The stem cell factor (SCF)/c-KIT signalling in testis and prostate cancer

Abstract

The stem cell factor (SCF) is a cytokine that specifically binds the tyrosine kinase receptor c-KIT. The SCF/c-

Expression of tumour progression‐associated genes in circulating tumour cells of patients at different stages of prostate cancer

“…In addition to TYMS expression, other alterations, such as c‐met and c‐kit , also contribute to the development of the castration‐resistant phenotype . Clinical studies indicate that elevated c‐met expression is frequently seen in metastatic and CRPC tissues .…”

“…Moreover, PI3Kα can also be indirectly activated by c‐kit through its binding to the tyrosine phosphorylated adaptor protein GAB2 (growth factor receptor bound protein 2‐associated protein 2). PI3Kα activation in response to c‐kit is followed by the phosphorylation of downstream signalling molecules in the PI3Kα cascade .…”

Association between Circulation Indole-3-Acetic Acid Levels and Stem Cell Factor in Maintenance Hemodialysis Patients: A Cross-Sectional Study

“…SCF, one of the important MAPK cascade proteins, known as a ligand for the receptor-type protein-tyrosine kinase KIT, plays an essential role in cell proliferation, apoptosis, differentiation and migration in several tissues. The activity of the SCF/c-KIT system is linked with the PI3K/Akt pathway, the JAK/STAT pathway, and the MAPK pathway [39]. The average serum concentration of SCF is 3.3 ng/mL in a normal human, 5-6 fold higher in CKD and HD patients [40].…”

Exploring the molecular aspects associated with testicular germ cell tumors: a review

“…Its ligand KITLG (or stem cell factor, SCF), is located on chromosome region 12q21.3.2, which is necessary to carry out c-KIT dimerization and auto-phosphorylation, activating the c-KIT-KITLG signaling pathway and its downstream targets (e.i. k-ras) for proliferation and survival [ 34 ]. Variations in KITLG sequence (rs3782179, rs4474514 and rs995030) responsible for the predisposition to develop TGCTs have been recently documented, and also have been correlated with the role for KITLG in pigmentation, and with the greater incidence of TGCTs in Caucasian than in African-Americans males [ 17 ].…”

“…Moreover, the risk SNPs identified so far represent the most frequent alleles in Caucasian population, in general, and less frequent in the Black and Asian populations, possibly explaining TGCTs specific ethnic distributions. The KIT pathway has been suggested to be constitutively activated in human TGCTs as a result of gain of function mutations in the KIT oncogene and/or overexpression of KIT [ 34 , 35 ]. In mouse models, KITLG germline heterozygous deletions induce an increase in TGCTs incidence [ 35 ].…”