Abstract
Metastasis is a multistep process including dissociation of cancer cells from primary sites, survival in the vascular system, and proliferation in distant target organs. As a barrier to metastasis, cells normally undergo an apoptotic process known as “anoikis,” a form of cell death due to loss of contact with the extracellular matrix or neighboring cells. Cancer cells acquire anoikis resistance to survive after detachment from the primary sites and travel through the circulatory and lymphatic systems to disseminate throughout the body. Because recent technological advances enable us to detect rare circulating tumor cells, which are anoikis resistant, currently, anoikis resistance becomes a hot topic in cancer research. Detailed molecular and functional analyses of anoikis resistant cells may provide insight into the biology of cancer metastasis and identify novel therapeutic targets for prevention of cancer dissemination. This paper comprehensively describes recent investigations of the molecular and cellular mechanisms underlying anoikis and anoikis resistance in relation to intrinsic and extrinsic death signaling, epithelial-mesenchymal transition, growth factor receptors, energy metabolism, reactive oxygen species, membrane microdomains, and lipid rafts.
Highlights
Development, differentiation, and homeostasis are controlled by cell-cell interactions, cell-extracellular matrix (ECM) interactions, and soluble cues [1, 2]
They referred to this form of programmed cell death that occurs upon detachment from the appropriate ECM as anoikis [4,5,6]
Normal epithelial cells require adhesion to the appropriate ECM for survival and proliferation, and loss of this adhesion induces a type of cell death known as anoikis
Summary
Development, differentiation, and homeostasis are controlled by cell-cell interactions, cell-extracellular matrix (ECM) interactions, and soluble cues (hormones, cytokines, and growth factors) [1, 2]. In 1994, Frisch and Francis noticed that loss of matrix attachment of epithelial cells resulted in apoptosis [3] They referred to this form of programmed cell death that occurs upon detachment from the appropriate ECM as anoikis [4,5,6]. Because anoikis prevents detached epithelial cells from colonizing elsewhere, thereby inhibiting dysplastic cell growth or attachment to an inappropriate matrix, anoikis is a physiologically relevant process for tissue homeostasis and development. Dysregulation of anoikis, such as anoikis resistance, is a critical mechanism in tumor metastasis. This paper will focus on the current understanding of cellular and molecular mechanisms of anoikis resistance
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