Overexpression of SNHG12 regulates the viability and invasion of renal cell carcinoma cells through modulation of HIF1α.

BACKGROUND: Cumulative evidences demonstrated the aberrant overexpression of Small Nucleolar RNA Host Gene 12 (SNHG12) in diverse human cancer. However, the expression status and involvement of SNHG12 in renal cell carcinoma is still elusive. METHODS: The expression of SNHG12 was determined by q-PCR. The transcriptional regulation was interrogated by luciferase reporter assay. Cell viability was measured with CCK-8 kit. The anchorage-independent was evaluated by soft agar assay. Cell apoptosis was analyzed by Annexin V/7-AAD double staining. The migration and invasion were determined by trans-well assay and wound scratch closure. The in vivo tumor growth was monitored in xenograft mice model. Protein expression was quantified by immunoblotting. RESULTS: SNHG12 was aberrantly up-regulated in renal carcinoma both in vivo and in vitro. High expression of SNHG12 associated with poor prognosis. Deficiency of SNHG12 significantly suppressed cell viability, anchorage-independent growth and induced apoptosis. In addition, SNHG12 silencing inhibited migrative and invasive in vitro and xenograft tumor growth in vivo. Mechanistically, SNHG12 modulated HIF1α expression via competing with miR-199a-5p, which consequently contributed to its oncogenic potential. MiR-199a-5p inhibition severely compromised SNHG12 silencing-elicited tumor repressive effects. CONCLUSION: Our data uncovered a crucial role of SNHG12-miR-199a-5p-HIF1α axis in human renal cancer.

The crystal structure of red fluorescent protein TagRFP-T reveals the mechanism of its superior photostability.

The red fluorescent protein variant TagRFP-T has greatly improved photostability over its parent molecule, TagRFP, but the underlying mechanism leading to this improvement is to date unknown. The 1.95 Å resolution crystallographic structure of TagRFP-T showed that its chromophore exists as a mixture of cis and trans coplanar isomers in roughly equal proportions. Interestingly, both isomers are able to fluoresce, a property that has never been observed in any other fluorescent protein. We propose a "circular restoration model" for TagRFP-T to explain its superior photostability: There are four co-existing chromophore states (cis/trans protonated/ionized state) that can be driven by light to transform from one state into another. This model also explains how TagRPF-T essentially eliminates the temporary dark state (reversible photobleaching).

MiR-378 suppresses prostate cancer cell growth through downregulation of MAPK1 in vitro and in vivo.

Prostate cancer is one of the biggest health problems for the aging male. To the present, the roles of dysregulated microRNAs in prostate cancer are still unclear. Here, we evaluated the anti-proliferative role of miR-378 in prostate cancer. And, we found that the expression of miR-378 was significantly downregulated in clinical prostate cancer tissues. In vitro assay suggested that overexpression of miR-378-suppressed prostate cancer cell migration and invasion promoted cell apoptosis. Furthermore, we identified and validated MAPK1 as a direct target of miR-378. Ectopic expression of MAPK1 rescues miR-378-suppressed cell migration and invasion. In vivo assay demonstrated that the stably miR-378-overexpressed prostate cancer cells displayed a significantly reduction in tumor growth. Taken together, our data suggested that miR-378 may act as a potential therapeutic target against human prostate cancer.

[The clinical analysis of 62 cases of the urothelial inverted papilloma].

OBJECTIVE: To investigate the clinical manifestation, biological behavior, diagnosis and treatment of the urothelial inverted papilloma. METHODS: Sixty-two cases of urothelial inverted papilloma were analyzed retrospectively from January 1990 to August 2008. Of the 62 patients, 51 were men and 11 were women. The average age at presentation was 56.4 years old. Fifty-six cases were solitary tumors and 6 were multiple. The most common compliant was macroscopic hematuria. The tumor located at the ureter in 5 cases. Of these cases, 4 were treated by local excision, 1 by nephroureterectomy. One case of multiple ureteral inverted papilloma with coexistent bladder inverted papilloma was treated by total cystectomy. The tumor located at the bladder in 52 cases, with 44 treated by transurethral resection of bladder tumor, 6 by partial cystectomy, 2 by total cystectomy. Four cases had the tumor located at the urethra, with 1 treated by transurethral resection of tumor, 3 by tumorectomy. RESULTS: The postoperative pathological diagnosis of all the 62 cases was inverted papilloma, synchronous urothelial carcinoma in 7. Follow-up data were available in 49 cases. Two cases had a recurrence at 7 months and 79 months, respectively. Three case of subsequent transitional cell carcinoma developed 18 months, 2 years and 6 years later, respectively. CONCLUSIONS: Inverted urothelial papilloma is a kind of benign tumor. It should be differentiated from malignant urothelial tumors. Surgical operation is the main treatment choice. Cystoscopic surveillance and followup are necessary after the operation regularly.

MiR-345 suppresses proliferation, migration and invasion by targeting Smad1 in human prostate cancer.

INTRODUCTION: The roles of dysregulated microRNAs in prostate cancer metastasis are still unknown. In this study, we found that the expression of miR-345 was significantly downregulated in prostate cancer and clinical prostate cancer tissues. MATERIALS, METHODS AND RESULTS: Overexpression of miR-345 in prostate cancer cells suppressed proliferation, migration and invasion. Using nude mice model, we revealed that miR-345 inhibits the growth of prostate cancer cells in vivo and in vitro. Furthermore, we identified and validated Smad1 as a direct target of miR-345. Ectopic expression of Smad1 without its 3'-UTR rescued miR-345-induced cell migration and invasion inhibition. CONCLUSION: Taken together, our data suggest that miR-345 exerts a suppressive effect on prostate cancer proliferation, invasion and migration through downregulation of Smad1.