Anoikis

Gilmore, Andrew

doi:10.1038/sj.cdd.4401723

Cited by 579 publications

(505 citation statements)

References 58 publications

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“…When anchorage-dependent cells remain in a detached state for extended periods, they undergo a process termed anoikis. 43 Interestingly, Bim is required for cell death induced by anoikis, 44 suggesting that downregulation of Bim during mitosis may prevent cell death in response to extracellular matrix detachment.…”

Section: Discussionmentioning

confidence: 99%

BimEL is phosphorylated at mitosis by Aurora A and targeted for degradation by βTrCP1

et al. 2013

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Section: Discussionmentioning

confidence: 99%

BimEL is phosphorylated at mitosis by Aurora A and targeted for degradation by βTrCP1

et al. 2013

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“…Integrins regulate cell viability through their interaction with the ECM, sensing mechanical forces arising from contacts and converting them into intracellular signals [2]. Hence, anoikis is a physiologically relevant process for development and tissue homeostasis and is often deregulated in several diseases [3,4]. Anoikis has been described in several cell types, although it appears that cells of different tissue origin activate dissimilar pathways leading to anoikis.…”

Section: Physiological Role Of Anoikismentioning

confidence: 99%

“…The initiation and execution of anoikis could be driven by different pathways that terminally converge into the activation of caspases and DNA fragmentation. In keeping with classical apoptosis, anoikis could follow either the intrinsic pathway, due to the perturbation of mitochondria, or the extrinsic pathway triggered by cell surface death receptors ( Figure 1) [4,5]. Proteins of the Bcl-2 family are key players of both intrinsic and extrinsic pathways [6].…”

Section: Physiological Role Of Anoikismentioning

confidence: 99%

Anoikis: an emerging hallmark in health and diseases

Taddei

Giannoni

Fiaschi

et al. 2011

The Journal of Pathology

506

404

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Anoikis is a programmed cell death occurring upon cell detachment from the correct extracellular matrix, thus disrupting integrin ligation. It is a critical mechanism in preventing dysplastic cell growth or attachment to an inappropriate matrix. Anoikis prevents detached epithelial cells from colonizing elsewhere and is thus essential for tissue homeostasis and development. As anchorage-independent growth and epithelial-mesenchymal transition, two features associated with anoikis resistance, are crucial steps during tumour progression and metastatic spreading of cancer cells, anoikis deregulation has now evoked particular attention from the scientific community. The aim of this review is to analyse the molecular mechanisms governing both anoikis and anoikis resistance, focusing on their regulation in physiological processes, as well as in several diseases, including metastatic cancers, cardiovascular diseases and diabetes.

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“…9 Adhesion to the ECM is important to determine whether a cell is in the correct location and to remove displaced cells by apoptosis and anoikis following loss of cell anchorage is of physiological relevance for development, tissue homeostasis and disease. 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.…”

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 579 publications

References 58 publications

BimEL is phosphorylated at mitosis by Aurora A and targeted for degradation by βTrCP1

BimEL is phosphorylated at mitosis by Aurora A and targeted for degradation by βTrCP1

Anoikis: an emerging hallmark in health and diseases

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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