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Your search keyword '"Tripura, Chaturvedula"' showing total 19 results
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19 results on '"Tripura, Chaturvedula"'

9. Synthesis and biological evaluation of novel imidazo[1,2-a]pyridine-oxadiazole hybrids as anti-proliferative agents: Study of microtubule polymerization inhibition and DNA binding

Author

Sigalapalli, Dilep Kumar, primary, Kiranmai, Gaddam, additional, Parimala Devi, G., additional, Tokala, Ramya, additional, Sana, Sravani, additional, Tripura, Chaturvedula, additional, Jadhav, Govinda Shivaji, additional, Kadagathur, Manasa, additional, Shankaraiah, Nagula, additional, Nagesh, Narayana, additional, Babu, Bathini Nagendra, additional, and Tangellamudi, Neelima D., additional

Published
2021
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13. Targeting tubulin polymerization and DNA binding of 4-thiazolidinone–umbelliferone hybrids: synthesis and cytotoxicity evaluation

Author

Sigalapalli, Dilep Kumar, primary, Kiranmai, Gaddam, additional, Tokala, Ramya, additional, Tripura, Chaturvedula, additional, Ambatwar, Ramesh, additional, Nunewar, Saiprasad N., additional, Kadagathur, Manasa, additional, Shankaraiah, Nagula, additional, Nagesh, Narayana, additional, Nagendra Babu, Bathini, additional, and Tangellamudi, Neelima D., additional

Published
2021
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17. Vitamin C enhances epigenetic modifications induced by 5-azacytidine and cell cycle arrest in the hepatocellular carcinoma cell lines HLE and Huh7

Author

Sajadian, Sahar Olsadat, Tripura, Chaturvedula, Samani, Fazel Sahraneshin, Ruoss, Marc, Dooley, Steven, Baharvand, Hossein, and Nussler, Andreas K.

Subjects
TETs, Carcinoma, Hepatocellular, Epithelial-Mesenchymal Transition, Cell Survival, Research, Liver Neoplasms, 5-Azacytidine, Drug Synergism, Ascorbic Acid, Cell Cycle Checkpoints, GADD45B, EMT/MET, DNA Methylation, Epigenesis, Genetic, Gene Expression Regulation, Neoplastic, Snail, Cell Line, Tumor, Azacitidine, Humans, 5hmC, Vitamin C, neoplasms, Cell Proliferation
Abstract

Background 5-Azacytidine (5-AZA), a DNA methyl transferase inhibitor, is a clinically used epigenetic drug for cancer therapy. Recently, we have shown that 5-AZA upregulates ten-eleven translocation (TET) protein expression in hepatocellular carcinoma (HCC) cells, which induce active demethylation. Vitamin C facilitates TET activity and enhances active demethylation. The aim of this study is to investigate whether vitamin C is able to enhance the effect of 5-AZA on active demethylation and to evaluate its consequence in HCC cell lines. Methods HCC cell lines (Huh7 and HLE) were treated with 5-AZA and vitamin C. After 48 h of treatment, viability (resazurin conversion), toxicity (lactose dehydrogenase (LDH) release), and proliferation ((proliferating cell nuclear antigen (PCNA)) of single- and combined-treated cells were assessed. The effect of the treatment on 5-hydroxymethylcytosine (5hmC) intensity (immunofluorescence (IF) staining), TET, Snail, GADD45B, and P21 mRNA (real-time PCR) and protein expression (Western blot) were investigated. Results Our results indicated that vitamin C enhances the anti-proliferative and apoptotic effect of 5-AZA in HCC cell lines. By further analyzing the events leading to cell cycle arrest, we have shown for the first time in HCC that the combination of 5-AZA and vitamin C leads to an enhanced downregulation of Snail expression, a key transcription factor governing epithelial-mesenchymal transition (EMT) process, and cell cycle arrest. Conclusions We conclude that when combined with 5-AZA, vitamin C enhances TET activity in HCC cells, leading to induction of active demethylation. An increase in P21 expression as a consequence of downregulation of Snail accompanied by the induction of GADD45B expression is the main mechanism leading to cell cycle arrest in HCCs.

Published
2016

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