NDLI: CD44v6 Coordinates Tumor Matrix-triggered Motility and Apoptosis Resistance*

Content Provider	PubMed Central
Author	Jung, Thorsten Gross, Wolfgang Zöller, Margot
Copyright Year	2011
Abstract	Tumor progression requires a crosstalk with the tumor surrounding, where the tumor matrix plays an essential role. We recently reported that only the matrix delivered by a CD44v6-competent (ASMLwt), but not that of a CD44v6-deficient (ASML-CD44vkd) rat pancreatic adenocarcinoma line supports metastasis formation. We here describe that this matrix provides an important feedback toward the tumor cell and that CD44v6 accounts for orchestrating signals received from the matrix. ASMLwt cells contain more hyaluronan synthase-3 and secrete higher amounts of >50 kDa HA than ASML-CD44vkd cells, which secrete more hyaluronidase. Only the ASMLwt-matrix supports migration and apoptosis resistance, which both can be initiated via CD44v6, c-Met, and α6β4 ligand binding and proceed via FAK, PI3K/Akt, and MAPK activation, respectively. However, c-Met- and α6β4-initiated signaling are strongly augmented by the association with CD44v6 as only very weak effects are observed in CD44v6-deficient cells. The same CD44v6-dependent convergence of motility- and apoptosis resistance-related signals also accounts for human tumor lines. Thus, CD44v6 promotes motility and apoptosis resistance via its involvement in assembling a matrix that, in turn, triggers activation of signaling cascades, which proceeds, independent of the initiating receptor-ligand interaction, in a concerted action via CD44v6.
Related Links	http://dx.doi.org/10.1074/jbc.m110.208421
Ending Page	15874
Page Count	13
Starting Page	15862
File Format	PDF
ISSN	00219258
e-ISSN	1083351X
Journal	The Journal of Biological Chemistry
Issue Number	18
Volume Number	286
Language	English
Publisher	American Society for Biochemistry and Molecular Biology
Publisher Date	2011-05-06
Access Restriction	Open
Rights Holder	American Society for Biochemistry and Molecular Biology
Subject Keyword	Cell Biology Biochemistry Molecular Biology Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Cell Biology Biochemistry Molecular Biology

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

CD44v6 Coordinates Tumor Matrix-triggered Motility and Apoptosis Resistance

CD44/CD44v6 a Reliable Companion in Cancer-Initiating Cell Maintenance and Tumor Progression

Involvement of Protective Autophagy in TRAIL Resistance of Apoptosis-defective Tumor Cells* S⃞

Atm Is Dispensable for p53 Apoptosis and Tumor Suppression Triggered by Cell Cycle Dysfunction

Intracellular acidification triggered by mitochondrial-derived hydrogen peroxide isan effector mechanism for drug-induced apoptosis in tumor cells.

HGF Promotes Motility in Primary Human Melanocytes through CD44v6 via a NF-kappa B/Egr-1/C/EBP-beta complex

Tumor Necrosis Factor (TNF) Signaling, but Not TWEAK (TNF-like Weak Inducer of Apoptosis)-triggered cIAP1 (Cellular Inhibitor of Apoptosis Protein 1) Degradation, Requires cIAP1 RING Dimerization and E2 Binding

A Unified Mechanism for Aminopeptidase N-based Tumor Cell Motility and Tumor-homing Therapy

A Unified Mechanism for Aminopeptidase N-based Tumor Cell Motility and Tumor-homing Therapy

CD44v6 Coordinates Tumor Matrix-triggered Motility and Apoptosis Resistance*

Similar Documents

CD44v6 Coordinates Tumor Matrix-triggered Motility and Apoptosis Resistance

CD44/CD44v6 a Reliable Companion in Cancer-Initiating Cell Maintenance and Tumor Progression

Involvement of Protective Autophagy in TRAIL Resistance of Apoptosis-defective Tumor Cells* S⃞

Atm Is Dispensable for p53 Apoptosis and Tumor Suppression Triggered by Cell Cycle Dysfunction

Intracellular acidification triggered by mitochondrial-derived hydrogen peroxide isan effector mechanism for drug-induced apoptosis in tumor cells.

HGF Promotes Motility in Primary Human Melanocytes through CD44v6 via a NF-kappa B/Egr-1/C/EBP-beta complex

Tumor Necrosis Factor (TNF) Signaling, but Not TWEAK (TNF-like Weak Inducer of Apoptosis)-triggered cIAP1 (Cellular Inhibitor of Apoptosis Protein 1) Degradation, Requires cIAP1 RING Dimerization and E2 Binding

A Unified Mechanism for Aminopeptidase N-based Tumor Cell Motility and Tumor-homing Therapy

A Unified Mechanism for Aminopeptidase N-based Tumor Cell Motility and Tumor-homing Therapy

CD44v6 Coordinates Tumor Matrix-triggered Motility and Apoptosis Resistance*