A
Alpna Tyagi
Researcher at University of Colorado Denver
Publications - 32
Citations - 1526
Alpna Tyagi is an academic researcher from University of Colorado Denver. The author has contributed to research in topics: Silibinin & Apoptosis. The author has an hindex of 20, co-authored 30 publications receiving 1405 citations. Previous affiliations of Alpna Tyagi include University of Montana & University of Colorado Hospital.
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Journal ArticleDOI
Resveratrol causes Cdc2-tyr15 phosphorylation via ATM/ATR-Chk1/2-Cdc25C pathway as a central mechanism for S phase arrest in human ovarian carcinoma Ovcar-3 cells.
Alpna Tyagi,Rana P. Singh,Chapla Agarwal,Sunitha Siriwardana,Robert A. Sclafani,Rajesh Agarwal +5 more
TL;DR: Findings for the first time identify that resveratrol causes Cdc2-tyr15 phosphorylation via ATM/ATR-Chk1/2-Cdc25C pathway as a central mechanism for DNA damage and S phase arrest selectively in ovarian cancer cells, and provide a rationale for the potential efficacy of ATM/ ATR agonists in the prevention and intervention of cancer.
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Gallic acid causes inactivating phosphorylation of cdc25A/cdc25C-cdc2 via ATM-Chk2 activation, leading to cell cycle arrest, and induces apoptosis in human prostate carcinoma DU145 cells.
TL;DR: This is the first report identifying gallic acid efficacy and associated mechanisms in an advanced and androgen-independent human prostate carcinoma DU145 cells, suggesting future in vivo efficacy studies with this agent in preclinical prostate cancer models.
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Silibinin inhibits constitutive activation of Stat3, and causes caspase activation and apoptotic death of human prostate carcinoma DU145 cells.
TL;DR: Results showed that silibinin inhibits constitutively active Stat3 and induces apoptosis in DU145 cells, and thus might have potential significance in therapeutic intervention of this deadly malignancy.
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Growth inhibition and regression of lung tumors by silibinin: modulation of angiogenesis by macrophage-associated cytokines and nuclear factor-kappaB and signal transducers and activators of transcription 3.
Alpna Tyagi,Rana P. Singh,Kumaraguruparan Ramasamy,Komal Raina,Elizabeth F. Redente,Lori D. Dwyer-Nield,Richard A. Radcliffe,Alvin M. Malkinson,Rajesh Agarwal +8 more
TL;DR: Therapeutic efficacy of silibinin in lung tumor growth inhibition and regression by antiangiogenic mechanisms seem to be mediated by decreased tumor-associated macrophages and cytokines, inhibition of hypoxia-inducible factor-1α, NF-κB, and STAT-3 activation, and up-regulation of the angiogenic inhibitors, Ang-2 and Tie-2.
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Silibinin Suppresses Growth of Human Colorectal Carcinoma SW480 Cells in Culture and Xenograft through Down-regulation of β-Catenin-Dependent Signaling
TL;DR: It is suggested that silibinin inhibits the growth of SW480 tumors carrying the mutant APC gene by down-regulating CDK8 and beta-catenin signaling and, therefore, could be an effective agent against CRC.