Department Of Botany
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Item Vitex negundo and its medicinal value(Springer, 2018) Gill, Balraj Singh; Mehra, Richa; Navget; Kumar, SanjeevNatural products are rich in several potent bioactive compounds, targeting complex network of proteins involved in various diseases. Vitex negundo (VN), commonly known as “chaste tree”, is an ethnobotanically important plant with enormous medicinal properties. Different species of Vitex vary in chemical composition, thus producing different phytochemicals. Several bioactive compounds have been extracted from leaves, seeds, roots in form of volatile oils, flavonoids, lignans, iridoids, terpenes, and steroids. These bioactive compounds exhibit anti-inflammatory, antioxidant, antidiabetic, anticancer, antimicrobial. VN is typically known for its role in the modulation of cellular events like apoptosis, cell cycle, motility of sperms, polycystic ovary disease, and menstrual cycle. VN, reportedly, perturbs many cancer-signaling pathways involving p-p38, p-ERK1/2, and p-JNK in LPS-elicited cells, N-terminal kinase (JNK), COX-1 pathways, MAPK, NF-κB, tumor necrosis factor α (TNF-α), Akt, mTOR, vascular endothelial growth factor, hypoxia-inducible factor (HIF-1α). Several bioactive compounds obtained from VN have been commercialized and others are under investigation. This is the first review presenting up-to-date information about the VN, its bioactive constituents and their mode of action.Item Metformin inhibits human breast cancer cell growth by promoting apoptosis via a ROS-independent pathway involving mitochondrial dysfunction: pivotal role of superoxide dismutase (SOD)(Springer, 2018) Sharma, Prateek; Kumar, SanjeevPurpose Despite a growing body of evidence indicating a potential efficacy of the anti-diabetic metformin as anti-cancer agent, the exact mechanism underlying this efficacy has remained largely unknown. Here, we aimed at assessing putative mechanisms associated with the ability of metformin to reduce the proliferation and migration of breast cancer cells. Methods A battery of in vitro assays including MTT, colony formation, NBT and scratch wound healing assays were performed to assess the viability, proliferation, anti-oxidative potential and migration of breast cancer-derived MCF-7, MDA-MB-231 and T47D cells, respectively. Reactive oxygen species (ROS) assays along with fluorescence microscopy were used to assess apoptotic parameters. Quantification of SOD, Bcl-2, Bax, MMPs, miR-21 and miR-155 expression was performed using qRT-PCR. Results We found that metformin inhibited the growth, proliferation and clonogenic potential of the breast cancer-derived cells tested. ROS levels were found to be significantly reduced by metformin and, concomitantly, superoxide dismutase (SOD) isoforms were found to be upregulated. Mitochondrial dysfunction was observed in metformin treated cells, indicating apoptosis. In metastatic MDA-MB-231 cells, migration was found to be suppressed by metformin through deregulation of the matrix metalloproteinases MMP-2 and MMP-9. The oncogenic microRNAs miR-21 and miR-155 were found to be downregulated by metformin, which may be correlated with the suppression of cell proliferation and/or migration. Conclusions Our data indicate that metformin may play a pivotal role in modulating the anti-oxidant system, including the SOD machinery, in breast cancer-derived cells. Our observations were validated by in silico analyses, indicating a close interaction between SOD and metformin. We also found that metformin may inhibit breast cancer-derived cell proliferation through apoptosis induction via the mitochondrial pathway. Finally, we found that metformin may modulate the pro-apoptotic Bax, anti-apoptotic Bcl-2, MMP-2, MMP-9, miR-21 and miR-155 expression levels. These findings may be instrumental for the clinical management and/or (targeted) treatment of breast cancer.Item Ganoderma lucidum targeting lung cancer signaling: A review(SAGE Publications Ltd, 2017) Gill, Balraj Singh; Navgeet; Kumar, Sanjeev; Gill, B.S.; Navgeet, Kumar, S.Lung cancer causes huge mortality to population, and pharmaceutical companies require new drugs as an alternative either synthetic or natural targeting lung cancer. The conventional therapies cause side effects, and therefore, natural products are used as a therapeutic candidate in lung cancer. Chemical diversity among natural products highlights the impact of evolution and survival of fittest. One such neglected natural product is Ganoderma lucidum used for promoting health and longevity for a longer time. The major bioconstituents of G. lucidum are mainly terpenes, polysaccharides, and proteins, which were explored for various activities ranging from apoptosis to autophagy. The bioconstituents of G. lucidum activate plasma membrane receptors and initiate various downstream signaling leading to nuclear factor-?B, phosphoinositide 3-kinase, Akt, and mammalian target of rapamycin in cancer. The bioconstituents regulate the expression of various genes involved in cell cycle, immune response, apoptosis, and autophagy in lung cancer. This review highlights the inextricable role of G. lucidum and its bioconstituents in lung cancer signaling for the first time. ? The Author(s) 2017.Item Ganoderic acid modulating TNF and its receptors: in silico and in vitro study(Springer, 2017) Gill, Balraj Singh; Navgeet; Kumar, SanjeevCancer is a multifactorial disease with a network of genes causing genetic alterations. The sophisticated techniques in molecular biology revealed different cancer pathway, but their mechanistic approach is still shrouded. Tumor necrosis factor and TNF-related apoptosis-inducing ligand receptors (DR5) emerged as potential target drug for the cancer therapy. Among natural products basidiomycete fungus, Ganoderma lucidum and its constituents endowed with a plethora of activities modulating signaling in cancer. Ganoderic acid, a triterpene with lanosteroidal skeleton play an inextricable role in modulating signaling cascades in various mitogenic pathways. In the present study, receptor-based molecular docking was performed to study the dynamic behavior of the docked complexes and the molecular interactions between ganoderic acid and its isoforms with tumor necrosis factor and its receptor (DR5). The top scoring compounds were compared with the already documented natural inhibitor of tumor necrosis factor, DR5-curcumin, catechin, bupropion, pentoxyphyllin for their binding affinity and other absorption, distribution, metabolism, excretion, and toxicity properties. Ganoderic acid A interact more promising as compared with other isoforms with GScore (−9.858 (kcal/mol), Lipophilic EvdW (−1.7), H Bond (−0.9), Glide emodel (−40.5) with the involvement of Tyr 151, Leu 120 and Gln 149 residues during binding with tumor necrosis factor. During docking of ganoderic acid with DR5, ganoderic acid A exhibits GScore (−8.7), HBond (−2.9), Glide emodel (−30.0) with the involvement of hydrogen bonding inMet99, Arg101, Pro97, Glu98 residues. Natural inhibitors already documented exhibit low-binding energy and other docking parameters, which have an edge of ganoderic acid A to tumor necrosis factor and DR5. Ganoderic acid A efficiently inhibits the proliferation, viability, and intracellular reactive oxygen