NDLI: DDB2 (damaged-DNA binding 2) protein: a new modulator of nanomechanical properties and cell adhesion of breast cancer cells

Content Provider	Royal Society of Chemistry (RSC)
Author	Barbieux, Claire Razafitianamaharavo, Angélina Hupont, Sébastien Soussen, Charles Klotz, Rémi Bécuwe, Philippe Pannequin, Rémi Brie, David Bacharouche, Jalal Grandemange, Stéphanie Francius, Grégory
Copyright Year	2016
Abstract	DDB2, known for its role in DNA repair, was recently shown to reduce mammary tumor invasiveness by inducing the transcription of IκBα, an inhibitor of NF-κB activity. Since cellular adhesion is a key event during the epithelial to mesenchymal transition (EMT) leading to the invasive capacities of breast tumor cells, the aim of this study was to investigate the role of DDB2 in this process. Thus, using low and high DDB2-expressing MDA-MB231 and MCF7 cells, respectively, in which DDB2 expression was modulated experimentally, we showed that DDB2 overexpression was associated with a decrease of adhesion abilities on glass and plastic areas of breast cancer cells. Then, we investigated cell nanomechanical properties by atomic force microscopy (AFM). Our results revealed significant changes in the Young's Modulus value and the adhesion force in MDA-MB231 and MCF7 cells, whether DDB2 was expressed or not. The cell stiffness decrease observed in MDA-MB231 and MCF7 expressing DDB2 was correlated with a loss of the cortical actin-cytoskeleton staining. To understand how DDB2 regulates these processes, an adhesion-related gene PCR-Array was performed. Several adhesion-related genes were differentially expressed according to DDB2 expression, indicating that important changes are occurring at the molecular level. Thus, this work demonstrates that AFM technology is an important tool to follow cellular changes during tumorigenesis. Moreover, our data revealed that DDB2 is involved in early events occurring during metastatic progression of breast cancer cells and will contribute to define this protein as a new marker of metastatic progression in this type of cancer.
Starting Page	5268
Ending Page	5279
Page Count	12
File Format	HTM / HTML PDF
ISSN	20403364
Volume Number	8
Issue Number	9
Journal	Nanoscale
DOI	10.1039/c5nr09126h
Language	English
Publisher	Royal Society of Chemistry
Access Restriction	Open
Subject Keyword	MCF-7 Enzyme inhibitor Breast cancer DNA repair Carcinogenesis Protein DDB2 IκBα NF-κB Atomic-force microscopy Gene The Cell Stiffness Mammary tumor Cancer
Content Type	Text
Resource Type	Article
Subject	Nanoscience and Nanotechnology

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

Damaged dna binding protein 2 plays a role in breast cancer cell growth.

Revisiting the role of the immunoproteasome in the activation of the canonical NF-κB pathway

Retinoic acid receptor 2 is a growth suppressor epigenetically silenced in mcf-7 human breast (2002).

BRCA1 Transcriptionally Regulates Damaged DNA Binding Protein (DDB2) In the DNA Repair Response Following UV-Irradiation

The inhibitor of κB kinase β (IKKβ) phosphorylates IκBα twice in a single binding event through a sequential mechanism.

Glycolytic enzyme HK2 promotes PD-L1 expression and breast cancer cell immune evasion

Furanodiene Induces Extrinsic and Intrinsic Apoptosis in Doxorubicin-Resistant MCF-7 Breast Cancer Cells via NF-κB-Independent Mechanism

Corrigendum: Furanodiene Induces Extrinsic and Intrinsic Apoptosis in Doxorubicin-Resistant MCF-7 Breast Cancer Cells via NF-κB-Independent Mechanism

Co-culture of primary human mammary fibroblasts and mcf-7 cells as an invitro breast cancer model (2004).

DDB2 (damaged-DNA binding 2) protein: a new modulator of nanomechanical properties and cell adhesion of breast cancer cells

Similar Documents

Damaged dna binding protein 2 plays a role in breast cancer cell growth.

Revisiting the role of the immunoproteasome in the activation of the canonical NF-κB pathway

Retinoic acid receptor 2 is a growth suppressor epigenetically silenced in mcf-7 human breast (2002).

BRCA1 Transcriptionally Regulates Damaged DNA Binding Protein (DDB2) In the DNA Repair Response Following UV-Irradiation

The inhibitor of κB kinase β (IKKβ) phosphorylates IκBα twice in a single binding event through a sequential mechanism.

Glycolytic enzyme HK2 promotes PD-L1 expression and breast cancer cell immune evasion

Furanodiene Induces Extrinsic and Intrinsic Apoptosis in Doxorubicin-Resistant MCF-7 Breast Cancer Cells via NF-κB-Independent Mechanism

Corrigendum: Furanodiene Induces Extrinsic and Intrinsic Apoptosis in Doxorubicin-Resistant MCF-7 Breast Cancer Cells via NF-κB-Independent Mechanism

Co-culture of primary human mammary fibroblasts and mcf-7 cells as an invitro breast cancer model (2004).

DDB2 (damaged-DNA binding 2) protein: a new modulator of nanomechanical properties and cell adhesion of breast cancer cells