Anoikis

Valentijn, Anthony; Zouq, Nadia K.; Gilmore, Abigail

doi:10.1042/bst0320421

Cited by 127 publications

(97 citation statements)

References 49 publications

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“…1H), E-cadherin, and N-cadherin; it was never detected in engrafted cells expressing junctional and adhesion proteins. This phenomenon is consistent with anoikis of the nonengrafted cells, which is one of the aspects of programmed cell death triggered by the lack of cell-to-cell contacts (8). Quantitative measurements at 2 days showed that only Ϸ5% (4,800 Ϯ 2,600) of the 80,000 -100,000 injected nonactivated CPCs were present in the myocardium whereas Ϸ50% (48,000 Ϯ 18,000) of activated CPCs were detected.…”

Section: Cpc Survival and Engraftmentsupporting

confidence: 54%

Formation of large coronary arteries by cardiac progenitor cells

Tillmanns

Rota

Hosoda

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

146

117

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Coronary artery disease is the most common cause of cardiac failure in the Western world, and to date there is no alternative to bypass surgery for severe coronary atherosclerosis. We report that c-kitpositive cardiac progenitor cells (CPCs) activated with insulin-like growth factor 1 and hepatocyte growth factor before their injection in proximity of the site of occlusion of the left coronary artery in rats, engrafted within the host myocardium forming temporary niches. Subsequently, CPCs divided and differentiated into endothelial cells and smooth muscle cells and, to a lesser extent, into cardiomyocytes. The acquisition of vascular lineages appeared to be mediated by the up-regulation of hypoxia-inducible factor 1␣, which promoted the synthesis and secretion of stromal-derived factor 1 from hypoxic coronary vessels. Stromal-derived factor 1 was critical in the conversion of CPCs to the vascular fate. CPCs formed conductive and intermediate-sized coronary arteries together with resistance arterioles and capillaries. The new vessels were connected with the primary coronary circulation, and this increase in vascularization more than doubled myocardial blood flow in the infarcted myocardium. This beneficial effect, together with myocardial regeneration attenuated postinfarction dilated myopathy, reduced infarct size and improved function. In conclusion, locally delivered activated CPCs generate de novo coronary vasculature and may be implemented clinically for restoration of blood supply to the ischemic myocardium.coronary blood flow ͉ infarct size ͉ myocardial regeneration ͉ stem cells ͉ vasculogenesis

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Section: Cpc Survival and Engraftmentsupporting

confidence: 54%

Formation of large coronary arteries by cardiac progenitor cells

Tillmanns

Rota

Hosoda

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

146

117

View full text Add to dashboard Cite

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“…Anoikis, apoptotic cell death due to loss of cell adhesion, is critical for regulation of tissue homeostasis in tissue remodeling, development, fibrosis and tumor metastasis (Valentijn et al, 2004). Here, we showed that decreased CRT was associated with increase of anoikis in ESCC cells.…”

Section: Discussionmentioning

confidence: 68%

Calreticulin promotes cell motility and enhances resistance to anoikis through STAT3–CTTN–Akt pathway in esophageal squamous cell carcinoma

Yang

et al. 2009

Oncogene

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We have shown earlier that overexpression of Calreticulin (CRT) contributed to a poor prognosis for patients with esophageal squamous cell carcinoma (ESCC). Here, we have shown an important role of CRT in tumorigenesis through enhancing cell motility and anoikis resistance. SiRNA-mediated knockdown of CRT caused impaired cell migration, invasion and resistance to anoikis. Notably, CRT downregulation decreased the expression of Cortactin (CTTN), which has been previously reported as a candidate oncogene associated with anoikis through the PI3K-Akt pathway. In addition, Akt phosphorylation was abolished after CRT downregulation and its activation can be refreshed by CRT upregulation, suggesting that CRT-enhanced cell resistance to anoikis through the CRT-CTTN-PI3K-Akt pathway. Moreover, the CTTN mRNA level was decreased in CRT-siRNA cells, coupled with the inactivation of STAT3. Expression of both CTTN and p-STAT3 was reduced in tumor cells following incubation with the JAK-specific inhibitor, AG490. Chromatin immunoprecipitation assay showed direct binding of p-STAT3 to the conservative STAT3-binding sequences in CTTN promoter. Furthermore, overexpression of CTTN in CRT-downregulated ESCC cells restored its motility and resistance to anoikis. This study not only reveals a role of CRT in motility promotion and anoikis resistance in ESCC cells, but also identifies CRT as an upstream regulator in the CRT-STAT3-CTTNAkt pathway.

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“…10,11 The physiological relevance of anoikis has been confirmed by the fact that cancer cell lines, rather than normal epithelial cells, are usually not sensitive to anoikis and many have developed anchorage independence, which means that they do not require adhesion to ECM for proliferation and survival. [12][13][14][15] Anoikis has also been suggested to act as a physiological barrier to metastasis, and anoikis suppression is the first step taken by metastatic cells. 16 Hepatocyte growth factor (HGF) mediates tumor-stromal interactions that confer invasive, angiogenic and metastatic potential to various cancers through HGF/c-Met receptor binding.…”

mentioning

confidence: 99%

Co‐expression of hepatocyte growth factor and c‐Met predicts peritoneal dissemination established by autocrine hepatocyte growth factor/c‐Met signaling in gastric cancer

Toiyama¹,

Yasuda²,

Saigusa³

et al. 2011

Intl Journal of Cancer

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Epithelial–mesenchymal transition (EMT) promotes and facilitates migration and invasion of epithelial tumor cells. EMT is induced by factors such as hepatocyte growth factor (HGF). This study aimed to establish whether the HGF/c‐Met pathway is associated with gastric cancer metastasis; especially peritoneal dissemination. HGF and c‐Met expression and EMT‐related molecules were evaluated using real‐time PCR and immunohistochemistry. The role of the HGF/c‐Met pathway in EMT and anoikis was determined, and kinase inhibitor SU11274 was tested for its ability to block HGF‐induced biological effects. In HGF−/c‐Met+ gastric cancer cells, recombinant HGF promoted an EMT phenotype that was characterized by morphology, impaired E‐cadherin and induction of vimentin. HGF promoted cell growth, invasiveness and migration and inhibition of anoikis. SU11274 blocked HGF‐induced EMT and biological effects in vitro. In HGF+/c‐Met+ gastric cancer cells, HGF did not affect the biological outcome of EMT and anoikis, but SU11274 exerted the same inhibitory effects as in HGF−/c‐Met+ cells. In vivo, HGF+/c‐Met+ gastric cancer cells only established peritoneal dissemination and SU11274 inhibited tumor growth. Clinically, HGF expression was significantly correlated with c‐Met expression in gastric cancer. Increased HGF and c‐Met had a significant association with poor prognosis and predicted peritoneal dissemination. We demonstrated that the HGF/c‐Met pathway induces EMT and inhibition of anoikis in gastric cancer cells. Co‐expression of HGF and c‐Met has the potential to promote peritoneal dissemination in gastric cancer. Blockade of the autocrine HGF/c‐Met pathway could be clinically useful for the treatment of peritoneal dissemination in gastric cancer.

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Anoikis

Cited by 127 publications

References 49 publications

Formation of large coronary arteries by cardiac progenitor cells

Formation of large coronary arteries by cardiac progenitor cells

Calreticulin promotes cell motility and enhances resistance to anoikis through STAT3–CTTN–Akt pathway in esophageal squamous cell carcinoma

Co‐expression of hepatocyte growth factor and c‐Met predicts peritoneal dissemination established by autocrine hepatocyte growth factor/c‐Met signaling in gastric cancer

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