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PATZ1 ChIP-Seq

ABSTRACT: Liver cancer is the third most common cause of cancer death in the world. POZ/BTB and AT-hook-containing zinc finger protein 1 (PATZ1) is a transcription factor associated with various cancers. However, the role of PATZ1 in cancer progression remains controversial. Here we report that PATZ1 regulates cell proliferation by directly regulating CDKN1B (p27) in hepatocellular carcinoma HepG2 cells. PATZ1 level was found to be ectopically expressed in hepatocellular carcinoma cells compared to normal primary human hepatocytes, thus affirming its relevance in liver cancer. Our gene expression microarray and PATZ1 ChIP-seq analysis further revealed strong enrichment in gene ontology terms related to cellular proliferation. Importantly, siRNA-mediated PATZ1 knockdown in HepG2 cells led to an increased rate of colony formation, elevated Ki-67 expression and greater S phase entry. Furthermore, the increased cancer cell proliferation was accompanied with suppressed expression of the cyclin-dependent kinase inhibitor CDKN1B. Consistently, PATZ1 binds to the genomic loci flanking the transcriptional start site of CDKN1B and positively regulates its promoter activity. Additionally, we found that PATZ1 associates with p53 and the absence of p53 abrogated the PATZ1-mediated regulation of CDKN1B expression. In conclusion, our study provides novel mechanistic insights into the role of PATZ1 in liver cancer progression, thereby providing a promising therapeutic intervention to alleviate tumor burden in liver cancer.

ORGANISM(S): Homo sapiens

PROVIDER: GSE114030 | GEO | 2020/12/31

REPOSITORIES: GEO

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Genome-wide expression of PATZ1 knockdown in HepG2 cells

Project description:Liver cancer is the third most common cause of cancer death in the world. POZ/BTB and AT-hook-containing zinc finger protein 1 (PATZ1) is a transcription factor associated with various cancers. However, the role of PATZ1 in cancer progression remains controversial. Here we report that PATZ1 regulates cell proliferation by directly regulating CDKN1B (p27) in hepatocellular carcinoma HepG2 cells. PATZ1 level was found to be ectopically expressed in hepatocellular carcinoma cells compared to normal primary human hepatocytes, thus affirming its relevance in liver cancer. Our gene expression microarray and PATZ1 ChIP-seq analysis further revealed strong enrichment in gene ontology terms related to cellular proliferation. Importantly, siRNA-mediated PATZ1 knockdown in HepG2 cells led to an increased rate of colony formation, elevated Ki-67 expression and greater S phase entry. Furthermore, the increased cancer cell proliferation was accompanied with suppressed expression of the cyclin-dependent kinase inhibitor CDKN1B. Consistently, PATZ1 binds to the genomic loci flanking the transcriptional start site of CDKN1B and positively regulates its promoter activity. Additionally, we found that PATZ1 associates with p53 and the absence of p53 abrogated the PATZ1-mediated regulation of CDKN1B expression. In conclusion, our study provides novel mechanistic insights into the role of PATZ1 in liver cancer progression, thereby providing a promising therapeutic intervention to alleviate tumor burden in liver cancer.

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