Chromatin as a Target for the DNA-Binding Anticancer Drugs

Majumder, Pritha; Pradhan, Suman; Devi, Pukhrambam Grihanjali; Pal, Sudipta; Dasgupta, Dipak

doi:10.1007/1-4020-5466-1_8

Cited by 10 publications

(5 citation statements)

References 175 publications

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“…It is speculated that the efficacy of anticancer drugs in cancer cells depends mostly on their binding mode to DNA . The interaction with DNA is a very important mechanism of the cytostatic and antiproliferative activity of organometallic compounds and complexes with anticancer activity, and has long been the subject of intense study for biotechnology and medical application, still representing the main target in the development of new anticancer drugs …”

Section: Resultsmentioning

confidence: 99%

Insights into the in vitro Anticancer Effects of Diruthenium‐1

et al. 2016

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The in vitro anticancer activity of the dinuclear trithiolato-bridged arene ruthenium complex diruthenium-1 (DiRu-1) was evaluated against a panel of human cancer cell lines used as in vitro models for hepatocellular carcinoma (HepG2 cells), estrogen-responsive breast adenocarcinoma (MCF-7 cells), and triple-negative breast adenocarcinoma (MDA-MB-231 cells). DiRu-1 is highly cytotoxic to these cell lines, demonstrating half-maximal inhibitory concentrations (IC ) in the low-nanomolar range (77±1.4 to 268.2±4.4 nm). The main molecular mechanisms responsible for the high cytotoxicity of DiRu-1 against the most responsive MCF-7 cell line (IC =77±1.4 nm) were investigated on the basis of the capacity of DiRu-1 to induce oxidative stress, apoptosis, and DNA damage, and to inhibit the cell cycle and proliferation. The results show that DiRu-1 triggers caspase-dependent apoptosis in MCF-7 cells on both the intrinsic and extrinsic pathways. Moreover, the Ru complex also causes necrosis, mitotic catastrophe, and autophagy. DiRu-1 increases the intracellular levels of reactive oxygen species (ROS), which play a significant role in its cytotoxicity and pro-apoptotic activity. An important mechanism of the anticancer activity of DiRu-1 appears to be the induction of DNA lesions, mainly due to apoptotic DNA fragmentation and cell-cycle arrest at the G /M checkpoint. These changes are correlated with the concentration of DiRu-1, the duration of the cell treatment, and the post-treatment time.

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Section: Resultsmentioning

confidence: 99%

Insights into the in vitro Anticancer Effects of Diruthenium‐1

et al. 2016

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“…Small molecules which are bind to DNA, inhibit enzymatic DNA substrate such as DNA polymerase and topoisomerase activity [57].…”

Section: Resultsmentioning

confidence: 99%

Arylstyrylimidazo[1,2-a]pyridine-based donor–acceptor acidochromic fluorophores: Synthesis, photophysical, thermal and biological properties

Aydıner

Yalçın

Ihmels

et al. 2015

Journal of Photochemistry and Photobiology A: Chemistry

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“…These enzymes carry out strand passage to maintain appropriate DNA structure during semiconservative DNA replication, transcription, recombination as well as chromosome condensation and decondensation [25] . All cells have topoisomerases that fall into 2 major classes: type I enzymes that make single-stranded cuts in DNA and type II enzymes that cut and pass double-stranded DNA [26] .…”

Section: Discussionmentioning

confidence: 99%

Somatostatin Elevates Topoisomerase II Alpha and Enhances the Cytotoxic Effect of Doxorubicin on Gallbladder Cancer Cells

Quan

Yue²,

Li³

et al. 2008

Chemotherapy

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Background: Gallbladder cancer is a common and lethal digestive malignancy which is nonsensitive to routine chemotherapy. Doxorubicin (DOX) is one of the major chemotherapeutic drugs for patients with gallbladder cancer. We tried to evaluate if combined use of somatostatin (SST) and DOX could have synergistic effect in the treatment of gallbladder cancer. Methods: Cells from the human gallbladder cancer cell line GBC-SD were treated with SST. Cell cycle analysis was determined by flow cytometry. Western blot analysis was performed to determine the protein levels of topoisomerase IIα (Topo IIα) after SST treatment. RT-PCR was utilized to detect SST receptors in GBC-SD cells. Finally, the chemotherapeutic effect of DOX combined with SST treatment on cellular growth was measured by MTT assay. Results: SST could induce cell cycle arrest in S phase and upregulate Topo IIα expression in GBC-SD cells. GBC-SD cells expressed all 5 subtypes of SST receptors. Finally, combined use of DOX with SST had a synergistic cytotoxic effect on GBC-SD cells. Conclusion: SST, a naturally occurring, nontoxic compound, may represent a novel adjuvant chemotherapeutic agent for patients with gallbladder cancer.

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Chromatin as a Target for the DNA-Binding Anticancer Drugs

Cited by 10 publications

References 175 publications

Insights into the in vitro Anticancer Effects of Diruthenium‐1

Insights into the in vitro Anticancer Effects of Diruthenium‐1

Arylstyrylimidazo[1,2-a]pyridine-based donor–acceptor acidochromic fluorophores: Synthesis, photophysical, thermal and biological properties

Somatostatin Elevates Topoisomerase II Alpha and Enhances the Cytotoxic Effect of Doxorubicin on Gallbladder Cancer Cells

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