Cancer stem cells (CSCs) have recently emerged as key contributors to drug resistance based on their enhanced abilities to evade apoptosis and survive unfavorable microenvironments. CSCs represent a subpopulation of cells that can self-renew, propagate, reconstitute the tumor heterogeneity, and resist many types of cancer therapies.1 Determining the specific pathways involved in regulating the development of CSC populations will open doors for novel CSC-targeted therapeutic strategies in malignant cancers. A collection of cell surface markers that are either specific for the cancer's tissue of origin or expressed by normal stem cells are commonly used for isolation of sub-populations enriched for CSCs.2 Integrins have long been appreciated as a family of cell surface receptors that are formed by specific combinations of a and beta subunits, and certain of these integrins are enriched in CSC populations for various types of cancers.
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