Sn- and Ge- triorganometallics exert different cytotoxicity and modulation of migration in triple-negative breast cancer cell line MDA-MB-231

Hunáková, Ľuba; Brtko, Július

doi:10.1016/j.toxlet.2017.07.879

Cited by 8 publications

(12 citation statements)

References 30 publications

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“…Triorganotin compounds have been gaining importance in oncology due to their cytotoxic properties against various human cell lines including breast carcinoma [11,13,16,25]. Recently, we studied selected Sn- and Ge-triorganometallic compounds and have reported the different cytotoxicity and modulation of migration in triple-negative breast cancer cell line MDA-MB-231 [17]. Also, the in vitro effects of selected triorganotin ligands of nuclear retinoid X receptors have been studied in human MCF 7 breast cancer cells [19].…”

Section: Discussionmentioning

confidence: 99%

“…The cytotoxicity of tributyltin (TBT) in neuroblastoma cells [14] has been described at very low concentrations (0.1–1 μM), while in mammalian endothelial cells the IC50 value of TBT exceeded 1 μM concentration [15]. It has been suggested that some of the organotin compounds might be involved in cancer treatment via different mechanisms at the molecular level [16,17], thus opening up a new research subarea on organotin compounds [5,18,19].…”

Section: Introductionmentioning

confidence: 99%

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Genotoxic Effects of Tributyltin and Triphenyltin Isothiocyanates, Cognate RXR Ligands: Comparison in Human Breast Carcinoma MCF 7 and MDA-MB-231 Cells

Hunáková

Horváthová

Majerova

et al. 2019

IJMS

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The cytotoxicity of two recently synthesized triorganotin isothiocyanate derivatives, nuclear retinoid X receptor ligands, was tested and compared in estrogen-receptor-positive MCF 7 and -negative MDA-MB-231 human breast carcinoma cell lines. A 48 h MTT assay indicated that tributyltin isothiocyanate (TBT-ITC) is more cytotoxic than triphenyltin isothiocyanate (TPT-ITC) in MCF 7 cells, and the same trend was observed in the MDA-MB-231 cell line. A comet assay revealed the presence of both crosslinks and increasing DNA damage levels after the 17 h treatment with both derivatives. Differences in cytotoxicity of TBT-ITC and TPT-ITC detected by FDA staining correspond to the MTT data, communicating more pronounced effects in MCF 7 than in the MDA-MB-231 cell line. Both derivatives were found to cause apoptosis, as shown by the mitochondrial membrane potential (MMP) depolarization and caspase-3/7 activation. The onset of caspase activation correlated with MMP dissipation and the total cytotoxicity more than with the amount of active caspases. In conclusion, our data suggest that the DNA damage induced by TBT-ITC and TPT-ITC treatment could underlie their cytotoxicity in the cell lines studied.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Genotoxic Effects of Tributyltin and Triphenyltin Isothiocyanates, Cognate RXR Ligands: Comparison in Human Breast Carcinoma MCF 7 and MDA-MB-231 Cells

Hunáková

Horváthová

Majerova

et al. 2019

IJMS

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“…[ 26 ] Hunakova and Brtko reported the cytotoxicity of several tri‐ n ‐butyltin ( 1 and 4 – 6 ) and triphenyltin ( 2 , 3 , and 7 ) derivatives in MDA‐MB‐231 cells. [ 19 ] Tri ‐n‐ butyltin chloride ( 1 ), bromide ( 4 ), and iodide ( 5 ) were more cytotoxic in general, whereas tri ‐n‐ butyltin hydride ( 6 ) and triphenyltin hydride ( 7 ) were equally cytotoxic; triphenyltin hydroxide ( 3 ) was the least cytotoxic. [ 19 ]…”

Section: In Vitro Cytotoxicity In Cancer Cellsmentioning

confidence: 99%

“…[ 19 ] Tri ‐n‐ butyltin chloride ( 1 ), bromide ( 4 ), and iodide ( 5 ) were more cytotoxic in general, whereas tri ‐n‐ butyltin hydride ( 6 ) and triphenyltin hydride ( 7 ) were equally cytotoxic; triphenyltin hydroxide ( 3 ) was the least cytotoxic. [ 19 ]…”

