Detection of differentially expressed HES-6 gene in metastatic colon carcinoma by combination of suppression subtractive hybridization and cDNA library array

HES6 gene is selectively overexpressed in glioma and represents an important transcriptional regulator of glioma proliferation

“…HES6 has been previously implicated in metastatic neuroendocrine prostate cancer, breast cancer and metastatic colon carcinoma (Swearingen et al, 2003;Vias et al, 2008;Hartman et al, 2009). In the GeneSapiens database, neuroblastoma, melanoma, colon cancer and some breast cancers display somewhat elevated expression of HES6, but it is 5-10 times higher in the gliomas.…”

“…Its overexpression has been reported in metastatic colon and prostate cancers (Swearingen et al, 2003;Vias et al, 2008), and in cancers of the lung, breast and kidney (Swearingen et al, 2003;Hartman et al, 2009). Hes6 inhibits Hes1 activity by forming heterodimers with Hes1, supports achaete-scute complex homolog-1 (Ascl1) activity and promotes neuronal differentiation (Bae et al, 2000;Koyano-Nakagawa et al, 2000).…”

Upregulation of ASCL1 and inhibition of Notch signaling pathway characterize progressive astrocytoma

“…HES6 has been found to be overexpressed in human primary tumors derived from breast, lung and kidney, suggesting that HES6 overexpression may have an oncogenic role (Swearingen et al, 2003). Indeed, HES6 has been located in chromosome 2q37, a region known to be amplified in common adenocarcinomas such as that of the lung, breast, prostate, kidney and ovary (Mitelman et al, 2002).…”

HES-1 inhibits 17β-estradiol and heregulin-β1-mediated upregulation of E2F-1

“…Furthermore, HES-1 is expressed in many cancer cell lines indicating the presence of a mechanism for inactivation of HES-1. A recent paper reporting increased expression of HES-6 in primary cancer and in metastases might explain how HES-1 activity is neutralized (Swearingen et al, 2003), since HES-6 antagonizes HES-1 by forming a nonfunctional HES-6/ Figure 4 Exogenous expression of HES-1 inhibits induction of cyclin E and NPAT by E 2 ; HES-1 expression is needed for inhibitory effect by atRA. (a) T47D dnHES-1 cells were synchronized and treated with 10 nM E 2 , 1 mM atRA and 1 mg/ml of tet as indicated for 24 h. cDNA was prepared and real-time PCR was performed with cyclin E and NPAT specific primers.…”

“…Interestingly, amplification of the genomic region where HES-6 is located has been found in several cancers (Swearingen et al, 2003). Many hormone-independent breast tumors overexpress ErbB-receptors and/or HER-2, and these proteins could be involved in development of the hormoneindependent phenotype (Pietras et al, 1995;Tang et al, 1996).…”