NDLI: Dioxin-mediated tumor progression through activation of mitochondria-to-nucleus stress signaling

Content Provider	PubMed Central
Author	Biswas, Gopa Srinivasan, Satish Anandatheerthavarada, Hindupur K. Avadhani, Narayan G.
Copyright Year	2007
Abstract	The environmental toxin 2,3,7,8-tetrachlorodibenzodioxin (TCDD) is a known human carcinogen; however, its precise mechanism of action remains unclear. Here we show that TCDD induces mitochondrial dysfunction, stress signaling, and tumor invasion by a mechanism similar to that described for mtDNA-depleted cells. Treatment of C2C12 cells with TCDD disrupted mitochondrial transmembrane potential in a time-dependent fashion and inhibited mitochondrial transcription and translation. TCDD also increased cytosolic [Ca2+]c and RyR1-specific Ca2+ release. These changes were associated with increased calcineurin (CnA) levels and activation of CnA-sensitive NF-κB/Rel (IκBβ-dependent) factors. Cells treated with TCDD displayed resistance to apoptosis, increased expression of the tumor marker cathepsin L, and a high degree of invasiveness as tested by the Matrigel membrane invasion assay. These effects were reversed by the CnA inhibitor FK506, and CnA mRNA silencing suggesting that TCDD triggers a signaling pathway similar to mtDNA depletion. Taken together, these results reveal that TCDD may promote tumor progression in vivo by directly targeting mitochondrial transcription and induction of mitochondrial stress signaling.
Related Links	http://dx.doi.org/10.1073/pnas.0706183104
Starting Page	186
File Format	PDF
ISSN	10916490
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	1
Volume Number	105
Language	English
Publisher	National Academy of Sciences
Publisher Date	2008-01-08
Access Restriction	Open
Rights Holder	National Academy of Sciences
Subject Keyword	Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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

Mitochondria to nucleus stress signaling

Mitochondria-to-nucleus stress signaling induces phenotypic changes, tumor progression and cell invasion

Hyaluronan-mediated CD44 activation of RhoGTPase signaling and cytoskeleton function promotes tumor progression

Suppression of ATAD2 inhibits hepatocellular carcinoma progression through activation of p53- and p38-mediated apoptotic signaling

Cadmium Induces Apoptosis in Pancreatic β-Cells through a Mitochondria-Dependent Pathway: The Role of Oxidative Stress-Mediated c-Jun N-Terminal Kinase Activation

Aryl hydrocarbon receptor activation by cAMP vs. dioxin: Divergent signaling pathways

Epigenetic modification of miR-663 controls mitochondria-to-nucleus retrograde signaling and tumor progression

Neurotrophin-mediated dendrite-to-nucleus signaling revealed by microfluidic compartmentalization of dendrites

Mitochondria-to-nucleus stress signaling in mammalian cells: Nature of nuclear gene targets, transcription regulation, and induced resistance to apoptosis

Dioxin-mediated tumor progression through activation of mitochondria-to-nucleus stress signaling

Similar Documents

Mitochondria to nucleus stress signaling

Mitochondria-to-nucleus stress signaling induces phenotypic changes, tumor progression and cell invasion

Hyaluronan-mediated CD44 activation of RhoGTPase signaling and cytoskeleton function promotes tumor progression

Suppression of ATAD2 inhibits hepatocellular carcinoma progression through activation of p53- and p38-mediated apoptotic signaling

Cadmium Induces Apoptosis in Pancreatic β-Cells through a Mitochondria-Dependent Pathway: The Role of Oxidative Stress-Mediated c-Jun N-Terminal Kinase Activation

Aryl hydrocarbon receptor activation by cAMP vs. dioxin: Divergent signaling pathways

Epigenetic modification of miR-663 controls mitochondria-to-nucleus retrograde signaling and tumor progression

Neurotrophin-mediated dendrite-to-nucleus signaling revealed by microfluidic compartmentalization of dendrites

Mitochondria-to-nucleus stress signaling in mammalian cells: Nature of nuclear gene targets, transcription regulation, and induced resistance to apoptosis

Dioxin-mediated tumor progression through activation of mitochondria-to-nucleus stress signaling