Section: In Vitro Cytotoxicity In Cancer Cellsmentioning

confidence: 99%

“…[ 95 ] In a comparison of triphenyltin and tri ‐n‐ butyltin derivatives ( 7 and 32 ), the tri ‐n‐ butyltin derivatives were found to activate caspase‐3 and caspase‐7 more rapidly than did the positive control, staurosporine, or the triphenyltin derivative. [ 19 ] Indeed, an apoptotic activity measured using fluorescein diacetate and annexin assays also showed that tri ‐n‐ butyltin derivatives induced apoptosis much earlier than it was induced by triphenyltin derivatives. The authors suggested that these differences could be due to the faster metabolic rate of the tri ‐n‐ butyltin molecule compared with that of the triphenyltin complex, which was observed in rat, hamster, and human hepatic microsomes.…”

Section: Mechanism Of Action Of Triorganotin Complexesmentioning

confidence: 99%

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Triorganotin complexes in cancer chemotherapy: Mechanistic insights and future perspectives

Anasamy

Chee

Wong

et al. 2020

Applied Organom Chemis

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Current anticancer drug discovery and development efforts are aimed at identifying new complexes that can potently and selectively target DNA and modulate the functions of target proteins. Tin complexes, categorized as monoorganotin (RSnL3), diorganotin (R2SnL2), triorganotin (R3SnL), or tetraorganotin (R4SnL), are one of the most studied complexes in the metal‐based anticancer drug discovery and development field. Among these, diorganotins and triorganotins are widely reported to possess promising anticancer properties, with triorganotins offering several potential advantages over diorganotins, such as a higher total surface area causing higher lipophilicity and hence higher cytotoxicity in cancer cells. However, information on triorganotins' direct therapeutic targets, an in‐depth understanding of their mechanism of action, and useful therapeutic strategies are still lacking. In this review, we discuss the results from in vitro and in vivo mechanistic studies of triorganotin complexes as reported in recent years (2007–2019) and elaborate on the underlying mechanisms that could aid in the identification of triorganotin complex molecular targets. We conclude by identifying present obstacles faced by triorganotin complexes that avert their translation to the clinical phase and current strategies employed to overcome the aforementioned obstacles, and we offer considerations for their future development. These findings are anticipated to stimulate further developments of novel and innovative triorganotin complexes as anticancer drug candidates.

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Exploring the Potential of Metallodrugs as Chemotherapeutics for Triple Negative Breast Cancer

Nayeem

Contel

2021

Chemistry A European J

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This review focuses on studies of coordination and organometallic compounds as potential chemotherapeutics against triple negative breast cancer (TNBC) which has one of the poorest prognoses and worst survival rates from all breast cancer types. At present, chemotherapy is still the standard of care for TNBC since only one type of targeted therapy has been recently developed. References for metal-based compounds studied in TNBC cell lines will be listed, and those of metal-specific reviews, but a detailed overview will also be provided on compounds studied in vivo (mostly in mice models) and those compounds for which some preliminary mechanistic data was obtained (in TNBC cell lines and tumors) and/or for which bioactive ligands have been used. The main goal of this review is to highlight the most promising metalbased compounds with potential as chemotherapeutic agents in TNBC.

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Sn- and Ge- triorganometallics exert different cytotoxicity and modulation of migration in triple-negative breast cancer cell line MDA-MB-231

Cited by 8 publications

References 30 publications

Genotoxic Effects of Tributyltin and Triphenyltin Isothiocyanates, Cognate RXR Ligands: Comparison in Human Breast Carcinoma MCF 7 and MDA-MB-231 Cells

Genotoxic Effects of Tributyltin and Triphenyltin Isothiocyanates, Cognate RXR Ligands: Comparison in Human Breast Carcinoma MCF 7 and MDA-MB-231 Cells

Triorganotin complexes in cancer chemotherapy: Mechanistic insights and future perspectives

Exploring the Potential of Metallodrugs as Chemotherapeutics for Triple Negative Breast Cancer

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