Excision repair cross complementing-group 1: Gene expression and platinum resistance (Review) parameters in human breast cancer

Altaha, Ramin; Liang, Xin; Yu, Jing; Reed, Eddie

doi:10.3892/ijmm.14.6.959

Cited by 116 publications

(120 citation statements)

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“…Little is known about potential ZNF143 target genes for DNA repair pathways. Among several DNA repair pathways, it has been extensively studied that excision repair crosscomplementation group 1 (ERCC1) has the critical role in nucleotide excision repair pathway and high ERCC1 ZNF143 and cisplatin resistance T Wakasugi et al expression is associated with cisplatin resistance (Altaha et al, 2004). Both BRCA1 and Rad51 have been shown to be involved in recombinational repair and also associated with cisplatin resistance (Bhattacharyya et al, 2000;Spiro and McMurray, 2003).…”

Section: Discussionmentioning

confidence: 99%

ZNF143 interacts with p73 and is involved in cisplatin resistance through the transcriptional regulation of DNA repair genes

et al. 2007

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Zinc-finger protein 143 (ZNF143) is a human homolog of Xenopus transcriptional activator staf that is involved in selenocystyl tRNA transcription. We previously showed that ZNF143 expression is induced by treatment with DNA-damaging agents and that it preferentially binds to cisplatin-modified DNA. In this study, the potential function of ZNF143 was investigated. ZNF143 was overexpressed in cisplatin-resistant cells. ZNF143 knockdown in prostate cancer caused increased sensitivity for cisplatin, but not for oxaliplatin, etoposide and vincristine. We also showed that ZNF143 is associated with tumor suppressor gene product p73 but not with p53. p73 could stimulate the binding of ZNF143 to both ZNF143 binding site and cisplatin-modified DNA, and modulate the function of ZNF143. We provide a direct evidence that both Rad51 and flap endonuclease-1 are target genes of ZNF143 and overexpressed in cisplatin-resistant cells. Taken together, these experiments demonstrate that an interplay of ZNF143, p73 and ZNF143 target genes is involved in DNA repair gene expression and cisplatin resistance.

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Section: Discussionmentioning

confidence: 99%

ZNF143 interacts with p73 and is involved in cisplatin resistance through the transcriptional regulation of DNA repair genes

et al. 2007

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“…Drug resistance of cancer cells primarily attribute to two mechanisms: one is the decreased effective concentration of drugs in the cell which is induced by the altered cell membrane proteins that work as the drug pumps to decrease drug influx into cells and/or increase drug efflux out of cells (12); the other is the decreased sensitivity of the cancer cell to drugs which is mediated by the increased capacity of DNA repair pathways (35,36). In the present study, no significant difference was found in the accumulation of cisplatin between H1299/E and H1299/V cells (Fig.…”

Section: Discussionmentioning

confidence: 99%

Excision repair cross complementation group 1 is a chemotherapy-tolerating gene in cisplatin-based treatment for non-small cell lung cancer

Wang

Pan

Liu

et al. 2014

International Journal of Oncology

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Abstract. This study aimed to evaluate the biological functions of excision repair cross complementation goup 1 (ERCC1) in cell proliferation, cell cycle, invasion and cisplatin response of non-small cell lung cancer (NSCLC) cells. Firstly, ERCC1 gene was successfully transfected into H1299 cells by gene cloning and transfection techniques. Then, cell proliferation was determined with the cell growth curve and colony-forming assays. Flow cytometry (FCM) was employed to investigate the cell cycle distribution. The ability of cell invasion was estimated by means of Matrigel invasion assays. Response of NSCLC cells to cisplatin was detected utilizing MTT assays, and the intracellular drug concentrations were determined by the high performance liquid chromatography (HPLC) analysis. Expression of the two cell membrane proteins, P-glycoprotein (P-gp) and multidrug resistanceassociated protein (MRP), was also evaluated utilizing FCM technique. By contrast, ERCC1 expression in the NSCLC A549 cells was silenced by small interfering RNA (siRNA) through RNAi technique. In addition, the cytotoxic effect of cisplatin on A549 cells was detected by MTT assays. In the present study, the results demonstrated that ERCC1 had no effect on cell proliferation, cell cycle and the ability of invasion, but showed significant impact on cisplatin response of the NSCLC H1299 cells. Furthermore, siRNA-induced suppression of ERCC1 evidently enhanced sensitivity to cisplatin of NSCLC A549 cells. Therefore, it is confirmed that ERCC1 is a chemotherapy-tolerating gene and a promising predictor in tailoring chemotherapy of NSCLC.

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“…The DNA repair systems are critical for repairing DNA damage induced by carcinogens. Moreover, they also play an important role in repairing the cross-linking and oxidative damage caused by chemotherapy drugs (Altaha et al, 2004). Therefore, the impaired DNA repair capacity may not only increase carcinogenesis and lead to more biologically aggressive tumors and decrease survival, but also contribute to the persistence of functional platinum-DNA adducts that confer anti-tumor activity and impart more favorable prognoses.…”

Section: Discussionmentioning

confidence: 99%

DNA Repair Gene ERCC1 and XPD Polymorphisms Predict Glioma Susceptibility and Prognosis

Chen

Yao²,

Zhao³

et al. 2012

Asian Pacific Journal of Cancer Prevention

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Aims: We conducted a case-control study in a Chinese population to clarify the association between polymorphisms in ERCC1 and XPD and susceptibility and survival of glioma. Methods: A total of 393 cases and 410 controls were selected from March 2007 to December 2011. Genotyping of ERCC1 and XPD was conducted by TaqMan assays using the ABI Prism 7911HT Sequence Detection System. All analyses were performed using the STATA statistical package. Results: Polymorphisms in ERCC1 118C/T, ERCC1 8092C/A and XPD Asp312Asn showed no statistically significant difference between glioma cases and controls. However, individuals with the XPD 751Gln/Gln genotype had an increased risk of developing glioma compared with those with the Lys/Lys genotype (adjusted OR=1.64, 95% CI: 1.06-2.89). The ERCC1 118T/T genotype was associated with significantly higher median survival than the ERCC1 C/C genotype (HR=0.67, 95%CI=0.35-0.96). In addition, individuals with XPD 751Gln/Gln had a lower median survival time than XPD Lys/Lys carriers (HR=0.54, 95%CI=0.37-0.93). Conclusion: In conclusion, we observed that the XPD 751Gln/Gln genotype is associated with glioma susceptibility, and ERCC1 118 T/T and XPD 751Gln/Gln genotypes confer a significantly better prognosis.

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Excision repair cross complementing-group 1: Gene expression and platinum resistance (Review) parameters in human breast cancer

Cited by 116 publications

References 0 publications

ZNF143 interacts with p73 and is involved in cisplatin resistance through the transcriptional regulation of DNA repair genes

ZNF143 interacts with p73 and is involved in cisplatin resistance through the transcriptional regulation of DNA repair genes

Excision repair cross complementation group 1 is a chemotherapy-tolerating gene in cisplatin-based treatment for non-small cell lung cancer

DNA Repair Gene ERCC1 and XPD Polymorphisms Predict Glioma Susceptibility and Prognosis

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