C-Terminal Tensin-Like Gene Functions as an Oncogene and Promotes Cell Motility in Pancreatic Cancer

Alghamdi, Saleh; Cachat, Julien; Albasri, Abdulkader M.; Ahmed, Mohammed; Jackson, Darryl; Zaitoun, Abed M.; Guppy, Naomi; Otto, W; Alison, Malcolm R.; Kindle, Karin B.; Ilyas, Mohammad

doi:10.1097/mpa.0b013e3182557ceb

Cited by 32 publications

(39 citation statements)

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“…Similar effects are observed in a variety of cancer cell lines (Liao et al, 2009, Albasri et al, 2009, Albasri et al, 2011b, Al-Ghamdi et al, 2011, Al-Ghamdi et al, 2013) and are believed to contribute to the tumorigenicities of these cancer cells. Several molecular mechanisms underlying ctenmediated cell migration have been established.…”

Section: Biological Functionsupporting

confidence: 54%

“…Despite of its low expression in the normal kidney, cten is further downregulated in kidney cancers (Martuszewska et al, 2009). Although it may not be expressed in other normal tissues, cten expression has been found to increase significantly in many types of cancer including thymoma, gastric, colorectal, breast, lung, skin, and pancreatic cancer (Liao et al, 2009, Sasaki et al, 2003b, Sasaki et al, 2003a, Katz et al, 2007, Albasri et al, 2011b, Albasri et al, 2011c, Al-Ghamdi et al, 2011, Sjoestroem et al, 2013, Li et al, 2010, Al-Ghamdi et al, 2013, Sakashita et al, 2008), suggesting that overexpression of cten in certain tissues may play a critical role in tumorigenesis.…”

Section: Expression Activation and Turnovermentioning

confidence: 99%

“…In cancer cells, cten levels appear to correlate with their tumorigenicities as measured by cell invasion, anchorage-independent growth, colony formation, and xenograft assays (Liao et al, 2009, Albasri et al, 2009, Albasri et al, 2011b, Al-Ghamdi et al, 2011, Al-Ghamdi et al, 2013). However, cten does not contribute to tumorigenicity by promoting cell proliferation, since overexpression of cten has limited effects on cancer cell growth (Lo et al, 2005, Albasri et al, 2009, Al-Ghamdi et al, 2013).…”

Section: Biological Functionmentioning

confidence: 99%

“…However, cten does not contribute to tumorigenicity by promoting cell proliferation, since overexpression of cten has limited effects on cancer cell growth (Lo et al, 2005, Albasri et al, 2009, Al-Ghamdi et al, 2013). In addition to mechanisms involving cten-mediated cell migration and EGFR homeostasis mentioned above, cten interaction with β-catenin also contributes to enhancing tumorigenicity (Liao et al, 2009).…”

Section: Biological Functionmentioning

confidence: 99%

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C-terminal tensin-like (CTEN): A promising biomarker and target for cancer

2014

The International Journal of Biochemistry & Cell Biology

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C-terminal tensin-like (cten, also known as tensin4, TNS4) is a member of the tensin family. Cten protein, like the other three tensin family members, localizes to focal adhesion sites but only shares sequence homology with other tensins at its C-terminal region, which contains the Src SH2 and PTB domains. Cten is abundantly expressed in normal prostate and placenta and is down-regulated in prostate cancer. However, overexpression of cten frequently associates with tumors derived from breast, colon, lung, stomach, skin and pancreas. A variety of cancer-associated growth factors and cytokines induce cten expression. Up-regulated cten promotes cell motility, prolongs epidermal growth factor receptor signaling, and enhances tumorigenicity. Emerging findings suggest that cten is a promising biomarker and therapeutic target for various cancers.

