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Rottlerin induces autophagy which leads to apoptotic cell death through inhibition of PI3K/Akt/mTOR pathway in human pancreatic cancer stem cells
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TLDR
The data demonstrate that ROT can induce autophagy which leads to cell death in pancreatic CSCs and that gene silencing of Atg7 and Beclin1, or cotreatment of the autophagosome inhibitor, 3-methyladenine, inhibited ROT-inducedAutophagy and accelerated Rottlerin-induced apoptosis.About:
This article is published in Biochemical Pharmacology.The article was published on 2012-11-01. It has received 180 citations till now. The article focuses on the topics: Programmed cell death & PI3K/AKT/mTOR pathway.read more
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Apoptosis, autophagy, necroptosis, and cancer metastasis
TL;DR: This review summarizes the recent advances in the understanding of the mechanisms by which key regulators of apoptosis, autophagy, and necroptosis participate in cancer metastasis and discusses the crosstalk between apoptosis-autophagy-and-novoptosis involved in the regulation of cancer metastatic processes.
Journal Article
PI3K/Akt/mTOR signaling pathway in cancer stem cells: from basic research to clinical application.
Pu Xia,Xiao-Yan Xu +1 more
TL;DR: Overall, the current available data suggest that the PI3K/Akt/mTOR signaling pathway could be a promising target for development of CSC-target drugs.
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Cancer stem cells and chemoresistance: The smartest survives the raid
TL;DR: This review briefly introduces the basics of the conventional chemotherapies, updates the CSC theories, highlights the molecular and cellular mechanisms by which CSC smartly designs and utilizes multiple lines of self-defense to avoid being killed by chemotherapy, and concisely summarizes recent progress in studies on CSC-targeted therapies.
Journal ArticleDOI
Inhibition of PI3K/Akt/mTOR pathway by apigenin induces apoptosis and autophagy in hepatocellular carcinoma cells.
TL;DR: In vivo data showed that administration of apigenin decreased tumor growth and autophagy inhibition by 3-MA significantly enhanced the anticancer effect of apigin, and results reveal that apigen in inhibits cell proliferation and induces autophagic via suppressing the PI3K/Akt/mTOR pathway.
Journal ArticleDOI
Alternative Pathways of Cancer Cell Death by Rottlerin: Apoptosis versus Autophagy
Claudia Torricelli,Sara Salvadori,Giuseppe Valacchi,Giuseppe Valacchi,Karel Souček,Eva Slabáková,Michela Muscettola,Nila Volpi,Emanuela Maioli +8 more
TL;DR: It is found that Rottlerin induced a noncanonical, Bcl-2, Beclin 1, Akt, and ERK-independent autophagic death in the former- and the caspases-mediated apoptosis in the latter, in not starved conditions and in the absence of any other treatment.
References
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Autophagy in the Pathogenesis of Disease
TL;DR: This Review summarizes recent advances in understanding the physiological functions of autophagy and its possible roles in the causation and prevention of human diseases.
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Specificity and mechanism of action of some commonly used protein kinase inhibitors
TL;DR: The results demonstrate that the specificities of protein kinase inhibitors cannot be assessed simply by studying their effect on kinases that are closely related in primary structure, and proposes guidelines for the use of protein Kinase inhibitors in cell-based assays.
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Self-eating and self-killing: crosstalk between autophagy and apoptosis
TL;DR: The functional relationship between apoptosis and autophagy is complex in the sense that, under certain circumstances,autophagy constitutes a stress adaptation that avoids cell death (and suppresses apoptosis), whereas in other cellular settings, it constitutes an alternative cell-death pathway.
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Induction of autophagy and inhibition of tumorigenesis by beclin 1.
Xiao Huan Liang,Saadiya Jackson,Matthew N.J. Seaman,Kristy A. Brown,Bettina Kempkes,Hanina Hibshoosh,Beth Levine +6 more
TL;DR: It is shown that beclin 1 is a mammalian autophagy gene that can inhibit tumorigenesis and is expressed at decreased levels in human breast carcinoma, suggesting that decreased expression of Autophagy proteins may contribute to the development or progression of breast and other human malignancies.
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mTOR Inhibition Induces Upstream Receptor Tyrosine Kinase Signaling and Activates Akt
Kathryn E. O'Reilly,Fredi Rojo,Qing-Bai She,David B. Solit,Gordon B. Mills,Debra G. Smith,Heidi Lane,Francesco Hofmann,Daniel J. Hicklin,Dale L. Ludwig,José Baselga,Neal Rosen +11 more
TL;DR: The data suggest that feedback down-regulation of receptor tyrosine kinase signaling is a frequent event in tumor cells with constitutive mTOR activation, and reversal of this feedback loop by rapamycin may attenuate its therapeutic effects, whereas combination therapy that ablates mTOR function and prevents Akt activation may have improved antitumor activity.