scholarly journals Influence of gap junction intercellular communication composed of connexin 43 on the antineoplastic effect of adriamycin in breast cancer cells

2016 ◽  
Vol 13 (2) ◽  
pp. 857-866 ◽  
Author(s):  
Guojun Jiang ◽  
Shuying Dong ◽  
Meiling Yu ◽  
Xi Han ◽  
Chao Zheng ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Gap Junction ◽  
Cancer Cells ◽  
Intercellular Communication ◽  
Connexin 43 ◽  
Breast Cancer Cells ◽  
Antineoplastic Effect ◽  
Gap Junction Intercellular Communication

scholarly journals Implication of Connexin 43 as a Tumor Suppressor in Pathogenesis of Breast Cancer

2021 ◽  
Author(s):  
Rabiya Rashid ◽  
Shazia Ali ◽  
Mahboob-Ul-Hussain
Keyword(s):  
Breast Cancer ◽  
Gap Junction ◽  
Intercellular Communication ◽  
Connexin 43 ◽  
Global Public Health ◽  
Down Regulation ◽  
Public Health Burden ◽  
Functional Dynamics ◽  
Gap Junction Intercellular Communication ◽  
Tumor Types

Breast cancer (BC) is a global public health burden, constituting the highest cancer incidence in women worldwide. Connexins 43 proteins propagate intercellular communication, gap junction intercellular communication (GJIC), remarkably expressed in several tumor types including liver, prostate, and breast. This domain of Cx43 possesses functionally critical sites identical to those involved in gating of channel and phosphorylation sites for various kinases. However, the mechanism by which Cx43 down regulation occurs in breast cancer is far from clear. Several mechanisms like Cx43 promoter hyper-methylation or a cancer-specific reduction of Cx43 expression/trafficking by the modulation of various components of the Cx43 life cycle give the idea to be involved in the down regulation of Connexins in mammary glands, but irreversible mutational alterations have not yet been proved to be among them. Summarily, the efficacy or specificity of these drugs can be increased by a combinatory approach considering an effect on both the Connexins and their regulatory molecules. This chapter will summarize the knowledge about the connexins and gap junction activities in breast cancer highlighting the differential expression and functional dynamics of connexins in the pathogenesis of the disease.

SDF-1α regulation in breast cancer cells contacting bone marrow stroma is critical for normal hematopoiesis

Blood ◽  
2006 ◽  
Vol 108 (10) ◽  
pp. 3245-3252 ◽  
Author(s):  
Anabella L. Moharita ◽  
Marcelo Taborga ◽  
Kelly E. Corcoran ◽  
Margarette Bryan ◽  
Prem S. Patel ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Bone Marrow ◽  
Cancer Cells ◽  
Connexin 43 ◽  
Breast Cancer Cells ◽  
Critical Role ◽  
Contact Inhibition ◽  
Enzyme Linked Immunosorbent Assay ◽  
Hematopoietic Regulation

Abstract Breast cancer cells (BCCs) show preference for the bone marrow (BM). An animal model showed 2 populations of BCCs in the BM with regard to their cycling states. An in vitro model of early BC entry into BM showed normal hematopoiesis. Here, we show a critical role for BCC-derived SDF-1α in hematopoietic regulation. The studies used a coculture of BM stroma and BCCs (cell lines and stage II BCCs). Northern blots and enzyme-linked immunosorbent assay (ELISA) showed gradual decreases in SDF-1α production in BCCs as they contact BM stroma, indicating partial microenvironmental effects caused by stroma on the BCCs. SDF-1 knock-down BCCs and increased exogenous SDF-1α prevented contact inhibition between BCCs and BM stroma. Contact inhibition was restored with low SDF-1α levels. Long-term culture-initiating assays with CD34+/CD38–/Lin– showed normal hematopoiesis provided that SDF-1α levels were reduced in BCCs. Gap junctions (connexin-43 [CX-43]) were formed between BCCs and BM stroma, with concomitant interaction between CD34+/CD38–/Lin– and BM stroma but not with the neighboring BCCs. In summary, SDF-1α levels are reduced in BCCs that contact BM stroma. The low levels of SDF-1α in BCCs regulate interactions between BM stroma and hematopoietic progenitors, consequently facilitating normal hematopoiesis.

scholarly journals Dysregulated connexin 43 in HER2-positive drug resistant breast cancer cells enhances proliferation and migration

Oncotarget ◽  
2017 ◽  
Vol 8 (65) ◽  
pp. 109358-109369 ◽  
Author(s):  
Elizabeth S. Yeh ◽  
Christina J. Williams ◽  
Carly Bess Williams ◽  
Ingrid V. Bonilla ◽  
Nancy Klauber-DeMore ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Connexin 43 ◽  
Breast Cancer Cells ◽  
Drug Resistant ◽  
Her2 Positive ◽  
And Migration ◽  
Proliferation And Migration
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