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Section: Biological Functionsupporting

confidence: 54%

Section: Expression Activation and Turnovermentioning

confidence: 99%

Section: Biological Functionmentioning

confidence: 99%

Section: Biological Functionmentioning

confidence: 99%

See 2 more Smart Citations

C-terminal tensin-like (CTEN): A promising biomarker and target for cancer

2014

The International Journal of Biochemistry & Cell Biology

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“…China has established a proteomic 2-DE database for human gastric tissues, providing crucial information for the proteomic analysis of normal tissues and those with pathological changes (Liao et al, 2009;Al-Ghamdi et al, 2013). Proteomic analysis revealed that 283 proteins were upregulated and 242 were downregulated in the CTEN-siRNA-1 group, of which the expression levels of E-cadherin and ERK proteins changed significantly.…”

Section: Discussionmentioning

confidence: 99%

Proteomic analysis of susceptibility in intestinal stromal tumors

Yang

Chen²,

Zhang

et al. 2015

Genet. Mol. Res.

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ABSTRACT. We analyzed the susceptibility of intestinal stromal tumors using cell culture and proteomics. Human SGC7901 gastric cells were selected and divided into a blank control group (untransfected SGC7901 cells), a negative control group [SGC7901 cells transfected with negative interference control-small interfering RNA (siRNA)], and a COOHterminus tensin-like molecule (CTEN)-siRNA-1 group (SGC7901 cells transfected with CTEN-siRNA-1). The cells were successfully transfected and subjected to analyses of cell proliferation, cell cycle, cell invasion, CTEN expression, and proteomics. The percentages of cells in the G0/ G1, S, and G2/M phases were similar in the three groups (P > 0.05), and the OD values were also similar at 24, 48, and 72 h (P > 0.05). Compared with the levels in the blank and negative control groups, CTEN protein in the CTEN-siRNA-1 group decreased by 66 and 65%, respectively, and significantly fewer cells in the CTEN-siRNA-1 group were capable of invasion (P < 0.05). Proteomic analysis showed that in the CTEN-siRNA-1 group, 283 proteins were upregulated and 242 were downregulated; from these, the expression levels of E-cadherin and ERK proteins changed significantly. Silencing the expression of CTEN in intestinal stromal tumor cells reduces their invasion capability. Moreover, silencing CTEN at different stages can also regulate the expression levels of E-cadherin and ERK proteins.

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Investigating TNS4 in the Colorectal Tumor Microenvironment Using 3D Spheroid Models of Invasion

2020

Self Cite

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TNS4 (Tensin 4 or Cten) is a putative oncogene in colorectal cancer (CRC) with a role in regulating cell adhesion, motility, invasion, and epithelial to mesenchymal transition (EMT). The objective is to study the role of TNS4 in CRC using more realistic models of the tumor microenvironment. CRC cells expressing TdTomato protein and shTNS4/shLUC hairpin oligos are grown in 3D spheroids with and without cancer‐associated fibroblasts (CAFs). Adhesiveness to collagen I and CAFs is assessed in 2D and cell proliferation, volume, and invasion are assessed in 3D conditions. The role of TNS4 knockdown in gefitinib chemosensitivity and epidermal growth factor receptor (EGFR) and Ras protein levels are also tested. In general, TNS4 knockdown increases cell proliferation in cell lines producing compact spheroids. The addition of CAFs in spheroids supports CRC cell proliferation, whereas CAFs themselves do not proliferate, but increases ECM degradation. TNS4 knockdown reduces adhesiveness and 3D invasion and disrupts EGFR signaling which results in increased sensitivity to Gefitinib. In conclusion, in a 3D spheroid model, TNS4 inhibits cell proliferation and promotes cell invasion into the ECM, possibly by adhesion to the ECM and stromal cells. TNS4 knockdown enhances sensitivity to the EGFR inhibitor gefitinib and may be helpful for Kirsten ras oncogene homolog mutant CRC patients.

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C-Terminal Tensin-Like Gene Functions as an Oncogene and Promotes Cell Motility in Pancreatic Cancer

Abstract: These are the first data showing an oncogenic role for CTEN in pancreatic cancer through promotion of colony formation and cell motility. The latter may be mediated by signaling through focal adhesion kinase and inhibiting E-cadherin.

Cited by 32 publications

References 1 publication

C-terminal tensin-like (CTEN): A promising biomarker and target for cancer

C-terminal tensin-like (CTEN): A promising biomarker and target for cancer

Proteomic analysis of susceptibility in intestinal stromal tumors

Investigating TNS4 in the Colorectal Tumor Microenvironment Using 3D Spheroid Models of Invasion

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