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Background Heterogeneous nuclear ribonucleoprotein K (HnRNPK) is a nucleic acid-binding protein that regulates diverse biological events. Pathologically, HnRNPK proteins are frequently overexpressed and clinically correlated with poor prognosis in various types of human cancers and are therefore pursued as attractive therapeutic targets for select patients. However, both the transcriptional regulation and degradation of HnRNPK in prostate cancer remain poorly understood. Methods qRT-PCR was used to detect the expression of HnRNPK mRNA and miRNA; Immunoblots and immunohistochemical assays were used to determine the levels of HnRNPK and other proteins. Flow cytometry was used to investigate cell cycle stage. MTS and clonogenic assays were used to investigate cell proliferation. Immunoprecipitation was used to analyse the interaction between SPOP and HnRNPK. A prostate carcinoma xenograft mouse model was used to detect the in vivo effects of HnRNPK and miRNA. Results In the present study, we noted that HnRNPK emerged as an important player in the carcinogenesis process of prostate cancer. miR-206 and miR-613 suppressed HnRNPK expression by targeting its 3’-UTR in PrCa cell lines in which HnRNPK is overexpressed. To explore the potential biological function, proliferation and colony formation of PrCa cells in vitro and tumor growth in vivo were also dramatically suppressed upon reintroduction of miR-206/miR-613. We have further provided evidence that Cullin 3 SPOP is a novel upstream E3 ubiquitin ligase complex that governs HnRNPK protein stability and oncogenic functions by promoting the degradation of HnRNPK in polyubiquitination-dependent proteolysis in the prostate cancer setting. Moreover, prostate cancer-associated SPOP mutants fail to interact with and promote the destruction of HnRNPK proteins. Conclusion Our findings reveal new posttranscriptional and posttranslational modification mechanisms of HnRNPK regulation via miR-206/miR-613 and SPOP, respectively. More importantly, given the critical oncogenic role of HnRNPK and the high frequency of SPOP mutations in prostate cancer, our results provide a molecular rationale for the clinical investigation of novel strategies to combat prostate cancer based on SPOP genetic status.

Background Heterogeneous nuclear ribonucleoprotein K (hnRNPK) is a nucleic acid-binding protein that regulates diverse biological events. Pathologically, hnRNPK proteins are frequently overexpressed and clinically correlated with poor prognosis to various types of human cancers, therefore pursued as attractive therapeutic targets for selective patients. However, both the transcriptional regulation and degradation of hnRNPK in prostate cancer are remain poorly understood. Methods qRT-PCR was used to detect the expression of hnRNPK and miRNA; Immunoblots and immunohistochemical assays were used to determine the levels of hnRNPK and other proteins. Flow cytometry was used to investigate cell cycle stage. MTS and clonogenic assays were used to investigate cell proliferation. Immunoprecipitation was used to analyze the interaction between SPOP and hnRNPK. A prostate carcinoma xenograft mouse model was used to detect the in vivo effects of hnRNPK and miRNA. Results In the present study, we observed that hnRNPK emerged as an important player in carcinogenesis process of PrCa. miR-206 and miR-613 suppressed hnRNPK expression by targeting the 3’-UTR of hnRNPK in PrCa cell lines, where hnRNP K is overexpressed. In biological effects studies, proliferation and colony formation of PrCa cells in vitro, and tumor growth in vivo, were also dramatically suppressed upon reintroduction of miR-206/ miR-613. We have further provided clear evidence that Cullin 3 SPOP as a novel upstream E3 ubiquitin ligase complex that governs hnRNPK proteins stability and oncogenic functions through promoting the degradation of HnRNP K in a poly-ubiquitinaion dependent proteolysis in the prostate cancer setting. Moreover, prostate cancer-associated SPOP mutants fail to interact with and promote the destruction of hnRNPK proteins. Conclusion Our finding reveal new post-transcriptional and post-translational modifications mechanism of hnRNPK regulation via miR-206/ miR-613 and SPOP, respectively. More important, given the critical oncogenic role of hnRNPK and high frequency of SPOP mutation in prostate cancer, our results provide a molecular rationale for the clinical investigation of novel strategies to combat prostate cancer based on SPOP genetic status.

A new leaf yellowing disease was observed on periwinkle (Catharanthus roseus) in Taiwan in 2005. Sequence analysis of a 1.8 kb region of 16S rDNA, 16S-23S intergenic spacer region and partial 23S rDNA revealed that the periwinkle leaf yellowing (PLY) disease was associated with a phytoplasma from the 16SrI group. In addition, five cultivated plants including chrysanthemum (Chrysanthemum sp.), cosmos (Cosmos bipinnatus), torenia (Torenia fournieri), Persian violet (Exacum affine), and cucumber (Cucumis sativus), and one weed, goosegrass (Eleusine indica) were identified as host plants of this phytoplasma. Leafhoppers, Macrosteles orientalis, Cicadulina bipunctella, Phlogotettix cyclops and Balclutha sp., were identified as potential insect vectors due to the positive results in PCR detection. The name, “Candidatus Phytoplasma asteris” strain PLY, is proposed for this new phytoplasma. The in silico restriction fragment length polymorphism analysis of the Fn2R2 region sequence showed that the periwinkle leaf yellowing phytoplasma is closest to the 16SrI-B subgroup and may be a new 16SrI subgroup. Transmission experiments with field-collected M. orientalis and C. bipunctella indicated that both leafhoppers can transmit the PLY phytoplasma to healthy periwinkle plants. This work is the first description of a new 16SrI subgroup phytoplasma in Taiwan.

An investigation on the average number v of prompt neutrons emitted per thermal neutron induced fission of U235 has been made with the Fermi gas statistical model. Weizsacker-Fermi semi-empirical mass equation has been used in calculating the neutron binding energies of the fission fragments. Using Stern's value for the mass of U235, the total excitation energy Ee of the fission fragments has been estimated to be of the order of 10 to 20 Mev for different hypotheses regarding the primary fission products. The results of calculation (given in the third table) show that only the hypothesis of equal radioactive chain lengths together with the assumption (A) that the excitation energy Ee is shared by the two fragments in proportion to their masses yields values of v exceeding 2. The latter assumption is not in accord with the experimental finding of Fraser that the light fragment group emits on the average 30% more neutrons than does the heavy. However, a shift of mass of U235 towards larger values or of kinetic energy of fission fragments towards lower values so that 5 Mev more excitation energy is available would make v considerably larger than 2 even with the assumption (B) that the excitation energy is shared by the two fragments in inverse proportion to their masses, thus making possible conformity with Fraser's discovery. Even then, in no case has the value of v thus calculated exceeded 3 (as shown in the fourth table), which may then be taken as a theoretical upper bound for the value of ν for thermal neutron induced fission of U235. The results of this investigation are thus seen to be in harmony with the recently announced experimental value 2.5 ±0.1 for ν.