Abstract
To investigate the role of miR-1297 and the tumor suppressor gene PTEN in cell proliferation of testicular germ cell tumors (TGCT). MTT assays were used to test the effect of miR-1297 on proliferation of the NCCIT testicular germ cell tumor cell line. In NCCIT cells, the expression of PTEN was assessed by Western blotting further. In order to confirm target association between miR-1297 and 3'-UTR of PTEN, a luciferase reporter activity assay was employed. Moreover, roles of PTEN in proliferation of NCCIT cells were evaluated by transfection of PTEN siRNA. Proliferation of NCCIT cells was promoted by miR-1297 in a concentration-dependent manner. In addition, miR-1297 could bind to the 3'-UTR of PTEN based on luciferase reporter activity assay, and reduced expression of PTEN at protein level was found. Proliferation of NCCIT cells was significantly enhanced after knockdown of PTEN by siRNA. miR-1297 as a potential oncogene could induce cell proliferation by targeting PTEN in NCCIT cells.
Highlights
Testicular germ cell tumor (TGCT) is the most common cancer in young men, with peak incidence among those aged 25 to 34 years in the United States (Chung et al, 2013)
Regulation of NCCIT cell proliferation by miR-1297 To explore the effect of miR-1297 on testicular germ cell tumor proliferation, miR-1297 mimics were transfected into the human NCCIT cell line, and proliferation was assessed by MTT assay
Luciferase activity was significantly decreased following co-transfection of psiCHECK-2/PTEN wild type 3’ untranslated region (3’-UTR) (WT) with miR-1297, compared with psiCHECK-2/ PTEN mutated 3’-UTR (Mutant) or the miR-negative control (Control) (Figure 2B). These results indicate that miR-1297 binds to the 3’-UTR of PTEN in NCCIT cells
Summary
Testicular germ cell tumor (TGCT) is the most common cancer in young men, with peak incidence among those aged 25 to 34 years in the United States (Chung et al, 2013). It is well known that TGCT is originate from transformed primordial germ cells (PGCs) during early embryonic development (Rajpert-De et al, 2007; Andreassen et al, 2013). TGCT is relatively rare, but the incidence has increased several folds during the last decades in most western countries (Huyghe et al, 2003; 2007). Most of patients with newly diagnosed TGCT are eventually cured, the treatment-associated morbidity is still significant at higher stages (Feldman et al, 2008; Cost et al, 2012), in patients who have metastatic disease at diagnosis (Sokoloff et al, 2007). A better understanding of the detailed mechanisms might be helpful to find new therapeutic targets and strategies for the treatment of TGCT
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