MiR-492 exerts tumor-promoting function in prostate cancer through repressing SOCS2 expression.

OBJECTIVE: MiRNAs have been verified to play a role in the development and progression of prostate cancer (PCa). However, the role of miR-492 in PCa has not been mentioned. We aim to detect the expression of miR-492 in PCa and explore its underlying mechanism. PATIENTS AND METHODS: The relative expression of miR-492 in PCa tissue samples to normal prostate tissues was detected using quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The level of miR-492 in PCa-derived cell lines compared with the normal prostate cell line was also measured. Cell counting kit-8 (CCK-8) and colony formation assays were employed to investigate the cell proliferation ability. Transwell assay and wound-healing assays were utilized to explore the cell invasion and migration abilities. Luciferase assay and Western blot were utilized to explore the underlying mechanism of miR-492 in PCa cells. RESULTS: MiR-492 expressed significantly higher in PCa tissues than that in the normal tissues. Its expression level was also over-expressed in PCa cells compared with that in the normal cells. The up-regulation of miR-492 promoted the growth, invasion, and migration of the cells, while down-regulation had the opposite effects. SOCS2 was identified as a potential target for miR-492 in PCa. Silencing of SOCS2 could neutralize the inhibitory function of miR-492 inhibitor in PCa cells. CONCLUSIONS: This study demonstrated that miR-492 was over-expressed in PCa and exerted tumor-promoting function in PCa cells via repressing SOCS2 expression. This might provide a new sight for future accurate therapy for PCa.

MicroRNA-185-5p modulates chemosensitivity of human non-small cell lung cancer to cisplatin via targeting ABCC1.

OBJECTIVE: MicroRNA-185-5p (miR-185-5p) dysregulation is found in various human cancers. Our purpose is to investigate the association of miR-185-5p expression with the sensitivity of non-small cell lung cancer (NSCLC) to cisplatin. MATERIALS AND METHODS: Real-time PCR or Western blot assay was performed to detect the expression of mature miR-185-5p and ATP-binding cassette, subfamily C, member 1 (ABCC1) protein. Cell lines with abnormal expression of miR-185-5p were generated using miR-185-5p inhibitor and mimics. The viabilities of treated cells were analyzed using MTT assay. Cell apoptosis was evaluated by TUNEL assay. Apoptosis-related protein expressions were tested by Western blot. Dual-luciferase assay was applied to assess the target gene of miRNA. RESULTS: The expression level of miR-185-5p in A549 cell line was significantly higher than that in A549/DDP cell line (p < 0.05). Transfection of miR-185-5p mimics increased the sensitivity of A549 cells to cisplatin and the expression of an apoptosis-related factor, and restrained cell proliferation. MiR-185-5p inhibitor promoted cisplatin resistance and cell growth in A549 cells, and declined apoptosis-related factor levels. ABCC1 was verified as the target gene of miR-185-5p. MiR-185-5p exhibited negative correlation with ABCC1 in A549/DDP cells. CONCLUSIONS: The results of the present study demonstrated that inhibition of miR-185-5p was involved in chemo-resistance of NSCLC cells to cisplatin via down-regulating ABCC1.

[An exploration of animal behavior screen platform for novel gene function in central nervous system].

For the purpose of large-scale screening of novel gene functions in mammalian nervous system, we have developed an animal behavior-monitoring platform employing antisense-oligo technology. Twenty genes of different categories were chosen from a low abundant gene (c)DNA sub-library of rat brain. Antisense oligo-nucleotides of these genes were designed and synthesized according to the homologues of the genes in mouse for mouse behavior tests. These antisense oligos were injected into the lateral ventricles of mouse brain using a Hamilton micro-syringe, with saline and oligos of scramble sequences as controls. These mice were tested with the following behavior model paradigms: metabolism, open field behavior, tail flick latency, and step-down test. Out of the 20 genes tested, 14 genes showed significant behavioral differences from the control groups at the level of P value less than 0.05 or 0.001 in different behavior animal models.

Resection of meningiomas with implantable microwave coagulation.

Implantable microwave coagulation was used to perform resection on 62 patients that had intracranial meningiomas. When 20-60 W microwave power was applied for 15 s, the temperature at the center of the tumor tissue was 43-63 degrees C; 30 mm from the center, the temperature was under 40 degrees C. Histological changes in the center of the tumor showed coagulative necrosis, diminished nuclei, and obliterated blood vessels. The changes at 10-20 mm from the center of the tumor showed coagulative necrosis and degeneration and, 30-50 mm from the center of the tumor, showed normal cell morphology after microwave coagulation. The thermal field in brain tumor has an effective diameter of about 40 mm. No side effects on the normal brain tissues were observed. The amount of blood loss during the operation was minimal while the meningioma was coagulated, especially when the meningioma was located at the skull base or in the parasagittal or cerebral convexity region. After microwave coagulation, the entire tumor could easily be removed. Among the 62 surgically treated cases, gross total tumor excision was 85 percent. No postoperative complications occurred after microwave coagulation, and there was no operative mortality in the series. We believe that this new technique has the advantage of simplicity, less blood loss, and smooth postoperative procedures. Hemostatic effects during the operation are satisfactory, and blood transfusion can be reduced by 50-60 percent.