Department Of Human Genetics And Molecular Medicine

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Author: search.filters.author.Chander, HarishSubject: search.filters.subject.breast cancer

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    Cancer informatics analysis indicates high CHAC2 associated with unfavorable prognosis in breast cancer
    (Frontiers Media S.A., 2022-12-09T00:00:00) Chand, Subhash; Mehta, Vikrant; Sharma, Ratnesh K.; Anvikar, Anupkumar R.; Chander, Harish
    Breast cancer remains the most commonly diagnosed cancer worldwide and exhibits a poor prognosis. The induction of genetic changes deregulates several genes that increase the disposal towards this life-threatening disease. CHAC2, a member of the glutathione degrading enzyme family has been shown to suppress gastric and colorectal cancer progression, however, the expression of CHAC2 in breast cancer has not been reported. We did an analysis of CHAC2 expression in breast cancer patients from various online tools like UALCAN, GEPIA2, GENT2, TIMER2, and bcGenExminer v4.8. Further, we used the Kaplan-Meier plotter to establish the significance of CHAC2 in BC patient survival and prognosis while TISIDB and TIMER databases were used to investigate the filtration of immune cells. The results showed that CHAC2 levels were high in breast cancer patients and elevated CHAC2 was associated with low overall survival. Taken together, the results of the present study show that like its paralog CHAC1, CHAC2 may also be an important biomarker and could have a potential therapeutic implication in breast cancer. Copyright � 2022 Chand, Mehta, Sharma, Anvikar and Chander.
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    Wild-type p53 suppresses formin-binding protein-17 (FBP17) to reduce invasion
    (Oxford University Press, 2022-01-28T00:00:00) Suman, Prabhat; Mehta, Vikrant; Craig, Andrew W. B.; Chander, Harish
    Invading tumor cells develop membrane protruding structures called invadopodia to invade and metastasize. Previously, we have reported the role of formin-binding protein-17 (FBP17) in extracellular matrix degradation and invadopodia formation in breast cancer cells. Here, we report a novel axis between tumor-suppressor p53 and FBP17. We observed that cell lines with mutant p53 express FBP17 to a higher level. The expression of FBP17 was reduced upon stabilizing wild-type p53. Furthermore, the immunohistochemistry analysis of breast cancer tissue microarrays demonstrated the correlation between the accumulation of p53 and enhanced FBP17 staining in invasive ductal carcinomas. The double knockdown of p53 and FBP17 showed the contribution of FBP17 in the invasion of cancer cells where p53 lost the regulatory control over FBP17. Taken together, these studies indicate that FBP17 may be a marker to understand the invasion propensity of breast cancer. � 2022 The Author(s). Published by Oxford University Press. All rights reserved.
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    Mechanisms of Anti-Tumor Activity of Withania somnifera (Ashwagandha)
    (Routledge, 2020-06-17T00:00:00) Mehta, Vikrant; Chander, Harish; Munshi, Anjana
    Increasing herbal formulations have been used to treat several diseases including cancer. W. somnifera (Ashwagandha) is one such plant the extracts of which have been tested against a number of ailments including cancer, which remains as one of the most dreadful diseases on the globe. The ever-increasing number of cancer related mortality demands the development of novel chemopreventive agents with minimum side effects. Different compounds isolated from various parts of the plant like root, stem, and leaves have been reported to display significant anti-cancerous and immunomodulating properties and thus can be used alone or in combination with other chemotherapeutic drugs for cancer treatment. Through this review, we highlight the importance of W. somnifera in countering the potential oncogenic signaling mediators that are modulated by active constituents of W. somnifera in a variety of cancer types. Further, we hope that active constituents of W. somnifera will be tested in clinical trials so that they can be used as an important adjuvant in the near future for the effective treatment of cancer. � 2020 Taylor & Francis Group, LLC.