Gap junctional intercellular communication in adipose-derived stromal/stem cells is cell density-dependent and positively impacts adipogenic differentiation

2017 ◽  
Vol 233 (4) ◽  
pp. 3315-3329 ◽  
Author(s):  
Miriam Wiesner ◽  
Oliver Berberich ◽  
Christiane Hoefner ◽  
Torsten Blunk ◽  
Petra Bauer-Kreisel
Keyword(s):  
Stem Cells ◽  
Cell Density ◽  
Intercellular Communication ◽  
Adipogenic Differentiation ◽  
Gap Junctional Intercellular Communication ◽  
Density Dependent ◽  
Gap Junctional ◽  
Stromal Stem Cells

scholarly journals Cancer Prevention and Therapy of Two Types of Gap Junctional Intercellular Communication–Deficient “Cancer Stem Cell”

Cancers ◽  
2019 ◽  
Vol 11 (1) ◽  
pp. 87 ◽  
Author(s):  
James Trosko
Keyword(s):  
Stem Cells ◽  
Stem Cell ◽  
Cancer Stem Cells ◽  
Cancer Stem Cell ◽  
Intercellular Communication ◽  
Adult Stem Cells ◽  
Gap Junctional Intercellular Communication ◽  
Organ Specific ◽  
Connexin Genes ◽  
Gap Junctional

Early observations showed a lack of growth control and terminal differentiation with a lack of gap junctional intercellular communication (GJIC). Subsequent observations showed that epigenetic tumor promoters and activated oncogenes, which block gap junction function, provide insights into the multi-stage, multi-mechanism carcinogenic process. With the isolation of embryonic induced pluri-potent stem cells and organ-specific adult stem cells, gap junctions were linked to early development. While tumors and tumor cell lines are a heterogeneous mixture of “cancer stem cells” and “cancer non-stem cells”, the cancer stem cells seem to be of two types, namely, they express (a) no connexin genes or (b) connexin genes, but do not have functional GJIC. These observations suggest that these “cancer stem cells” originate from normal adult stem cells or from the de-differentiation or re-programming of somatic differentiated cells. This “Concept Paper” provides a hypothesis that “cancer stem cells” either originate from (a) organ-specific adult stem cells before the expression of the connexin genes or (b) organ-specific adult stem cells that just express gap junction genes but that the connexin proteins are rendered dysfunctional by activated oncogenes. Therefore, cancer prevention and therapeutic strategies must account for these two different types of “cancer stem cell”.

scholarly journals Specific N-cadherin–dependent pathways drive human breast cancer dormancy in bone marrow

2021 ◽  
Vol 4 (7) ◽  
pp. e202000969
Author(s):  
Garima Sinha ◽  
Alejandra I Ferrer ◽  
Seda Ayer ◽  
Markos H El-Far ◽  
Sri Harika Pamarthi ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Stem Cells ◽  
Intercellular Communication ◽  
Drug Targets ◽  
Connexin 43 ◽  
Gap Junctional Intercellular Communication ◽  
Bm Niche ◽  
Cancer Dormancy ◽  
Apoptotic Pathways ◽  
Gap Junctional

The challenge for treating breast cancer (BC) is partly due to long-term dormancy driven by cancer stem cells (CSCs) capable of evading immune response and resist chemotherapy. BC cells show preference for the BM, resulting in poor prognosis. CSCs use connexin 43 (Cx43) to form gap junctional intercellular communication with BM niche cells, fibroblasts, and mesenchymal stem cells (MSCs). However, Cx43 is an unlikely target to reverse BC dormancy because of its role as a hematopoietic regulator. We found N-cadherin (CDH2) and its associated pathways as potential drug targets. CDH2, highly expressed in CSCs, interacts intracellularly with Cx43, colocalizes with Cx43 in BC cells within BM biopsies of patients, and is required for Cx43-mediated gap junctional intercellular communication with BM niche cells. Notably, CDH2 and anti-apoptotic pathways maintained BC dormancy. We thereby propose these pathways as potential pharmacological targets to prevent dormancy and chemosensitize resistant CSCs.

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