GSE121017
RNA-Seq analysis of cSCC cells followed by siRNA-induced gene knockdown of C1s.
Keratinocyte-derived cutaneous squamous cell carcinoma (cSCC) is the most common metastatic skin cancer, and its incidence is increasing globally. Chronic inflammation has been recognized as a risk factor for cSCC and inflammation is a typical feature in the progression of premalignant actinic keratosis lesions to invasive and metastatic cSCC. The complement system is an important part of innate immunity, and activation of complement is detected in the microenvironment of tumors and has been considered a host defense mechanism against cancer cells. The complement cascade can be activated via three distinct pathways, namely the classic, lectin, or alternative pathways, which all lead to activation of lytic pathway and formation of the membrane attack complex, a pore-like structure on the target cell membrane resulting in the lysis of the target cell. The classical pathway of complement is typically activated by binding of C1 complex to antibodies bound to their target antigens. The C1 complex consists of six subcomponents of C1q, each with a collagenous triple helix of subunits C1qA, C1qB, and C1qC chains and two copies of serine proteases C1r and C1s subunits each. Whole transcriptome analysis of cSCC cells (n=8) and normal human epidermal keratinocytes (NHEKs, n=4) and oligonucleotide array-based expression analysis of cSCC cells (n=8) and normal human epidermal keratinocytes (NHEKs, n=5) revealed overexpression of C1s in cSCC cells (GSE66412 and GSE66368, respectively). Inthis respect, we have wanted to futher study the RNA expression profile of C1s knockdown cSCC cells. Overall design: Total RNAs from negative control siRNA and C1s siRNA-treated cSCC cell lines (n=3) were extracted. The samples were sequenced using Illumina sequencing.