Project description:The role of itraconazole in cSCC was still unclear. Our objective is to explore the therapeutic potential of itraconazole in cSCC and investigate its molecular mechanism. We proved itraconazole inhibits the growth of cSCC by several pathways.
Project description:Our objective is exploring the therapeutic potential of itraconazole in cSCC and investigate its molecular mechanism.Transcriptomic and proteomic analyses were used to explore the underlying anti-cancer mechanism.
Project description:TCF4 was silenced in cutaneous squamous cell carcinoma of A431 cells, and detected the mRNA profiles compared to the negative control and blank control.
Project description:Cutaneous squamous cell carcinoma (cSCC) is the most common metastatic skin cancer, and its incidence is increasing globally. In this study, Homeobox A9 (HOXA9), a direct target of onco-miR-365, was identified to be significantly down-regulated in CSCC tumors and cell lines. We conducted RNA sequencing to characterize gene expression changes in HOXA9-silenced cutaneous squamous cell carcinoma cells(A431).
Project description:Cutaneous squamous cell carcinoma (CSCC) is the most common metastatic skin cancer, and its incidence is increasing globally. In this study, metastasis-associated in lung adenocarcinoma transcript 1 (MALAT1), a long non-coding RNA, was identified to be significantly up-regulated in CSCC tumors and cell lines. We conducted RNA sequencing to characterize gene expression changes in MALAT1-silenced cutaneous squamous cell carcinoma cells (A431).
Project description:Genome wide DNA methylation profiling in cutaneous squamous cell carcinoma. The Infinium MethylationEPIC BeadChips 850K has been used to interrogate DNA methylation changes. The cohort included 23 patients in total, with precursors of squamous cell carcinoma (actinic keratosis group) and with cSCC at different stages.
Project description:To determine the differentially expressed miRNAs in human cutaneous squamous cell carcinoma biopsies versus normal skin samples using microarray analysis.
Project description:Organ transplant recipients (OTRs) on Cyclosporine A (CSA) are prone to catastrophic cutaneous squamous cell carcinoma (SCC). Allograft-sparing, cancer-targeting systemic treatments are unavailable. We have shown increased risk for catastrophic SCC in OTRs via CSA-mediated induction of Interleukin-22 (IL-22). Herein, we found CSA drives SCC proliferation and tumor growth through IL-22 and JAK/STAT pathway induction. We in turn inhibited SCC growth with an FDA-approved JAK 1/2 inhibitor, Ruxolitinib. In human SCC cells, greatest proliferative response to IL-22 and CSA treatment occurred in non-metastasizing lines. IL-22 treatment upregulated JAK1 and STAT1/3 in A431 SCC cells. JAK/STAT pathway genes were highly expressed in tumors from a cohort of CSA-exposed OTRs, and in SCC with high risk for metastasis. Compared to immunocompetent SCC, genes associated with innate immunity, response to DNA damage and p53 regulation were differentially expressed in SCC from OTRs. In nude mice engrafted with human A431 cells, IL-22 and CSA treatment increased tumor growth and upregulated IL-22 receptor, JAK1 and STAT 1/3 expression. Ruxolitinib treatment significantly reduced tumor volume and reversed the accelerated tumor growth. CSA and IL-22 exacerbate aggressive behavior in SCC. Targeting the IL-22 axis via selective JAK/STAT inhibition may reduce the progression of aggressive SCC in OTRs, without compromising immunosuppression. In this study, microarray data was used to compare normal skin to immunocompetent SCC, to transplant associated SCC (TSCC)