Browsing by Author "Bansal, Shivani"

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    Synthesis, in vitro Cytotoxicity Evaluation, and Docking Studies of Gloriosine Derivatives as Potential Anticancer Agents
    (John Wiley and Sons Inc, 2023) Goel, Bharat; Naik, Aliva; Tripathi, Nancy; Khan, Anjesh; Bansal, Sunil; Bansal, Shivani; Kumar Guru, Santosh; Jain, Shreyans K.
    In the present work, series of C10-amine and amide derivatives of gloriosine were synthesized and evaluated for in vitro cytotoxic activity against a panel of six human cancer cell lines (MDA-MB-231, U87, FaDu, SiHa, A549, and MCF-7) of multiple tissue origin. The synthesized compounds were characterized by 1H and 13C NMR and MS experiments. In vitro cytotoxicity study showed that most of the C10-amine derivatives demonstrated superior activity in two of the tested cell lines, namely U87 and FaDu cell lines, while C10-amide derivatives showed poor activity in all the cell lines. The C10-amine derivatives were subjected to molecular docking studies to explore their possible binding interactions with colchicine binding site of tubulin protein, and in-silico ADME profiling to study the drug-likeness. The C10-amine derivatives may be less toxic than gloriosine towards normal cells and may provide the lead for anticancer drug development. � 2023 Wiley-VCH GmbH.
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    Tgf? drives metabolic perturbations during epithelial mesenchymal transition in pancreatic cancer: Tgf? induced emt in pdac
    (MDPI, 2021) Rajagopal, Meena U.; Bansal, Shivani; Kaur, Prabhjit; Jain, Shreyans K.; Altadil, Tatiana; Hinzman, Charles P.; Li, Yaoxiang; Moulton, Joanna; Singh, Baldev; Bansal, Sunil; Chauthe, Siddheshwar Kisan; Singh, Rajbir; Banerjee, Partha P.; Mapstone, Mark; Fiandaca, Massimo S.; Federoff, Howard J.; Unger, Keith; Smith, Jill P.; Cheema, Amrita K.
    Pancreatic ductal adenocarcinoma (PDAC) is a highly lethal malignancy wherein a majority of patients present metastatic disease at diagnosis. Although the role of epithelial to mesenchymal transition (EMT), mediated by transforming growth factor beta (TGF?), in imparting an aggressive phenotype to PDAC is well documented, the underlying biochemical pathway perturbations driving this behaviour have not been elucidated. We used high-resolution mass spectrometry (HRMS) based molecular phenotyping approach in order to delineate metabolic changes concomitant to TGF?-induced EMT in pancreatic cancer cells. Strikingly, we observed robust changes in amino acid and energy metabolism that may contribute to tumor invasion and metastasis. Somewhat unexpectedly, TGF? treatment resulted in an increase in intracellular levels of retinoic acid (RA) that in turn resulted in increased levels of extracellular matrix (ECM) proteins including fibronectin (FN) and collagen (COL1). These findings were further validated in plasma samples obtained from patients with resectable pancreatic cancer. Taken together, these observations provide novel insights into small molecule dysregulation that triggers a molecular cascade resulting in increased EMT-like changes in pancreatic cancer cells, a paradigm that can be potentially targeted for better clinical outcomes. � 2021 by the authors. Licensee MDPI, Basel, Switzerland.