Piwi-like RNA-mediated Gene Silencing Research Articles

Piwil2 modulates the invasion and metastasis of prostate cancer by regulating the expression of matrix metalloproteinase-9 and epithelial-mesenchymal transitions.

Piwi-like RNA-mediated gene silencing 2 (Piwil2) is an oncogene that is highly expressed in breast, gastric, colorectal and papillary thyroid cancer. As a candidate oncogene, its role in prostrate cancer has yet to be elucidated. In the present study, 30 tumor specimens and four prostate cancer cell lines were analyzed. The total RNA and protein from the specimens and the cells were analyzed using quantitative polymerase chain reaction and western blotting, respectively. The expression of Piwil2 in PC-3 cells was knocked down using specific small hairpin RNA. Transwell assays and wound-healing models were used to assess cell invasion and migration. In addition, the expression of several factors associated with epithelial-mesenchymal transitions (EMT) were evaluated by western blotting. The results revealed that the Piwil2 gene was associated with the Gleason score and the tumor-node-metastasis stage of the tumor tissues. Cell invasion and migration decreased significantly in PC-3 cells with knocked-down Piwil2. In addition, silencing Piwil2 downregulated the expression of N-cadherin, Twist and vimentin and upregulated the expression of E-cadherin, factors associated with EMT, and also reduced the expression of matrix metalloproteinase-9. Piwil2 was demonstrated to possess an important role in the invasive ability of prostate cancer, and therefore, may be a potential therapeutic target for the treatment of this cancer.

PIWIL2 induces c-Myc expression by interacting with NME2 and regulates c-Myc-mediated tumor cell proliferation.

c-Myc serves as a crucial regulator in multiple cellular events. Cumulative evidences demonstrate that anomalous c-Myc overexpression correlates with proliferation, invasion and metastasis in various human tumors. However, the transcriptionally activating mechanisms responsible for c-Myc overexpression are complex and continue to be intangible. Here we showed that Piwi-Like RNA-Mediated Gene Silencing 2 (PIWIL2) can upregulate c-Myc via binding with NME/NM23 nucleoside diphosphate kinase 2 (NME2). PIWIL2 promotes c-Myc transcription by interacting with and facilitating NME2 to bind to G4-motif region within c-Myc promoter. Interestingly, in a c-Myc-mediated manner, PIWIL2 upregulates RhoA, which in turn induces filamentary F-actin. Deficiency of PIWIL2 results in obstacle for c-Myc expression, cell cycle progress and cell proliferation. Taken together, our present work demonstrates that PIWIL2 modulates tumor cell proliferation and F-actin filaments via promoting c-Myc expression.

PIWIL1 (piwi-like RNA-mediated gene silencing 1)

Review on PIWIL1 (piwi-like RNA-mediated gene silencing 1), with data on DNA, on the protein encoded, and where the gene is implicated.