Prof. Xuezhen Yang graduated from Peking University with a doctor’s degree in Surgery, studied under Professor Liqun Zhou and Academician Yinglu Guo. He have been studying in several world famous universities for 5 years and have rich clinical experience in the diagnosis and treatment of urinary system tumor. He is invited to give academic reports and won awards in international and domestic conferences for many times, and have served in many academic societies at home and abroad. Prof. Yang won one national and one provincial project, published many papers and participated in the translation and compilation of four monographs.
Objective: To evaluate the effects of protocadherin-PC (PCDH-PC) gene expression on epithelial–mesenchymal transition (EMT) in prostate cancer cells. Methods: Western blot analysis, morphological analysis, and in vitro wound closure assay were used to assess the effects of inhibition of PCDH-PC expression on EMT in the androgen-independent prostate cancer cell lines DU-145 and PC-3. Results: Inhibition of PCDH-PC expression promoted mesenchymal–epithelial transition (MET) of DU-145 and PC-3 cells, which changed the cytomorphology to resemble that of the androgen-dependent prostate adenocarcinoma cells LNCaP, and slowed down the growth rate. Conclusions: Inhibition of PCDH-PC expression reduced the invasiveness of androgen-independent prostate cancer cells.
Ms. Tian Yuyao got her master degree of biochemistry from Peking University. She got her doctoral degree of biomedical sciences from the Chinese University of Hong Kong.
Werner Syndrome (WS) is an autosomal recessive genetic disorder characterized by premature aging. This disease is caused by mutations in the WRN gene. WRN gene plays a vital role in genomic stability, DNA replication and transcription. The first sign of WS is short stature. Individuals with WS have an abnormally slow growth rate, and growth stops at puberty. However, the underlying mechanisms are not well understood. Here we report a potential downstream target gene, SHOX (short-stature homeobox), was involved in the failure of bone development in Werner Syndrome. Additionally, the wrn mutant zebrafish was generated. In vivo analysis of chondrogenesis confirmed the role of wrn was crucial on bone development. And in the wrn mutant zebrafish, the expression of shox also decreased. Together, we concluded that the depletion of WRN would be one of the causes of short stature.