Table 1.
Summary of factors that are shown to regulate tumour-initiating cell growth in cutaneous SCC.
| Factor | Potential Mechanism | References |
|---|---|---|
| CD44 | Cell surface marker elevated in subpopulations of SCC, i.e., putative tumour stem cell marker | [15] |
| CD133 | Putative tumour stem cell marker in SCC | [28] |
| TGF-β | Promotes chemotherapy resistance in SCC | [18] |
| BMI1 | Tumour self-renewal and tumourigenesis | [15] |
| Sox2 | Putative tumour stem cell marker in SCC | [29] |
| FRMD4A | Putative tumour stem cell marker in SCC; interacts with Hippo pathway | [39] |
| YAP1 | Key downstream effector of the Hippo pathway, influencing the behaviour of stem cells in the normal epithelium and in SCC | [58] |
| Lrig1 (loss) | Putative tumour stem cell marker in SCC and tumour suppressor. | [41] |
| Grhl3 (loss) | Conserved developmental transcription factor, essential for epidermal differentiation, barrier formation and SCC initiation | [51] |
| TARC/CCL17 | Cytokine driving hyperproliferation in Grhl3 deletion model | [51] |
| IL-1α | Cytokine driving papilloma formation in MEK1 overexpression model | [40] |
| IL-17R | Cytokine implicated in the mobilization of Lrig1-positive stem cells in wound healing experiments, and in tumorigenesis | [41] |
| Survivin | Overexpression of Survivin promotes the development of SCC in multiple tissue types and results in poor prognosis | [32] |
| miR-204 (loss) | Loss of miR-204 drives STAT3 pro-inflammatory response in sun-damaged skin leading to the development of SCC. | [55] |
| MEK1 | Overexpression promotes hyperproliferation and skin inflammation, leading to papilloma formation | [40] |