<unk>  has been suggested to regulate skin progenitor cell fusion and mediate chemotherapeutic drug resistance in stem-like tumor cell subpopulations in human malignant melanoma, colorectal cancer, and malignant pleural mesothelioma. It is commonly over-expressed on circulating melanoma tumour cells. Furthermore, the<unk> + melanoma- initiating cells were demonstrated to express FLT1 (VEGFR1) receptor tyrosine kinase which was functionally required for efficient xenograft tumor formation, as demonstrated by shRNA knockdown experiments. In colorectal cancer,<unk>  was shown to act as a mediator of 5-FU patient chemoresistance, and had a further direct role in tumorigenesis shown by shRNA-mediated colorectal cancer cell-line<unk>  knockdowns that impeded tumorigenesis in human-to-mouse xenografts. It has been shown that in some highly aggressive tumors, such as mesothelioma and melanoma,<unk>  contributes to multi-drug chemotherapy resistance, and tumor growth, controlling a proinflammatory signaling circuit utilizing TLR4, IL-1β, IL8 and CXCR1 signaling involving reciprocal paracrine interactions between the cancer stem cells and tumor bulk population (in a rheostat manner termed "cancer stem cell rheostasis").<unk>  was shown to maintain the slow-cycling melanoma stem cells using this cytokine signaling loop, which became more differentiated upon<unk>  interference (e.g. WFDC1 melanocyte differentiation marker increased, cancer cells were faster growing in vitro, tumors were more pigmented), or CXCR1 blockade (slow-cycling<unk> + cells entered the cell-cycle). In normal physiology,<unk>  is a functional marker for adult limbal stem cells of the cornea.<unk> + cells could regrow a human cornea on a mouse with limbal stem cell deficiency (LSCD - a blindness disease of the corneal limbus) while<unk> - cells could not, indicating a therapeutic potential for treating some types of blindness.<unk>  was further shown to be anti-apoptotic in these adult stem cells.
ABCB5
APOBEC3G
GP1BB
McN5652
GP1BA
CHCHD10
GRAd-COV2
PC3