MiR-192 inhibits nucleotide excision repair by targeting ERCC3 and ERCC4 in HepG2.2.15 cells

Xie, Qing; He, Xingxing; Chang, Ying; Sun, Shuzhen; Jiang, Xiang; Li, Peiyuan; Lin, Ju‐Sheng

doi:10.1016/j.bbrc.2011.05.153

Cited by 37 publications

(34 citation statements)

References 28 publications

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“…This association may be necessary to stabilise the target mRNAs in the early developing embryos to direct DNA repair until the embryonic genome activation. However both direct and indirect relationships were observed for the nucleotide excision repair genes as also reported previously for miR-192 and ERCC3 [11], double-strand break repair and interstrand cross-link repair genes. The down-regulatory effect of some miRNAs on BRCA1 and PARP1 was also reported previously [54,55].…”

Section: Discussionsupporting

confidence: 86%

“…miRNAs were selected to target more than one gene that is involved in different repair Genes involved in cell cycle checkpoint, nucleotide excision, base excision, double-strand break and mismatch repair pathways and the miRNAs targeting these genes are listed. These associations were either published previously [11,[47][48][49][50], or bioinformatics studies showed that these miRNAs target the mRNAs (http://www.targetscan.org/, http://www.microrna.org/microrna/home.do, http://mirdb.org/miRDB/) pathways to be able to have a general idea of the possible regulatory roles of miRNAs in DNA repair pathways. The expression of 20 miRNAs targeting these repair genes was analysed in 22 oocytes and 23 blastocysts, respectively.…”

Section: Resultsmentioning

confidence: 99%

“…Recent studies proposed that more than half of the human transcriptome is regulated by microRNAs (miRNAs) [2,3]. Several miRNAs have been shown to regulate and be regulated by genes functioning at cell cycle checkpoints [4][5][6][7][8][9][10] and in different repair mechanisms: nucleotide excision repair [11], mismatch repair [12][13][14][15] and double-strand break repair [16][17][18][19][20][21] in cancer cells and cell lines.…”

Section: Introductionmentioning

confidence: 99%

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Investigation of microRNA expression and DNA repair gene transcripts in human oocytes and blastocysts

Tulay

Naja

Cascales-Roman

et al. 2015

J Assist Reprod Genet

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Purpose The aim of the study is to investigate the regulation of DNA repair genes by microRNAs (miRNAs). miRNAs are short non-coding RNAs that regulate transcriptional and post-transcriptional gene silencing. Several miRNAs that are expressed during preimplantation embryo development have been shown or are predicted to target genes that regulate cell cycle checkpoints and DNA repair in response to DNA damage. Methods This study compares the expression level of 20 miRNAs and 9 target transcripts involved in DNA repair. The statistical significance of differential miRNA expression between oocytes and blastocysts was determined by t test analysis using the GraphPad Prism v6 software. The possible regulatory roles of miRNAs on their target messenger RNAs (mRNAs) were analysed using a Pearson correlation test. Results This study shows for the first time that several miRNAs are expressed in human oocytes and blastocysts that target key genes involved in DNA repair and cell cycle checkpoints. Blastocysts exhibited statistically significant lower expression levels for the majority of miRNAs compared to oocytes (p<0.05). Correlation analyses showed that there was both inverse and direct association between miRNAs and their target mRNAs. Conclusions miRNAs target many mRNAs including ones involved in DNA repair mechanisms. This study suggests that miRNAs and their target mRNAs involved in DNA repair are expressed in preimplantation embryos. Similar to the miRNAs expressed in adult tissues, these miRNAs seem to have regulatory roles on their target DNA repair mRNAs during preimplantation embryo development.

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Section: Discussionsupporting

confidence: 86%

Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Investigation of microRNA expression and DNA repair gene transcripts in human oocytes and blastocysts

Tulay

Naja

Cascales-Roman

et al. 2015

J Assist Reprod Genet

View full text Add to dashboard Cite

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“…miR-192 inhibited NER by suppressing ERCC3 and ERCC4 in HepG2 cells. 26 miR-103 and miR-107 directly targeted RAD51, which was an essential protein for catalyzing HR repair of DNA double-strand breaks (DSBs). 27 Additionally, another critical component of non-homologous end joining (NHEJ) for DSBs repair-Ku80, was a direct target of miR-526b.…”

Section: Discussionmentioning

confidence: 99%

DNA damage responsive miR-33b-3p promoted lung cancer cells survival and cisplatin resistance by targeting p21^WAF1/CIP1

