scholarly journals Dual phenotype of MDA-MB-468 cancer cells reveals mutual regulation of tensin3 and adhesion plasticity

2017 ◽  
Author(s):  
Astrid Veβ ◽  
Ulrich Blache ◽  
Laura Leitner ◽  
Angela R.M. Kurz ◽  
Anja Ehrenpfordt ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Focal Adhesion ◽  
Three Dimensional ◽  
Suspension Cells ◽  
Adhesion Protein ◽  
Cell Matrix ◽  
Mutual Regulation ◽  
Summary Statement ◽  
And Migration ◽  
Focal Adhesion Protein

AbstractPlasticity between adhesive and less-adhesive states is important for mammalian cell behaviour. To investigate adhesion plasticity, we have selected a stable isogenic subpopulation of MDA-MB-468 breast carcinoma cells which grows in suspension. These suspension cells are unable to re-adhere to various matrices or to contract three-dimensional collagen lattices. By transcriptome analysis, we identified the focal adhesion protein tensin3 (Tns3) as a determinant of adhesion plasticity. Tns3 is strongly reduced on mRNA and protein level in suspension cells. Furthermore, challenging breast cancer cells transiently with non-adherent conditions markedly reduces Tns3 expression, which is regained upon re-adhesion. Stable knockdown of Tns3 in parental cells results in defective adhesion, spreading and migration. Tns3 knockdown cells display impaired structure and dynamics of focal adhesion complexes as determined by immunostaining. Restoration of Tns3 expression in suspension cells partially rescues adhesion and focal contact composition. Our work identifies Tns3 as a critical focal adhesion component regulated by, and functionally contributing to, the switch between adhesive and non-adhesive states in MDA-MB-468 cancer cells.Summary statementWe identify the cell-matrix adapter protein tensin3 as a determinant of adhesion plasticity, using cancer cells selected for non-adherent growth. Tensin3 expression constitutes a feedback loop controlling adhesion and motility.

Novel focal adhesion protein kindlin-2 promotes the invasion of gastric cancer cells through phosphorylation of integrin β1 and β3

2013 ◽  
Vol 108 (2) ◽  
pp. 106-112 ◽  
Author(s):  
Zhanlong Shen ◽  
Yingjiang Ye ◽  
Tuuli Kauttu ◽  
Hanna Seppänen ◽  
Sanna Vainionpää ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Focal Adhesion ◽  
Integrin Β1 ◽  
Gastric Cancer Cells ◽  
Adhesion Protein ◽  
Focal Adhesion Protein

scholarly journals The focal adhesion protein Testin modulates KCNE2 potassium channel β subunit activity

Channels ◽  
2021 ◽  
Vol 15 (1) ◽  
pp. 229-238
Author(s):  
Maria Papanikolaou ◽  
Shawn M. Crump ◽  
Geoffrey W. Abbott
Keyword(s):  
Potassium Channel ◽  
Focal Adhesion ◽  
Β Subunit ◽  
Adhesion Protein ◽  
Focal Adhesion Protein

scholarly journals The extracellular-regulated protein kinase 5 (ERK5) enhances metastatic burden in triple-negative breast cancer through focal adhesion protein kinase (FAK)-mediated regulation of cell adhesion

Oncogene ◽  
2021 ◽  
Author(s):  
Qiuping Xu ◽  
Jingwei Zhang ◽  
Brian A. Telfer ◽  
Hao Zhang ◽  
Nisha Ali ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Protein Kinase ◽  
Tumor Growth ◽  
Focal Adhesion ◽  
Triple Negative Breast Cancer ◽  
Triple Negative ◽  
Metastatic Breast ◽  
Adhesion Protein ◽  
Focal Adhesion Protein

AbstractThere is overwhelming clinical evidence that the extracellular-regulated protein kinase 5 (ERK5) is significantly dysregulated in human breast cancer. However, there is no definite understanding of the requirement of ERK5 in tumor growth and metastasis due to very limited characterization of the pathway in disease models. In this study, we report that a high level of ERK5 is a predictive marker of metastatic breast cancer. Mechanistically, our in vitro data revealed that ERK5 was critical for maintaining the invasive capability of triple-negative breast cancer (TNBC) cells through focal adhesion protein kinase (FAK) activation. Specifically, we found that phosphorylation of FAK at Tyr397 was controlled by a kinase-independent function of ERK5. Accordingly, silencing ERK5 in mammary tumor grafts impaired FAK phosphorylation at Tyr397 and suppressed TNBC cell metastasis to the lung without preventing tumor growth. Collectively, these results establish a functional relationship between ERK5 and FAK signaling in promoting malignancy. Thus, targeting the oncogenic ERK5-FAK axis represents a promising therapeutic strategy for breast cancer exhibiting aggressive clinical behavior.

scholarly journals TRIM15 is a focal adhesion protein that regulates focal adhesion disassembly

Development ◽  
2014 ◽  
Vol 141 (19) ◽  
pp. e1906-e1906
Author(s):  
P. D. Uchil ◽  
T. Pawliczek ◽  
T. D. Reynolds ◽  
S. Ding ◽  
A. Hinz ◽  
...  
Keyword(s):  
Focal Adhesion ◽  
Adhesion Protein ◽  
Focal Adhesion Protein

Genomic structure and chromosomal mapping of the mouse hic-5 gene that encodes a focal adhesion protein

Gene ◽  
2000 ◽  
Vol 249 (1-2) ◽  
pp. 99-103 ◽  
Author(s):  
Jun'ichi Mashimo ◽  
Motoko Shibanuma ◽  
Hitoshi Satoh ◽  
Kazuhiro Chida ◽  
Kiyoshi Nose
Keyword(s):  
Focal Adhesion ◽  
Genomic Structure ◽  
Chromosomal Mapping ◽  
Adhesion Protein ◽  
Focal Adhesion Protein

scholarly journals Polycystins in Colorectal Cancer

2018 ◽  
Vol 20 (1) ◽  
pp. 104 ◽  
Author(s):  
Antonios Gargalionis ◽  
Efthimia Basdra ◽  
Athanasios Papavassiliou
Keyword(s):  
Colorectal Cancer ◽  
Calcium Influx ◽  
Cellular Functions ◽  
Selective Treatment ◽  
Adhesion Protein ◽  
Protein Molecules ◽  
Transduction Mechanisms ◽  
Novel Biomarkers ◽  
And Migration ◽  
Focal Adhesion Protein

Cell and extracellular matrix (ECM) biomechanics emerge as a distinct feature during the development and progression of colorectal cancer (CRC). Polycystins are core mechanosensitive protein molecules that mediate mechanotransduction in a variety of epithelial cells. Polycystin-1 (PC1) and polycystin-2 (PC2) are engaged in signal transduction mechanisms and during alterations in calcium influx, which regulate cellular functions such as proliferation, differentiation, orientation, and migration in cancer cells. Recent findings implicate polycystins in the deregulation of such functions and the formation of CRC invasive phenotypes. Polycystins participate in all aspects of the cell’s biomechanical network, from the perception of extracellular mechanical cues to focal adhesion protein and nuclear transcriptional complexes. Therefore, polycystins could be employed as novel biomarkers and putative targets of selective treatment in CRC.

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