NDLI: Thioridazine induces apoptosis by targeting the PI3K/Akt/mTOR pathway in cervical and endometrial cancer cells

Please wait, while we are loading the content...

Increased acetylation of lysine 317/320 of p53 caused by BCR-ABL protects from cytoplasmic translocation of p53 and mitochondria-dependent apoptosis in response to DNA damage

Low concentrations of isothiocyanates protect mesenchymal stem cells from oxidative injuries, while high concentrations exacerbate DNA damage

Protective effect of Homer 1a on tumor necrosis factor-α with cycloheximide-induced apoptosis is mediated by mitogen-activated protein kinase pathways

Thioridazine induces apoptosis by targeting the PI3K/Akt/mTOR pathway in cervical and endometrial cancer cells

Stimulation of platelet apoptosis by peptidoglycan from Staphylococcus aureus 113

Electronegative low-density lipoprotein induces cardiomyocyte apoptosis indirectly through endothelial cell-released chemokines

β-Arrestin prevents cell apoptosis through pro-apoptotic ERK1/2 and p38 MAPKs and anti-apoptotic Akt pathways

Apoptosis : Volume 17, Issue 8, August 2012

Apoptosis : Volume 17, Issue 7, July 2012

Apoptosis : Volume 17, Issue 6, June 2012

Apoptosis : Volume 17, Issue 5, May 2012

Apoptosis : Volume 17, Issue 4, April 2012

Apoptosis : Volume 17, Issue 3, March 2012

Apoptosis : Volume 17, Issue 2, February 2012

Apoptosis : Volume 17, Issue 1, January 2012

Apoptosis : Volume 16

Apoptosis : Volume 15

Apoptosis : Volume 14

Apoptosis : Volume 13

Apoptosis : Volume 12

Apoptosis : Volume 11

Apoptosis : Volume 10

Thioridazine induces apoptosis by targeting the PI3K/Akt/mTOR pathway in cervical and endometrial cancer cells

Content Provider	Springer Nature Link
Author	Kang, Sokbom Dong, Seung Myung Kim, Boh Ram Park, Mi Sun Trink, Barry Byun, Hyun Jung Rho, Seung Bae
Copyright Year	2012
Abstract	Recently, thioridazine (10-[2-(1-methyl-2-piperidyl) ethyl]-2-methylthiophenothiazine), a well-known anti-psychotic agent was found to have anti-cancer activity in cancer cells. However, the molecular mechanism of the agent in cellular signal pathways has not been well defined. Thioridazine significantly increased early- and late-stage apoptotic fraction in cervical and endometrial cancer cells, suggesting that suppression of cell growth by thioridazine was due to the induction of apoptosis. Cell cycle analysis indicated thioridazine induced the down-regulation of cyclin D1, cyclin A and CDK4, and the induction of p21 and p27, a cyclin-dependent kinase inhibitor. Additionally, we compared the influence of thioridazine with cisplatin used as a control, and similar patterns between the two drugs were observed in cervical and endometrial cancer cell lines. Furthermore, as expected, thioridazine successfully inhibited phosphorylation of Akt, phosphorylation of 4E-BP1 and phosphorylation of p70S6K, which is one of the best characterized targets of the mTOR complex cascade. These results suggest that thioridazine effectively suppresses tumor growth activity by targeting the PI3K/Akt/mTOR/p70S6K signaling pathway.
Starting Page	989
Ending Page	997
Page Count	9
File Format	PDF
ISSN	13608185
Journal	Apoptosis
Volume Number	17
Issue Number	9
e-ISSN	1573675X
Language	English
Publisher	Springer US
Publisher Date	2012-03-30
Publisher Place	Boston
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Thioridazine Apoptosis Anti-cancer activity mTOR signaling Cervical tumorigenesis Virology Biochemistry Oncology Cancer Research Cell Biology
Content Type	Text
Resource Type	Article
Subject	Pharmaceutical Science Biochemistry (medical) Cell Biology Clinical Biochemistry Cancer Research Pharmacology

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

Thioridazine induces apoptosis by targeting the PI3K/Akt/mTOR pathway in cervical and endometrial cancer cells

Thioridazine induces apoptosis by targeting the PI3K/Akt/mTOR pathway in cervical and endometrial cancer cells

ORIGINAL PAPER Thioridazine induces apoptosis by targeting the PI3K/Akt/mTOR pathway in cervical and endometrial cancer cells (2012)

Thymosin alpha 1 suppresses proliferation and induces apoptosis in breast cancer cells through PTEN-mediated inhibition of PI3K/Akt/mTOR signaling pathway

Grifolin induces apoptosis via inhibition of PI3K/AKT signalling pathway in human osteosarcoma cells

Growth factor progranulin promotes tumorigenesis of cervical cancer via PI3K/Akt/mTOR signaling pathway.

Bilobalide prevents apoptosis through activation of the PI3K/Akt pathway in SH-SY5Y cells

Knockdown of lncRNA TDRG1 Inhibits Tumorigenesis in Endometrial Carcinoma Through the PI3K/AKT/mTOR Pathway

LYG-202 exerts antitumor effect on PI3K/Akt signaling pathway in human breast cancer cells

Thioridazine induces apoptosis by targeting the PI3K/Akt/mTOR pathway in cervical and endometrial cancer cells

Similar Documents

Thioridazine induces apoptosis by targeting the PI3K/Akt/mTOR pathway in cervical and endometrial cancer cells

Thioridazine induces apoptosis by targeting the PI3K/Akt/mTOR pathway in cervical and endometrial cancer cells

ORIGINAL PAPER Thioridazine induces apoptosis by targeting the PI3K/Akt/mTOR pathway in cervical and endometrial cancer cells (2012)

Thymosin alpha 1 suppresses proliferation and induces apoptosis in breast cancer cells through PTEN-mediated inhibition of PI3K/Akt/mTOR signaling pathway

Grifolin induces apoptosis via inhibition of PI3K/AKT signalling pathway in human osteosarcoma cells

Growth factor progranulin promotes tumorigenesis of cervical cancer via PI3K/Akt/mTOR signaling pathway.

Bilobalide prevents apoptosis through activation of the PI3K/Akt pathway in SH-SY5Y cells

Knockdown of lncRNA TDRG1 Inhibits Tumorigenesis in Endometrial Carcinoma Through the PI3K/AKT/mTOR Pathway

LYG-202 exerts antitumor effect on PI3K/Akt signaling pathway in human breast cancer cells

Thioridazine induces apoptosis by targeting the PI3K/Akt/mTOR pathway in cervical and endometrial cancer cells