Huang

Chen

et al. 2016

Cell Cycle

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Cisplatin is the most potent and widespread used chemotherapy drug for lung cancer treatment. However, the development of resistance to cisplatin is a major obstacle in clinical therapy. The principal mechanism of cisplatin is the induction of DNA damage, thus the capability of DNA damage response (DDR) is a key factor that influences the cisplatin sensitivity of cancer cells. Recent advances have demonstrated that miRNAs (microRNAs) exerted critical roles in DNA damage response; nonetheless, the association between DNA damage responsive miRNAs and cisplatin resistance and its underlying molecular mechanism still require further investigation. The present study has attempted to identify differentially expressed miRNAs in cisplatin induced DNA damage response in lung cancer cells, and probe into the effects of the misexpressed miRNAs on cisplatin sensitivity. Deep sequencing showed that miR-33b-3p was dramatically down-regulated in cisplatin-induced DNA damage response in A549 cells; and ectopic expression of miR33b-3p endowed the lung cancer cells with enhanced survival and decreased gH2A.X expression level under cisplatin treatment. Consistently, silencing of miR-33b-3p in the cisplatin-resistant A549/DDP cells evidently sensitized the cells to cisplatin. Furthermore, we identified CDKN1A (p21) as a functional target of miR-33b-3p, a critical regulator of G1/S checkpoint, which potentially mediated the protection effects of miR-33b-3p against cisplatin. In aggregate, our results suggested that miR-33b-3p modulated the cisplatin sensitivity of cancer cells might probably through impairing the DNA damage response. And the knowledge of the drug resistance conferred by miR-33b-3p has great clinical implications for improving the efficacy of chemotherapies for treating lung cancers.

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“…Therefore, miR-375 downregulation could determine a proliferative advantage and also an increased DDR phenotype in ERCC1-positive tumors. The HBV-expressing HepG2.2.15 cell line, with impaired NER activity, showed upregulation of miR-192 [84]. ERCC3 and ERCC4, two proteins involved in NER pathway, were downregulated by miR-192, with consequent impairing of NER machinery.…”

Section: Micrornas In Dna Damage/repair Mechanisms and Cancermentioning

confidence: 99%

MicroRNAs in the DNA Damage/Repair Network and Cancer

Tessitore

Cicciarelli

Vecchio

et al. 2014

International Journal of Genomics

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Cancer is a multistep process characterized by various and different genetic lesions which cause the transformation of normal cells into tumor cells. To preserve the genomic integrity, eukaryotic cells need a complex DNA damage/repair response network of signaling pathways, involving many proteins, able to induce cell cycle arrest, apoptosis, or DNA repair. Chemotherapy and/or radiation therapy are the most commonly used therapeutic approaches to manage cancer and act mainly through the induction of DNA damage. Impairment in the DNA repair proteins, which physiologically protect cells from persistent DNA injury, can affect the efficacy of cancer therapies. Recently, increasing evidence has suggested that microRNAs take actively part in the regulation of the DNA damage/repair network. MicroRNAs are endogenous short noncoding molecules able to regulate gene expression at the post-transcriptional level. Due to their activity, microRNAs play a role in many fundamental physiological and pathological processes. In this review we report and discuss the role of microRNAs in the DNA damage/repair and cancer.

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MiR-192 inhibits nucleotide excision repair by targeting ERCC3 and ERCC4 in HepG2.2.15 cells

Cited by 37 publications

References 28 publications

Investigation of microRNA expression and DNA repair gene transcripts in human oocytes and blastocysts

Investigation of microRNA expression and DNA repair gene transcripts in human oocytes and blastocysts

DNA damage responsive miR-33b-3p promoted lung cancer cells survival and cisplatin resistance by targeting p21^WAF1/CIP1

MicroRNAs in the DNA Damage/Repair Network and Cancer

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MiR-192 inhibits nucleotide excision repair by targeting ERCC3 and ERCC4 in HepG2.2.15 cells

Cited by 37 publications

References 28 publications

Investigation of microRNA expression and DNA repair gene transcripts in human oocytes and blastocysts

Investigation of microRNA expression and DNA repair gene transcripts in human oocytes and blastocysts

DNA damage responsive miR-33b-3p promoted lung cancer cells survival and cisplatin resistance by targeting p21WAF1/CIP1

MicroRNAs in the DNA Damage/Repair Network and Cancer

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DNA damage responsive miR-33b-3p promoted lung cancer cells survival and cisplatin resistance by targeting p21^WAF1/CIP1