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Chromatin-associated OGT promotes hepatocellular carcinoma malignancy via activating ZNF263

ABSTRACT: OGT, the only facilitator which attaches the monosaccharide to many oncogenic factors or tumor suppressors, has been suggested to play an influential role in tumorigenesis and metastasis of HCC. OGT interactome analyses indicates that disordered OGT may serve as a hub protein to activate the building of aberrant transcriptional regulatory complexes, supporting that this unique enzyme is an essential regulator in tumor progression. However, the function and related mechanisms by which OGT triggers HCC malignancy are still largely unknown

ORGANISM(S): Homo Sapiens

SUBMITTER: Yubo Liu

PROVIDER: PXD039365 | iProX | Thu Jan 12 00:00:00 GMT 2023

REPOSITORIES: iProX

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Project description:Chromosomal DNA copy number alterations are a hallmark of human malignancies, including hepatocellular carcinoma (HCC). However, which oncogenes or tumor suppressors located on regions with DNA copy number aberration may contribute to HCC initiation and progression still remain obscure. Here we performed a genome-wide DNA copy number analysis on human HCC samples to identify novel potential oncogenes or tumor suppressors with DNA copy number aberrations. Genome-wide DNA copy numbers analysis was performed with single nucleotide polymorphism micoarray. RT-PCR and immunohistochemical staining were employed to evaluate the NOXIN expression in HCC samples. Colony formation, cell cycle analysis and tumor xenograft assays were performed to assess the role of NOXIN in HCC cells. Reciprocal co-immunoprecipitation experiments were used to detect the interaction between NOXIN and DNA polymerase a primase. Genome-wide DNA copy number analysis on 43 paired HCC samples indentified the smallest DNA amplification region containing NOXIN, along with the elevated transcript. NOXIN overexpression was significantly associated with HCC tumor stage. Enforced NOXIN promoted cellular proliferation, colony formation, cell migration and in vivo tumorigenicity, whereas RNA interference against NOXIN can attenuate these effects. Interestingly, NOXIN overexpression can accelerate the G1-S transition of cell cycle progression through enhancing DNA synthesis in HCC cells, as indicated by bromodeoxyuridine incorporation. Furthermore, NOXIN can interact with DNA polymerase a, implying that NOXIN may promote de novo DNA synthesis via affiliating formation of DNA polymerase-primase complex. Affymetrix SNP arrays were performed according to the manufacturer's directions on DNA extracted from hepatocellular carcinoma and adjacent liver tissue samples. Copy number analysis of Affymetrix 500K SNP arrays was performed for 43 hepatocellular carcinoma tissue samples, which their adjacent liver tissues were used as references for copy number inference.

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Chromatin-associated OGT promotes hepatocellular carcinoma malignancy via activating ZNF263

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