Abstract
The ability of cells to assume different phenotypes without changing their genotype is referred to as cellular plasticity. It is increasingly being recognized as a fundamental and essential property of cancer cells, which enables their adaptation to the changing environmental conditions, imposed by both disease progression and therapeutic intervention. Epithelial–mesenchymal transition (EMT) is a classical well-studied example of cellular plasticity during cancer progression that aids cancer spread by metastasis. A closely associated phenomenon that entails metastatic progression is the detachment of cancer cells from the extracellular matrix (ECM) at the primary tumor site, their passage and survival in the circulation in an anchorage-independent form, and subsequent re-attachment at a distant site to establish new tumor growth. In this review, we discuss molecular and metabolic plasticity in matrix-attached and -detached states of cancer cells that aid in metastatic cancer progression. Further, cellular plasticity enables cancer cells within a population to assume different phenotypic states, thus leading to cancer heterogeneity—an emerging evil that needs to be tackled for overcoming therapy failure and achieving better treatment outcomes.
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We acknowledge Ms. Neha Deshpande for proofreading the manuscript. The definitions were variably adapted from Encyclopaedia Britannica, Wikipedia, Khan Academy, and Genetics Home Reference.
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Ranganathan, S., Kumar, S., Mohanty, S.S. et al. Cellular Plasticity in Matrix-attached and -Detached Cells: Implications in Metastasis. J Indian Inst Sci 100, 525–536 (2020). https://doi.org/10.1007/s41745-020-00179-0
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DOI: https://doi.org/10.1007/s41745-020-00179-0