Preferential binding of cisplatin to mitochondrial DNA of Chinese hamster ovary cells

Olivero, Ofelia A.; Semino, Cristina; Kassim, Ahmed; López-Larraza, Daniel M.; Poirier, Miriam C.

doi:10.1016/0165-7992(95)90039-x

Cited by 68 publications

(40 citation statements)

References 32 publications

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“…Although there has been comparatively little study of direct cisplatin action on mitochondria, some studies have indicated that mtDNA-cisplatin adducts may be significantly more common than cisplatin adducts with nDNA in the same cell line treated with the same concentration of cisplatin (43,44). This has been attributed to a lack of mtDNA repair following cisplatin exposure (45).…”

Section: Discussionmentioning

confidence: 99%

Cisplatin Preferentially Binds Mitochondrial DNA and Voltage-Dependent Anion Channel Protein in the Mitochondrial Membrane of Head and Neck Squamous Cell Carcinoma: Possible Role in Apoptosis

Yang

Schumaker

Egorin

et al. 2006

Clinical Cancer Research

231

185

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Purpose: Cisplatin adducts to nuclear DNA (nDNA) are felt to be the molecular lesions that trigger apoptosis, but the mechanism linking nDNA adduct formation and cell death is unclear. Some literature in the last decade has suggested a possible direct effect of cisplatin on mitochondria independent of nDNA interaction. In this study, we define separately the sequelae of cisplatin interactions with nDNA and with mitochondria in head and neck squamous cell carcinoma (HNSCC) cell lines. Experimental Design: Cisplatin binding to mitochondrial DNA (mtDNA) and proteins was analyzed by atomic absorption spectroscopy and other methods.

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Section: Discussionmentioning

confidence: 99%

Cisplatin Preferentially Binds Mitochondrial DNA and Voltage-Dependent Anion Channel Protein in the Mitochondrial Membrane of Head and Neck Squamous Cell Carcinoma: Possible Role in Apoptosis

Yang

Schumaker

Egorin

et al. 2006

Clinical Cancer Research

231

185

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“…However, our data with flow cytometry demonstrated that there was no difference in the cell cycle between parental YES-2 and YES-2/Neo and YES-2/AS-12 (data not shown). Recent studies have shown that mitochondria play an important role in the cytotoxicity or apoptosis induced by cisplatin, but not 5-FU or etoposide (Andrews and Albright, 1992;Olivero et al, 1995). The MTT assay is considered to be a representative mitochondrial function assay (Berridge and Tan, 1993); therefore, it is possible that nm23-H1 may be directly related to mitochondrial dysfunction induced by cisplatin in OSCC.…”

Section: Discussionmentioning

confidence: 99%

The nm23-H1 gene as a predictor of sensitivity to chemotherapeutic agents in oesophageal squamous cell carcinoma

