Bo Luo1, Na Kang2, Yan Chen3, Lihong Liu4, Yongmei Zhang5. 1. Department of Urology, Songshan Hospital of Qingdao University Medical College, Qingdao, China. 2. Department of Blood Purification Center, First People's Hospital of Jinan, Jinan, China. 3. Department of Neurology, People's Hospital of Zhangqiu, Jinan, China. 4. Department of Electrocardiograms, People's Hospital of Zhangqiu, Jinan, China. 5. Department of Medical Records Room, People's Hospital of Weifang, Weifang, China - xialie5811@163.com.
Abstract
BACKGROUND: Prostate cancer (PCa) is the second leading contributor to male malignancy-associated death in developed countries. The study aimed to evaluate the effects of miR-106a on prostate cancer cells and the underlying molecular mechanism. METHODS: The cell proliferation was detected using MTT assay and colony formation, and cells migration and invasion were also analyzed. Luciferase reporter assay was carried out to explore the correlation between miR-106a and PTEN. Besides, reverse transcriptase-polymerase chain reaction and western blot were carried out to measure the mRNA and protein levels in prostate tissues and PCa cells. Immunocytochemical staining was performed to detect the PTEN level in PCa tissues. RESULTS: MiR-106a level was dramatically increased in the PCa tissues and PCa cell lines. The overexpression of miR-106a significantly promoted the proliferation, migration and invasion of PCa cells. Besides, we confirmed that PTEN was regulated by miR-106a expression and was a direct target of miR-106a. Most importantly, we further found that miR-106a could promote the PCa cells xenograft growth in the nude mice by targeting PTEN, which was significantly downregulated in PCa tissues and cell lines and was closely related with PCa metastasis. CONCLUSIONS: MiR-106a as an oncogene could promote proliferation and metastasis of prostate cancer cells by directly targeting PTEN in vivo and in vitro.
BACKGROUND:Prostate cancer (PCa) is the second leading contributor to male malignancy-associated death in developed countries. The study aimed to evaluate the effects of miR-106a on prostate cancer cells and the underlying molecular mechanism. METHODS: The cell proliferation was detected using MTT assay and colony formation, and cells migration and invasion were also analyzed. Luciferase reporter assay was carried out to explore the correlation between miR-106a and PTEN. Besides, reverse transcriptase-polymerase chain reaction and western blot were carried out to measure the mRNA and protein levels in prostate tissues and PCa cells. Immunocytochemical staining was performed to detect the PTEN level in PCa tissues. RESULTS:MiR-106a level was dramatically increased in the PCa tissues and PCa cell lines. The overexpression of miR-106a significantly promoted the proliferation, migration and invasion of PCa cells. Besides, we confirmed that PTEN was regulated by miR-106a expression and was a direct target of miR-106a. Most importantly, we further found that miR-106a could promote the PCa cells xenograft growth in the nude mice by targeting PTEN, which was significantly downregulated in PCa tissues and cell lines and was closely related with PCa metastasis. CONCLUSIONS:MiR-106a as an oncogene could promote proliferation and metastasis of prostate cancer cells by directly targeting PTEN in vivo and in vitro.