Complement C1q activates tumor suppressor WWOX to induce apoptosis in prostate cancer cells.

The genetic alterations observed in head and neck cancer are mainly due to oncogene activation (gain of function mutations) and tumor suppressor gene inactivation (loss of

Specific genes that are predominantly expressed or exclusively expressed in prostate cells, prostate cancer cells, and prostate metastasis cells at the level of DNA, RNA and

The data observed in this study demonstrate a signiicant increase in the serum levels of C3 and/or C4 complement components in the majority of patients with intermittent

Since thiazole antibiotics suppress the expression and the activity of FoxM1 and at the same time FoxM1 overexpression protects cancer cells from Siomycin A and thiostrepton

Silvers et al., “Selective expression of CD44, a putative prostate cancer stem cell marker, in neuroendocrine tumor cells of human prostate cancer,” The Prostate , vol.

Malignant prostate cells express CXCL16 and CXCR6 In order to investigate the roles of chemokines in prostate cancer, we screened prostate cancer cell lines and xenografts

Consequently, knockdown of SATB1 in highly aggressive human prostate cancer PC-3M cells inhibited invasiveness and tumor growth in vivo along with increase in E-cadherin

Although PSMA-speciic ligands are mainly used as prostate cancer imaging agents and targeting ligands for drug delivery systems, some of the PSMA inhibitors can also be used alone