et al. 1999

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Summary Recently, nm23-H1, an anti-metastasis gene, has been reported to correlate with sensitivity to chemotherapeutic agents including cisplatin in human breast and ovarian carcinoma cells. The aim of this study was to evaluate a role for nm23-H1 in responsiveness to cisplatin-based chemotherapy in patients with oesophageal squamous cell carcinoma (OSCC). The expression of nm23-H1 protein was examined immunohistochemically in 32 eligible patients with OSCC who underwent adjuvant chemotherapy with cisplatin, etoposide, and 5-fluorouracil after tumour resection. Fifteen (46.9%) of 32 patients were positive for nm23-H1 staining and 17 (53.1%) were negative. Both disease-free survival and overall survival rates of nm23-H1-negative patients were significantly shorter than in nm23-H1-positive patients (P < 0.01 for both). There was no significant difference in clinicopathologic characteristics between nm23-H1-positive and nm23-H1-negative groups. Multivariate analysis also showed that nm23-H1 expression was the most significant factor for overall survival of OSCC patients included in this study (P = 0.0007). To further study the role of nm23-H1, a human OSCC cell line (YES-2) was transfected with a plasmid containing a fragment of the nm23-H1 cDNA in an antisense orientation. Reduced expression of nm23-H1 protein in the antisensetransfected (AS) clones was found by Western blot analysis as compared to wild-type YES-2 and YES-2/Neo (clone transfected with the neomycin resistance gene alone). MTT (3-(4,5-dimethyl-2-thiazol)-2,5-diphenyl-2H tetrazolium bromide) assay showed that reduced expression of the nm23-H1 protein in AS clones was consistent with the degree of increased resistance to cisplatin but not etoposide or 5-fluorouracil. These data support the conclusion that reduced expression of nm23-H1 may be associated with resistance to cisplatin, suggesting the value of nm23-H1 expression as a prognostic marker for OSCC patients who are to undergo cisplatin-based chemotherapy. © 1999 Cancer Research Campaign Keywords: nm23; cisplatin; chemotherapy; prognosis; oesophageal squamous cell carcinoma 469British Journal of Cancer (1999) 81(3), 469-475 © 1999 Cancer Research Campaign Article no. bjoc.1999 Received 17 September 1998 Revised 1 February 1999 Accepted 21 April 1999Correspondence to: N Iizuka, Department of Bioregulatory Function, Yamaguchi University School of Medicine, Ube, Yamaguchi 755-8505, Japan follow-up periods respectively. One patient was excluded because of loss to follow-up. Therefore, the present study was undertaken in 32 patients retrospectively selected. One course of cisplatinbased chemotherapy consisted of etoposide 120 mg m -2 per day and 5-fluorouracil (5-FU) 500 mg m -2 per day by intravenous (i.v.) continuous infusion on days 3-5, and cisplatin 50 mg m -2 per day by i.v. bolus infusion on days 1 and 8. Seven (21.9%) of 32 patients underwent only 1 course of this regimen because of sideeffects, while 25 patients (78.1%) underwent two course of this regimen following resection. All patient...

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“…11 Mitochondria are likely the main such target since acute effects of cisplatin include induction of reactive oxygen species (ROS) [12][13][14] and direct binding to mitochondrial ReseaRCh papeR ReseaRCh papeR DNA (mtDNA). 12,15,16 In a study on dorsal root neurons, cisplatin-mtDNA adducts led to decreased transcription of mtDNA-encoded proteins 16 that are integral components of the complexes of the mitochondrial electron transport chain (ETC) and thus involved in normal oxidative phosphorylation (OxPhos) of ADP to ATP. Cisplatin has also been shown to inhibit OxPhos and ATP production in proximal tubular cells by directly inhibiting several of the complexes in the ETC.…”

Section: Introductionmentioning

confidence: 99%

“…Our initial, and then refuted, hypothesis that cisplatin might induce these features of tumor progression via damage to mtDNA was based on the ability of cisplatin to form numerous mtDNA adducts, 15,16 and on observations that depletion of mtDNA can be associated with EMT and motility, 22,23 and with properties of TICs and stem cells. 40,41 Interestingly, the SKOV-3-ρ 0 cells, Technologies).…”

mentioning

confidence: 99%

Repeated cisplatin treatment can lead to a multiresistant tumor cell population with stem cell features and sensitivity to 3-bromopyruvate

Wintzell

Löfstedt

Johansson

et al. 2012

Cancer Biology & Therapy

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Preferential binding of cisplatin to mitochondrial DNA of Chinese hamster ovary cells

Cited by 68 publications

References 32 publications

Cisplatin Preferentially Binds Mitochondrial DNA and Voltage-Dependent Anion Channel Protein in the Mitochondrial Membrane of Head and Neck Squamous Cell Carcinoma: Possible Role in Apoptosis

Cisplatin Preferentially Binds Mitochondrial DNA and Voltage-Dependent Anion Channel Protein in the Mitochondrial Membrane of Head and Neck Squamous Cell Carcinoma: Possible Role in Apoptosis

The nm23-H1 gene as a predictor of sensitivity to chemotherapeutic agents in oesophageal squamous cell carcinoma

Repeated cisplatin treatment can lead to a multiresistant tumor cell population with stem cell features and sensitivity to 3-bromopyruvate

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