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ZCCHC4 Interacts with AL133467.2 and gamma H2AX to Promote Chemoresistance in Hepatocellular Carcinoma

ABSTRACT: ZCCHC4 Interacts with AL133467.2 and gamma H2AX to Promote Chemoresistance in Hepatocellular Carcinoma

PROVIDER: PRJNA779966 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16930721.fastq.gz	Fastqsanger.gz
	SRR16930722.fastq.gz	Fastqsanger.gz
	SRR16930580.fastq.gz	Fastqsanger.gz
	SRR16930581.fastq.gz	Fastqsanger.gz
	SRR16930582.fastq.gz	Fastqsanger.gz

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ZCCHC4 Interacts with AL133467.2 and gamma H2AX to Promote Chemoresistance in Hepatocellular Carcinoma [UV-CLIP_ZCCHC4]

Project description:Purpose: We performed UV-CLIP-seq to investigate the RNAs interacting with ZCCHC4. The goal of this study is to investigate the role of ZCCHC4 in regulating the progression and prognosis of HCC. We have found that ZCCHC4 could inhibit DNA damage agent induced DNA damage and apoptosis of HCC, and promote chemoresistance. We proposed that ZCCHC4 could interact with RNAs to regulate chemoresistance.

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ZCCHC4 Interacts with AL133467.2 and gamma H2AX to Promote Chemoresistance in Hepatocellular Carcinoma [HepG2_ZCCHC4 KO]

Project description:ZCCHC4 Interacts with AL133467.2 and gamma H2AX to Promote Chemoresistance in Hepatocellular Carcinoma [HepG2_ZCCHC4 KO]

| PRJNA779967 | ENA

ZCCHC4 Interacts with AL133467.2 and gamma H2AX to Promote Chemoresistance in Hepatocellular Carcinoma [UV-CLIP_ZCCHC4]

Project description:ZCCHC4 Interacts with AL133467.2 and gamma H2AX to Promote Chemoresistance in Hepatocellular Carcinoma [UV-CLIP_ZCCHC4]

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ZCCHC4 Interacts with AL133467.2 and gamma H2AX to Promote Chemoresistance in Hepatocellular Carcinoma [HepG2_ZCCHC4 KO OXA]

Project description:ZCCHC4 Interacts with AL133467.2 and gamma H2AX to Promote Chemoresistance in Hepatocellular Carcinoma [HepG2_ZCCHC4 KO OXA]

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ZCCHC4 Interacts with AL133467.2 and gamma H2AX to Promote Chemoresistance in Hepatocellular Carcinoma [HepG2_ZCCHC4 KO]

Project description:Purpose: We performed RNA sequencing (RNA-seq) analysis of ZCCHC4 KO1 cells and wild type cells to find differentially expressed genes regulated by ZCCHC4 in HCC cells. The goal of this study is to investigate the biological effect of ZCCHC4 in HCC progression and prognosis.

2022-07-27 | GSE188702 | GEO

ZCCHC4 Interacts with AL133467.2 and gamma H2AX to Promote Chemoresistance in Hepatocellular Carcinoma [HepG2_ZCCHC4 KO OXA]

Project description:Purpose: We performed RNA sequencing (RNA-seq) analysis to investigate the role of ZCCHC4 in regulating OXA-induced genes in HepG2 cells. The goal of this study is to investigate the biological effect of ZCCHC4 in HCC progression and prognosis, and we have found that ZCCHC4 could promote chmoresistance of HCC to DNA damage agents including OXA, we conducted RNA-seq to figure out more clues for deep mechanisms.

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ZCCHC4 Interacts with AL133467.2 and gamma H2AX to Promote Chemoresistance in Hepatocellular Carcinoma

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-07-27 | GSE188704 | GEO

Whole-genome landscape of histone H2AX and γ-H2AX

Project description:Phosphorylation of the histone variant H2AX forms γ-H2AX that marks DNA double-strand break (DSB). Here we generated the sequencing-based maps of H2AX and γ-H2AX positioning in resting and proliferating cells before and after ionizing irradiation. Genome-wide locations of possible endogenous and exogenous DSBs were identified based on γ-H2AX distribution in dividing cancer cells without irradiation and that in resting cells upon irradiation, respectively. γ-H2AX-enriched regions of endogenous origin in replicating cells included telomeres and active transcription start sites, apparently reflecting replication- and transcription-mediated stress during rapid cell division. Surprisingly, H2AX itself, prior to phosphorylation, was specifically located at these endogenous hotspots. This phenomenon was only observed in dividing cancer cells but not in resting cells. Endogenous H2AX was concentrated on the transcription start site of actively transcribed genes but was irrelevant to pausing of RNA polymerase II (pol II), which precisely coincided with γ-H2AX of endogenous origin. γ-H2AX enrichment upon irradiation also coincided with actively transcribed regions, but unlike endogenous γ-H2AX, it extended into the gene body and was not specifically concentrated on the pausing site of pol II. Subtelomeres were not responsive to external DNA damage. Our findings provide insight into DNA repair programs of cancer and may have implications for cancer therapy.

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