Expression of FOXE1 in Cutaneous Squamous Cell Carcinoma

Cutaneous squamous cell carcinoma (cSCC) is one of the common non-melanoma skin malignant tumors with sophisticated pathogenesis. FOXE1 is considered to be a tumor suppressor involved in the development of various tumors; however, the expression and significance of FOXE1 in cSCC remains to be investigated.

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Extended UVB Exposures Alter Tumorigenesis and Treatment Efficacy in a Murine Model of Cutaneous Squamous Cell Carcinoma

Journal of Skin Cancer ◽

10.1155/2013/246848 ◽

2013 ◽

Vol 2013 ◽

pp. 1-10 ◽

Cited By ~ 2

Author(s):

Erin M. Burns ◽

Kathleen L. Tober ◽

Judith A. Riggenbach ◽

Donna F. Kusewitt ◽

Gregory S. Young ◽

...

Keyword(s):

Squamous Cell Carcinoma ◽

Cell Carcinoma ◽

Squamous Cell ◽

Malignant Tumors ◽

Tumor Development ◽

Sun Exposure ◽

Epidemiological Studies ◽

Cutaneous Squamous Cell Carcinoma ◽

Exposure Model ◽

Uvb Exposure

Epidemiological studies support a link between cumulative sun exposure and cutaneous squamous cell carcinoma (SCC) development. However, the presumed effects of extended ultraviolet light B (UVB) exposure on tumorigenesis in the sexes have not been formally investigated. We examined differences in ultimate tumorigenesis at 25 weeks in mice exposed to UVB for either 10 or 25 weeks. Additionally, we investigated the effect of continued UVB exposure on the efficacy of topical treatment with anti-inflammatory (diclofenac) or antioxidant (C E Ferulic or vitamin E) compounds on modulating tumorigenesis. Vehicle-treated mice in the 25-week UVB exposure model exhibited an increased tumor burden and a higher percentage of malignant tumors compared to mice in the 10-week exposure model, which correlated with increases in total and mutant p53-positive epidermal cells. Only topical diclofenac decreased tumor number and burden in both sexes regardless of UVB exposure length. These data support the commonly assumed but not previously demonstrated fact that increased cumulative UVB exposure increases the risk of UVB-induced SCC development and can also affect therapeutic efficacies. Our study suggests that cessation of UVB exposure by at-risk patients may decrease tumor development and that topical NSAIDs such as diclofenac may be chemopreventive.

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HOXA9 Transcriptionally Promotes Apoptosis and Represses Autophagy by Targeting NF-κB in Cutaneous Squamous Cell Carcinoma

Cells ◽

10.3390/cells8111360 ◽

2019 ◽

Vol 8 (11) ◽

pp. 1360 ◽

Cited By ~ 4

Author(s):

Shuo Han ◽

Xue Li ◽

Xiaoting Liang ◽

Liang Zhou

Keyword(s):

Squamous Cell Carcinoma ◽

Tumor Suppressor ◽

Cell Carcinoma ◽

Squamous Cell ◽

Cutaneous Squamous Cell Carcinoma ◽

Signaling Network ◽

Rna Seq

Tumor suppressor HOXA9 has been identified to promote apoptosis in cutaneous squamous cell carcinoma (cSCC). However, the mechanism of such pro-apoptotic role of HOXA9 remains obscure. KEGG (Kyoto Encyclopedia of Genes and Genomes) analysis of RNA-seq data showed that NF-κB, apoptosis and autophagy pathways are significantly regulated after HOXA9 knockdown. HOXA9 transcriptionally regulates RELA, the p65 subunit of NF-κB. Loss of HOXA9 in cSCC significantly upregulates RELA expression and thus enhances NF-κB pathway. Interestingly, RELA transcriptionally promotes not only anti-apoptotic factor BCL-XL but also autophagic genes including ATG1, ATG3, and ATG12. Our results reveal an enhanced NF-κB signaling network regulated by HOXA9, which contributes to repressed apoptosis and activated autophagy in cSCC development and may represent an intervention target for cSCC therapy.

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