NDLI: GRP78 modulates cell adhesion markers in prostate Cancer and multiple myeloma cell lines

Content Provider	Springer Nature : BioMed Central
Author	Cultrara, Christopher N. Kozuch, Stephen D. Ramasundaram, Poornema Heller, Claudia J. Shah, Sunil Beck, Adah E. Sabatino, David Zilberberg, Jenny
Abstract	Background Glucose regulated protein 78 (GRP78) is a resident chaperone of the endoplasmic reticulum and a master regulator of the unfolded protein response under physiological and pathological cell stress conditions. GRP78 is overexpressed in many cancers, regulating a variety of signaling pathways associated with tumor initiation, proliferation, adhesion and invasion which contributes to metastatic spread. GRP78 can also regulate cell survival and apoptotic pathways to alter responsiveness to anticancer drugs. Tumors that reside in or metastasize to the bone and bone marrow (BM) space can develop pro-survival signals through their direct adhesive interactions with stromal elements of this niche thereby resisting the cytotoxic effects of drug treatment. In this study, we report a direct correlation between GRP78 and the adhesion molecule N-cadherin (N-cad), known to play a critical role in the adhesive interactions of multiple myeloma and metastatic prostate cancer with the bone microenvironment. Methods N-cad expression levels (transcription and protein) were evaluated upon siRNA mediated silencing of GRP78 in the MM.1S multiple myeloma and the PC3 metastatic prostate cancer cell lines. Furthermore, we evaluated the effects of GRP78 knockdown (KD) on epithelial-mesenchymal (EMT) transition markers, morphological changes and adhesion of PC3 cells. Results GRP78 KD led to concomitant downregulation of N-cad in both tumors types. In PC3 cells, GRP78 KD significantly decreased E-cadherin (E-cad) expression likely associated with the induction in TGF-β1 expression. Furthermore, GRP78 KD also triggered drastic changes in PC3 cells morphology and decreased their adhesion to osteoblasts (OSB) dependent, in part, to the reduced N-cad expression. Conclusion This work implicates GRP78 as a modulator of cell adhesion markers in MM and PCa. Our results may have clinical implications underscoring GRP78 as a potential therapeutic target to reduce the adhesive nature of metastatic tumors to the bone niche.
Related Links	https://bmccancer.biomedcentral.com/counter/pdf/10.1186/s12885-018-5178-8.pdf
Ending Page	14
Page Count	14
Starting Page	1
File Format	HTM / HTML
ISSN	14712407
DOI	10.1186/s12885-018-5178-8
Journal	BMC Cancer
Issue Number	1
Volume Number	18
Language	English
Publisher	BioMed Central
Publisher Date	2018-12-18
Access Restriction	Open
Subject Keyword	Cancer Research Oncology Surgical Oncology Health Promotion and Disease Prevention Biomedicine Medicine Public Health GRP78 Gene knockdown Epithelia-mesenchymal transition (EMT) Cell adhesion Medicine/Public Health
Content Type	Text
Resource Type	Article
Subject	Cancer Research Oncology Genetics
Journal Impact Factor	3.4/2023
5-Year Journal Impact Factor	3.8/2023

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

Cancer-initiating cells derived from established cervical cell lines exhibit stem-cell markers and increased radioresistance

HNF1α inhibition triggers epithelial-mesenchymal transition in human liver cancer cell lines

Loss of DIP2C in RKO cells stimulates changes in DNA methylation and epithelial-mesenchymal transition

MiR-200a inhibits epithelial-mesenchymal transition of pancreatic cancer stem cell

Involvement of DNMT 3B promotes epithelial-mesenchymal transition and gene expression profile of invasive head and neck squamous cell carcinomas cell lines

Grp78 promotes the invasion of hepatocellular carcinoma

Epithelial-mesenchymal transition markers screened in a cell-based model and validated in lung adenocarcinoma

PD-L1 knockdown suppresses vasculogenic mimicry of non-small cell lung cancer by modulating ZEB1-triggered EMT

Comparative gene co-expression network analysis of epithelial to mesenchymal transition reveals lung cancer progression stages

GRP78 modulates cell adhesion markers in prostate Cancer and multiple myeloma cell lines

Similar Documents

Cancer-initiating cells derived from established cervical cell lines exhibit stem-cell markers and increased radioresistance

HNF1α inhibition triggers epithelial-mesenchymal transition in human liver cancer cell lines

Loss of DIP2C in RKO cells stimulates changes in DNA methylation and epithelial-mesenchymal transition

MiR-200a inhibits epithelial-mesenchymal transition of pancreatic cancer stem cell

Involvement of DNMT 3B promotes epithelial-mesenchymal transition and gene expression profile of invasive head and neck squamous cell carcinomas cell lines

Grp78 promotes the invasion of hepatocellular carcinoma

Epithelial-mesenchymal transition markers screened in a cell-based model and validated in lung adenocarcinoma

PD-L1 knockdown suppresses vasculogenic mimicry of non-small cell lung cancer by modulating ZEB1-triggered EMT

Comparative gene co-expression network analysis of epithelial to mesenchymal transition reveals lung cancer progression stages

GRP78 modulates cell adhesion markers in prostate Cancer and multiple myeloma cell lines