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265 results on '"Babu, Phanithi Prakash"'

4. Reactive Oxygen Species in Glioma : Mechanisms and Challenges

Author

Deshpande, Ravindra Pramod, Babu, Phanithi Prakash, Walczak, Maria, Section editor, Chakraborti, Tapati, Section editor, Kar, Pulak, Section editor, Dam, Somasri, Section editor, Dey, Kuntal, Section editor, Kunnimalaiyaan, Muthusamy, Section editor, and Chakraborti, Sajal, editor

Published
2022
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22. Efficient Four‐Component Synthesis of 1,2,4‐Triazolo[1,5‐a]pyrimidines and Their In Vitro Antiproliferative Studies.

Author

Venkatesham, Papisetti, Kalonia, Mansi, Sangolkar, Akanksha Ashok, Mudiraj, Anwita, Babu, Phanithi Prakash, and Vedula, Rajeswar Rao

Subjects
AMINO acid residues, MOLECULAR docking, CELL migration, ACID catalysts, AROMATIC aldehydes, PYRIMIDINES
Abstract

Triazolopyrimidines are emerging as potential anticancer agents. Herein, we report a novel one‐pot four component synthesis of 2‐((2‐oxo‐2‐phenylethyl/benzyl)thio)‐10‐phenyl‐4,10‐dihydro‐9H‐indeno[1,2‐d][1,2,4]‐Triazolo[1,5‐a]pyrimidin‐9‐ones by the reaction of 1,3‐indanedione, aromatic aldehyde, 5‐amino‐4H‐1,2,4‐Triazol‐3‐thiol and phenacyl bromide in acetic acid with piperidine as catalyst at 90 °C for 13 hours. All the final compounds were identified on the basis of their FT‐IR, 1H NMR, 13C NMR and HRMS. The synthesized compounds were evaluated for their cell growth inhibition potential using MTT and wound healing assay, 13 compounds induced concentration dependent inhibition with IC50 below 10 μM against breast cancer cell lines (MCF‐7). Further, the molecular docking simulation were carried out for all the derivatives, amongst these thio phenacyl, 2,4‐dichlorophenyl 9H‐indeno [1,2,4]‐Triazolo[1,5‐a]pyrimidin‐9‐one (5 g) shows good binding interaction with amino acid residues. This is further confirmed by wound healing assay which shows that 5 g inhibits cell migration at increasing concentrations. [ABSTRACT FROM AUTHOR]

Published
2023
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33. The Tumor Suppressor MTUS1/ATIP1 Modulates Tumor Promotion in Glioma: Association with Epigenetics and DNA Repair

Author

Ranjan, Nikhil, Pandey, Vimal, Panigrahi, Manas Kumar, Klumpp, Lukas, Naumann, Ulrike, and Babu, Phanithi Prakash

Subjects
MTUS1/ATIP1, hypermethylation, recurrence, glioma, DNA repair, cell motility, lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens, lcsh:RC254-282, decitabine
Abstract

Glioblastoma (GBM) is a highly aggressive brain tumor. Resistance mechanisms in GBM present an array of challenges to understand its biology and to develop novel therapeutic strategies. We investigated the role of a TSG, MTUS1/ATIP1 in glioma. Glioma specimen, cells and low passage GBM sphere cultures (GSC) were analyzed for MTUS1/ATIP1 expression at the RNA and protein level. Methylation analyses were done by bisulfite sequencing (BSS). The consequence of chemotherapy and irradiation on ATIP1 expression and the influence of different cellular ATIP1 levels on survival was examined in vitro and in vivo. MTUS1/ATIP1 was downregulated in high-grade glioma (HGG), GSC and GBM cells and hypermethylation at the ATIP1 promoter region seems to be at least partially responsible for this downregulation. ATIP1 overexpression significantly reduced glioma progression by mitigating cell motility, proliferation and facilitate cell death. In glioma-bearing mice, elevated MTUS1/ATIP1 expression prolonged their survival. Chemotherapy, as well as irradiation, recovered ATIP1 expression both in vitro and in vivo. Surprisingly, ATIP1 overexpression increased irradiation-induced DNA-damage repair, resulting in radio-resistance. Our findings indicate that MTUS1/ATIP1 serves as TSG-regulating gliomagenesis, progression and therapy resistance. In HGG, higher MTUS1/ATIP1 expression might interfere with tumor irradiation therapy.

Published
2021

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