Induction of the c-myc but not the cH-ras promoter by platinum compounds

Eliopoulos, Aristides G.; Kerr, David; Maurer, H. R.; Hilgard, P.; Spandidos, Demetrios Α.

doi:10.1016/0006-2952(95)00085-e

Cited by 13 publications

(4 citation statements)

References 16 publications

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“…Numerous other markers were also identified as involved in platinum activity, with a marked difference between the group constituted of cisplatin and carboplatin and the one constituted of tetraplatin and oxaliplatin. For instance, the significant link that we observed between oxaliplatin sensitivity and c-MYC expression was rather unexpected, although platinum compounds have been shown to activate the c-MYC gene promoter (38). So, too, was the highly significant correlation between tetraplatin sensitivity and topoisomerase II expression.…”

Section: Discussionmentioning

confidence: 76%

Molecular Determinants of the Cytotoxicity of Platinum Compounds

Vekris¹,

Meynard

Haaz³

et al. 2004

Cancer Research

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Gene expression profiling of tumors allows the establishment of relationships between gene expression profiles and sensitivity to anticancer drugs. In an attempt to study the molecular determinants of the activity of platinum compounds, we explored the publicly available databases of the National Cancer Institute (NCI; http://dtp.nci.nih.gov), which allow access to the gene expression profiles of the 60 cell lines for which drug cytotoxicity patterns already existed. Using this database, we have conducted an in silico research to identify the genes the expression of which was positively or negatively correlated to the sensitivity to four platinum compounds (cisplatin, carboplatin, oxaliplatin and tetraplatin). Important similarities were noticed between cisplatin and carboplatin on one hand, and tetraplatin and oxaliplatin on the other hand. In the restricted panel of 1416 genes and molecular markers, we identified 204 markers, among which 120 corresponded to identified genes, that significantly correlated (P < 0.001) with the cytotoxicity of at least one platinum compound. For example, the functionality of the p53-activated pathway appeared positively correlated with the cytotoxicity of all platinum compounds. More specific are the positive correlations between RAS gene mutations and MYC expression and the cellular sensitivity to oxaliplatin. Among the parameters already known as related to the sensitivity to platinum compounds, we identified, in the complete set of 9400 genes, numerous significant relationships, such as the negative correlations between ERB-B2 and BCL-X L expressions and the cytotoxicity of the platinum compounds. Public databases mining, therefore, appears to be a valuable tool for the identification of determinants of anticancer drug activity in tumors.

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Section: Discussionmentioning

confidence: 76%

Molecular Determinants of the Cytotoxicity of Platinum Compounds

Vekris¹,

Meynard

Haaz³

et al. 2004

Cancer Research

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“…Lobaplatin (D-19466; 1, 2-diammino-methylcyclobutaneplatinum (II)-lactate) is a representative of the third-generation platinum compounds delivered as a diastereomeric mixture of S, S and R, R configurations of the carrier ligand, complex with DNA alkylating activity (Huang et al, 2013). It can obstruct the process of DNA replication and transcription by forming Pt-GG and Pt-AG intrachain cross-linking so as to interfere the running of tumor cell cycles (Eliopoulos et al, 1995). Compared with cisplatin, lobaplatin is considered to be less toxic, more soluble and stable in water and shows incomplete cross-resistance to cisplatin (McKeage et al, 2001;Deng et al, 2013).…”

mentioning

confidence: 99%

A Randomized Controlled Trial Comparing Clinical Outcomes and Toxicity of Lobaplatin- Versus Cisplatin-Based Concurrent Chemotherapy Plus Radiotherapy and High-Dose-Rate Brachytherapy for FIGO Stage II and III Cervical Cancer

Wang¹,

Wang²,

Shi³

et al. 2015

Asian Pacific Journal of Cancer Prevention

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Cervical cancer is second only to breast cancer as the most common female malignancy in both incidence and mortality worldwide (Seol et al., 2014). Platinum-based chemoradiotherapy has become an acceptable treatment for FIGO stage II and III disease. The platinum-based compounds cisplatin is among the most widely used and effective drugs. The activity of cisplatin-containing chemoradiotherapy in cervical cancer showed a reduction in the risk of recurrence of 40-60% (Whitney, et al., 1999). But there are approximately 275000 deaths annually because of treatment failure or recurrence of cervical cancer (Wiebe et al., 2012). Drug resistance to cisplatin is considered to be a major cause of treatment failure. Another problem for cisplatin, is its severe neuro

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“…In this study, we demonstrate that lobaplatin could inhibit prostate cancer in vitro and in vivo in part by suppressing both AR and ERG signaling pathways that are two major drivers of prostate cancer. Interestingly, although a previous study demonstrated that lobaplatin could induce c-MYC promoter activity [35], our study showed that lobaplatin downregulated c-MYC expression in multiple prostate cancer cell lines, which may be attributed to the fact that c-MYC is a downstream target of AR and ERG in prostate cancer setting [29,36]. Moreover, consistent with previous studies [37][38][39], our results also demonstrated that lobaplatin treatment dramatically elevated MDR1 expression, indicating that combination of lobaplatin and MDR1 specific inhibitor might achieve better outcomes for prostate cancer therapy.…”

Section: Discussionmentioning

confidence: 94%

Lobaplatin inhibits prostate cancer progression in part by impairing AR and ERG signal

Chen

Cao

et al. 2018

Fundamemntal Clinical Pharma

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Lobaplatin is the third-generation platinum drug that has been shown promising antitumor activity in preclinical studies and clinical trials for multiple human cancers except prostate cancer. In this study, we investigated the role of lobaplatin on prostate cancer progression and the underlying molecular mechanism. We treated a variety of prostate cancer cell lines with different doses of lobaplatin and examined cell cycle progression, cell apoptosis, cell proliferation, and cell migration. Moreover, we also assessed the in-vivo antitumor activity of lobaplatin using xenograft mouse model. Importantly, we further dissected the underlying molecular mechanism by examining the expression of AR and ERG, as well as their downstream targets. We found that lobaplatin arrested cell cycle progression in G2/M phase and trigged cell apoptosis. Lobaplatin also dramatically inhibited cell proliferation and migration in vitro. Consistently, lobaplatin significantly suppressed tumor growth in xenograft mouse model. Mechanistically, the expression of AR and ERG, as well as their downstream targets, was markedly decreased upon treatment with lobaplatin in prostate cancer cells. Altogether, our results suggest that lobaplatin displayed favorable antitumor activity on prostate cancer both in vitro and in vivo, providing molecular basis and rational for using lobaplatin to combat human prostate cancer.

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Induction of the c-myc but not the cH-ras promoter by platinum compounds

Cited by 13 publications

References 16 publications

Molecular Determinants of the Cytotoxicity of Platinum Compounds

Molecular Determinants of the Cytotoxicity of Platinum Compounds

A Randomized Controlled Trial Comparing Clinical Outcomes and Toxicity of Lobaplatin- Versus Cisplatin-Based Concurrent Chemotherapy Plus Radiotherapy and High-Dose-Rate Brachytherapy for FIGO Stage II and III Cervical Cancer

Lobaplatin inhibits prostate cancer progression in part by impairing AR and ERG signal

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