Es-SOX8 regulates the morphological changes of the sperm nucleus of Eriocheir sinensis by activating Es-BMP2 transcription

The SRY-related high mobility group(HMG)box(SOX)transcription factors participate in many physiological processes of animal growth,development,and reproduction and are related to spermatogenesis in many species.However,the relationship between SOX and spermatogenesis in Eriocheir sinensis is rarely reported.Here,we studied the role of Es-SOX8 in the spermatogenesis of E.sinensis and its possible regulation mechanism.Immunofluorescence results demonstrated Es-SOX8 signal in both cytoplasm and nucleus of spermatogonia,spermatocytes as well as spermatids,but not in mature spermatozoa.Hematoxylin and eosin staining showed a significant increase in the number of spermatozoa with abnormal nuclear morphology in vivo,described as prominent edges and corners,after the knockdown of Es-SOX8 through RNA interference.This indicated a possible role of Es-SOX8 in the nuclear deformation process in the spermatogenesis of E.sinensis.Analysis of the mRNA levels of Es-bone morphogenetic protein 2(BMP2)in the Es-Sox8 knocked-down testis tissue revealed significantly decreased transcription of Es-BMP2.Chromatin immunoprecipitation results showed the binding of Es-SOX8 protein to the promoter region of Es-BMP2.Thus,Es-SOX8 can directly regulate the transcription of Es-BMP2 by activating the promoter of Es-BMP2 and thus affects the sperm nucleus deformation of E.sinensis.

KIFC1 overexpression promotes prostate cancer cell survival and proliferation in vitro by clustering of amplified centrosomes via interaction with Centrin 2

Mitotic kinesin KIFC1 plays critical roles in mitosis by regulating the spindle length,pole formation,and known for clustering extra centrosomes in cancer cells.Centrosome clustering is associated with the survival of cancer cells,but this phenomenon remains obscure in prostate cancer(PCa).The present study demonstrated that PCa cells showed centrosome amplification and clustering during interphase and mitosis,respectively.KIFC1 is highly expressed in PCa cells and tumor tissues of prostatic adenocarcinoma(PAC)patients.Up-regulation of KIFC1 facilitated the PCa cell survival in vitro by ensuring bipolar mitosis through clustering the multiple centrosomes,suggesting centrosome clustering could be a leading cause of prostate carcinogenesis.Conversely,the silencing of KIFC1 resulted in normal centrosome number or multipolar mitosis by inhibiting the clustering of amplified centrosomes in PCa cells.Besides,knockdown of KIFC1 by RNAi in PCa cells reduced cancer cell survival,and proliferation.KIFC1 interacted with centrosome structural protein Centrin 2 in clustering of amplified centrosomes in PCa cells to ensure the bipolar mitotic spindle formation.Knockdown of Centrin 2 in PCa cells inhibited the centrosome amplification and clustering.Moreover,up-regulated KIFC1 promotes PCa cell proliferation via progression of cell cycle possibly through aberrant activation of cyclin dependent kinase 1(Cdk1).Therefore,KIFC1 can be a prognostic marker and therapeutic target of PCa for inhibiting the cancer cell proliferation.