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

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE188704 | GEO | 2022/07/27

REPOSITORIES: GEO

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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.

2022-07-27 | GSE188703 | GEO

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.

2022-07-27 | GSE190632 | GEO

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

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

| PRJNA779966 | ENA

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]

| PRJNA779970 | ENA

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]

| PRJNA787888 | ENA

Hepatocellular Carcinoma

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2014-12-10 | E-GEOD-57958 | biostudies-arrayexpress

Hepatocellular Carcinoma

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

2014-12-10 | GSE57958 | GEO

Zinc finger protein 668 interacts with Tip60 to promote H2AX acetylation after DNA damage.

Project description:Many tumor suppressors play an important role in the DNA damage pathway. Zinc finger protein 668 (ZNF668) has recently been identified as one of the potential tumor suppressors in breast cancer, but its function in DNA damage response is unknown. Herein, we report that ZNF668 is a regulator of DNA repair. ZNF668 knockdown impairs cell survival after DNA damage without affecting the ATM/ATR DNA-damage signaling cascade. However, recruitment of repair proteins to DNA lesions is decreased. In response to IR, ZNF668 knockdown reduces Tip60-H2AX interaction and impairs IR-induced histone H2AX hyperacetylation, thus impairing chromatin relaxation. Impaired chromatin relaxation causes decreased recruitment of repair proteins to DNA lesions, defective homologous recombination (HR) repair and impaired cell survival after IR. In addition, ZNF668 knockdown decreased RPA phosphorylation and its recruitment to DNA damage foci in response to UV. In both IR and UV damage responses, chromatin relaxation counteracted the impaired loading of repair proteins and DNA repair defects in ZNF668-deficient U2OS cells, indicating that impeded chromatin accessibility at sites of DNA breaks caused the DNA repair defects observed in the absence of ZNF668. Our findings suggest that ZNF668 is a key molecule that links chromatin relaxation with DNA damage response in DNA repair control.

| S-EPMC3737306 | biostudies-literature

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