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] |