MLF1 interacting protein: a potential gene therapy target for human prostate cancer?

• Published in: Medical oncology (Northwood, London, England) Vol. 32; no. 2; pp. 454 - 7
• Main Authors: Zhang, Lei, Ji, Guoqing, Shao, Yuzhang, Qiao, Shaoyi, Jing, Yuming, Qin, Rongliang, Sun, Huiming, Shao, Chen
• Format: Journal Article
• Language: English
• Published: Boston Springer US 01.02.2015; Springer Nature B.V
• Subjects: Apoptosis - genetics; Cell Line, Tumor; Cell Proliferation - genetics; Flow Cytometry; Genetic Therapy - methods; Hematology; Humans; Internal Medicine; Male; Medicine; Medicine & Public Health; Nuclear Proteins - biosynthesis; Nuclear Proteins - genetics; Oncology; Original Paper; Pathology; Prostatic Neoplasms - genetics; Prostatic Neoplasms - metabolism; Real-Time Polymerase Chain Reaction; Transcriptome; Transfection; Prostate carcinoma; MLF1IP; Prostate cancer
• ISSN: 1357-0560; 1559-131X
• DOI: 10.1007/s12032-014-0454-1

Here, we investigated the role of one gene that has been previously associated with human prostate carcinoma cells—myelodysplasia/myeloid leukemia factor 1 interacting protein (MLF1IP)—in order to better ascertain its role in human prostate carcinogenesis. The prostate cancer cell line PC-3 was lentivirally transfected to silence endogenous MLF1IP gene expression, which was confirmed by real-time quantitative PCR (RT-qPCR). Cellomics ArrayScan VTI imaging and MTT assays were conducted to assess cell proliferation. Cell cycle phase arrest and apoptosis were assayed by flow cytometry. Colony formation was assessed by fluorescence microscopy. MLF1IP gene expression was also analyzed by RT-qPCR in sixteen prostate cancer tissue samples and six healthy control prostate tissue samples from human patients. Cell proliferation was significantly inhibited in MLF1IP-silenced cells relative to control cells. G1 phase, S and G2/M phase cell counts were not significantly changed in MLF1IP-silenced cells relative to control cells. Apoptosis was significantly increased in MLF1IP-silenced cells, while MLF1IP-silenced cells displayed a significantly reduced number of cell colonies, compared to control cells. The 16 human prostate cancer tissue samples revealed no clear upregulation or downregulation in MLF1IP gene expression. MLF1IP significantly promotes prostate cancer cell proliferation and colony formation and significantly inhibits apoptosis without affecting cell cycle phase arrest. Further study is required to conclusively determine whether MLF1IP is upregulated in human prostate cancer tumors and to determine the precise cellular mechanism(s) for MLF1IP in prostate carcinogenesis.