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Cellular and molecular response to ruthenium(II)-arene complex with substituted picolinato ligand in HeLa cells

ABSTRACT: Ruthenium(II)-arene complexes are promising drug candidates for therapy of solid tumors. We have previously shown that ruthenium(II)-arene complex [Ru(η6-p-cymene)(L7)Cl] (RuT7) exerts cytotoxic effects in a panel of cancer cell lines (J. Organomet. Chem. 2014, 749, 343–349). In this study we analyzed in vitro cellular response and performed whole-transcriptome microarray gene expression analysis in HeLa cells in order to understand the cellular and molecular mechanism of response to RuT7 complex. Results on biological action of ruthenium complex obtained on cellular level were reflected on molecular level as well. Analysis of functional categories and signaling and biochemical pathways that are associated with HeLa cells' response to ruthenium complex revealed that RuT7 complex leads HeLa cells through intrinsic (mitochondrial) apoptotic pathway, via indirect DNA damage made by action of reactive oxygen species and through direct DNA binding of RuT7. Performed molecular toxicity analysis has shown that RuT7 has fewer associated toxicity profiles than cisplatin. Altogether these results provide the basis for development of RuT7 in animal and pre-clinical studies as a potential drug candidate.

ORGANISM(S): Homo sapiens

PROVIDER: GSE72905 | GEO | 2015/09/11

SECONDARY ACCESSION(S): PRJNA295298

REPOSITORIES: GEO

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Cellular and molecular response to ruthenium(II)-arene complex with substituted picolinato ligand in HeLa cells

Project description:Ruthenium(II)-arene complexes are promising drug candidates for therapy of solid tumors. We have previously shown that ruthenium(II)-arene complex [Ru(η6-p-cymene)(L7)Cl] (RuT7) exerts cytotoxic effects in a panel of cancer cell lines (J. Organomet. Chem. 2014, 749, 343–349). In this study we analyzed in vitro cellular response and performed whole-transcriptome microarray gene expression analysis in HeLa cells in order to understand the cellular and molecular mechanism of response to RuT7 complex. Results on biological action of ruthenium complex obtained on cellular level were reflected on molecular level as well. Analysis of functional categories and signaling and biochemical pathways that are associated with HeLa cells' response to ruthenium complex revealed that RuT7 complex leads HeLa cells through intrinsic (mitochondrial) apoptotic pathway, via indirect DNA damage made by action of reactive oxygen species and through direct DNA binding of RuT7. Performed molecular toxicity analysis has shown that RuT7 has fewer associated toxicity profiles than cisplatin. Altogether these results provide the basis for development of RuT7 in animal and pre-clinical studies as a potential drug candidate. We hybridized each condition (control, RuT7 and CDDP) at each time point (12 h and 24 h) in triplicate, for a total of 18 samples.

2015-09-11 | E-GEOD-72905 | biostudies-arrayexpress

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2024-10-22 | GSE235884 | GEO

Homo sapiens

Project description:Cellular and molecular response to ruthenium(II)-arene complex with substituted picolinato ligand in HeLa cells

| PRJNA295298 | ENA

New ruthenium-cyclopentadienyl complexes affect colorectal cancer hallmarks showing high therapeutic potential

Project description:Colorectal cancer (CRC) is one of the most lethal cancers worldwide. Current therapeutic strategies are accompanied by low success rates and several side effects, representing a relevant clinical problem and requiring the discovery of new and more effective therapeutic alternatives. Ruthenium drugs emerged as one of the most promising metallodrugs due to their high selectivity to cancer cells. In this work, we studied for the first time the anticancer properties and mechanisms of action of four lead Ru-cyclopentadienyl compounds, namely PMC79, PMC78, LCR134 and LCR220, in CRC-derived cell lines. Biological assays were performed in CRC cell lines to evaluate cellular distribution, colony formation, cell cycle, proliferation, apoptosis, motility as well as cytoskeleton and mitochondrial alterations. Our results showed that all compounds displayed high bioactivity and selectivity, as shown by low IC50 concentrations against CRC cells. We observed that all Ru compounds had different intracellular distributions and inhibited to a high extent the clonogenic ability and proliferation of CRC cells. In addition, PMC79, LCR134 and LCR220 induced apoptosis, increased the levels of reactive oxygen species, induced mitochondrial alterations and affected F-actin cytoskeleton organization and cellular motility. A proteomic analysis showed that these compounds induce alterations in several cellular proteins related to the phenotypic alterations induced. Overall, we demonstrated that Ru compounds, in special PMC79 and LCR220, present promising anticancer activity in CRC cells and potential to be used as new metallodrugs for CRC therapy.

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Genome-wide monitoring of gene expression in Saccharomyces cerevisiae upon KP1019 treatment

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RDC and cisplatin transcriptomes

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Project description:Four glioblastoma cell line U-343 MG, U-343 MGa, U-343 MGa 31L, U-343 MGa Cl2:6 were derived form the same glioblastoma U-343. The RNA-seq was performed to identify their difference and better understand the glioblastoma heterogeneity.

2020-08-10 | E-MTAB-8620 | biostudies-arrayexpress

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Project description:In order to understand the underline mechanism of SHMT2 (serine hydroxymethyltransferase 2) effect on tumor growth, proteome and metabolome analysis were carried on an engineered HeLa cell line (HeLa-SHMT2-shSHMT2, short as HeLa-Ss), which has inducible SHMT2 over-expression or suppression by treating cell with tetracycline or IPTG, respectively. SHMT2 over-expression in HeLa-ss cell increased cell proliferation in vitro and in vivo, deceased expression of several mitochondrial complex I and III proteins, and increased glycine and glutathione levels in cells. BioID method identified more than 20 SHMT2 associated proteins that are involved in oxidation-reduction process. These results indicate SHMT2 involves in the regulation of cellular redox balance. SHMT2 suppression only reduced growth of cells under glycine depletion condition in cell culture. It increased expression of several proteins involved in glutaminolysis and amino acid transporters, and elevated metabolites related to glutamine metabolism. These results indicate tumor cells have a compensatory reaction after SHMT2 suppression. Further reducing glycine levels in cells by sodium benzoate caused cell death in cultured cell and slightly reduced tumor growth in vivo. Benzoate treatment induces more changes in protein expressions and metabolite levels, and it may provide a new addition for tumor treatment.

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