that sequesters the HDAC6-TRIM28-ZNF354C transcriptional corepressor complex away from the specific genomic loci, and that it can potentially be a therapeutic target in HCC.
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PMID:Gain of LINC00624 Enhances Liver Cancer Progression by Disrupting the HDAC6-TRIM28-ZNF354C Corepressor Complex. 3286 73