DEPDC1 promotes cell proliferation and tumor growth via activation of E2F signaling in prostate cancer
Autor: | Fu-Chao Chen, Huiyong Shen, Xu-biao Chen, Zhaopeng Cai, Guo-xue Tang, Keng Chen, Wei-hua Zhao, Lin Huang, Xi Lin, Song-jie Yang |
---|---|
Rok vydání: | 2017 |
Předmět: |
Male
0301 basic medicine Biophysics Bone Neoplasms Biochemistry Bone and Bones 03 medical and health sciences Prostate cancer 0302 clinical medicine Cell Line Tumor medicine Animals Humans E2F1 E2F Molecular Biology Cell Proliferation Mice Inbred BALB C Cell growth Chemistry Cell Cycle GTPase-Activating Proteins Prostate Prostatic Neoplasms Bone metastasis Cell Biology Cell cycle medicine.disease E2F Transcription Factors Neoplasm Proteins Up-Regulation Gene Expression Regulation Neoplastic 030104 developmental biology Cell culture 030220 oncology & carcinogenesis DEP domain Cancer research Signal Transduction |
Zdroj: | Biochemical and Biophysical Research Communications. 490:707-712 |
ISSN: | 0006-291X |
DOI: | 10.1016/j.bbrc.2017.06.105 |
Popis: | DEP domain containing 1 (DEPDC1) is recently reported to be overexpressed in several types of human cancer; however the role of DEPDC1 in prostate cancer remains to be investigated. Herein, we identified that the DEPDC1 mRNA and protein expression levels were dramatically increased in prostate cancer tissues and cell lines. Overexpression of DEPDC1 promoted, but depletion of DEPDC1 inhibited cell proliferation by regulating the G1-S phase cell cycle transition. Importantly, we found that DEPDC1 was essential for the tumor growth and formation of bone metastases of prostate cancer cells in vivo. Finally, we demonstrated that DEPDC1 interacted with E2F1 and increased its transcriptional activity, leading to hyper-activation of E2F signaling in prostate cancer cells. Our findings reveal an oncogenic role of DEPDC1 in prostate cancer progression via activation of E2F signaling, and suggest DEPDC1 might be a potential therapeutic target against the disease. |
Databáze: | OpenAIRE |
Externí odkaz: |