School Of Basic And Applied Sciences

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    To Study the Dose and Time Dependent Effect of Human Insulin and Metformin on the Growth of Breast Cancer Cells
    (Central University of Punjab, 2012) Cholia, Ravi Prakash; Thakur, Sanjeev
    Cancer and diabetes, both are leading causes of mortality globally. Both the diseases are multifactorial and share number of common risk factors. Hyperglycemia and hyperinsulinemia which are the characteristic features of diabetes influences the growth rate and proliferation of tumor cells directly or indirectly. Type 2 diabetes shows stronger association with various cancers. Breast cancer is one of the malignancy affecting females worldwide. This study demonstrates that glucose not only acts as energy source in tumor cell but also acts as mitogen. Insulin not only regulates the blood glucose level but also induces growth and proliferation in MCF 7 and MDA MB 231 breast cancer cell lines independently and in combination with glucose. Metformin inhibit proliferation of MCF 7 and MDA MB 231 breast cancer cell lines independently and also in presence of glucose and insulin, but shows more inhibitory effect in presence of insulin as compare to glucose. Recently discovered insulin receptor antagonist S961 did not showed any significant response in breast cancer cell lines MCF 7 and MDA MB 231. The ineffectiveness is probably due to blocking effect of higher insulin dose. So with this investigation it can be concluded that metabolic alteration leads to proliferation of breast cancer cell lines.
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    Nischarin inhibition alters energy metabolism by activating AMP-activated protein kinase
    (American Society for Biochemistry and Molecular Biology Inc., 2017) Dong, Shengli; Baranwal, Somesh; Garcia, Anapatricia; Serrano-Gomez, Silvia; Eastlack, Steven; Iwakuma, Tomoo; Mercante, Donald; Mauvais-Jarvis, Franck; Alahari, Suresh K.; Dong, S.; Baranwal, S.; Garcia, A.; Serrano-Gomez, S.J.; Eastlack, S.; Iwakuma, T.; Mercante, D.; Mauvais-Jarvis, F.; Alahari, S.K.
    Nischarin (Nisch) is a key protein functioning as a molecular scaffold and thereby hosting interactions with several protein partners. To explore the physiological importance of Nisch, here we generated Nisch loss-of-function mutant mice and analyzed their metabolic phenotype. Nisch-mutant embryos exhibited delayed development, characterized by small size and attenuated weight gain. We uncovered the reason for this phenotype by showing that Nisch binds to and inhibits the activity of AMP-activated protein kinase (AMPK), which regulates energy homeostasis by suppressing anabolic and activating catabolic processes. The Nisch mutations enhanced AMPK activation and inhibited mechanistic target of rapamycin signaling in mouse embryonic fibroblasts as well as in muscle and liver tissues of mutant mice. Nisch-mutant mice also exhibited increased rates of glucose oxidation with increased energy expenditure, despite reduced overall food intake. Moreover, the Nisch-mutant mice had reduced expression of liver markers of gluconeogenesis associated with increased glucose tolerance. As a result, these mice displayed decreased growth and body weight. Taken together, our results indicate that Nisch is an important AMPK inhibitor and a critical regulator of energy homeostasis, including lipid and glucose metabolism. ? 2017 by The American Society for Biochemistry and Molecular Biology, Inc.