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Updated: Dec 30, 2025

An Orthotopic Murine Model of Human Prostate Cancer Metastasis
Published on: September 18, 2013
TRIM66 promotes malignant progression of prostate carcinoma through the JAK/STAT pathway
Hongwen Cao1, Renjie Gao1, Lei Chen1
1Surgical Department I (Urology Department), LongHua Hospital Shanghai University of Traditional Chinese Medicine, China.
Abstract:
Prostate cancer is the fifth leading cause of cancer-related deaths in males globally. Tripartite Motif Containing 66 (TRIM66) functions as transcriptional repressor and exerts its effect at least partially through promotion of deacetylase. TRIM66 has been previously reported to play an oncogenic role in a number of human cancers. Here, we investigated the potential oncogenic properties of TRIM66 in prostate cancer. We report that shRNA-mediated knockdown of TRIM66 significantly suppressed viability and proliferation of both PC-3 and DU145 prostate cancer cell lines. Furthermore, TRIM66 deficiency inhibited migration and invasion of prostate cancer cells. Mechanistically, TRIM66 positively regulated signal transducer and activator of transcription 2 (STAT2) and interleukin-2 (IL-2) expression. The predominance of STAT2-IL-2 in mediating the oncogenic properties of TRIM66 was determined using a rescue assay, wherein overexpression of either STAT2 or IL-2 almost completely abolished the inhibitory effects on cell proliferation, migration and invasion elicited by TRIM66 deficiency in prostate cancer cells. Our study highlights the importance of the TRIM66-STAT2-IL-2 signaling axis in the tumor biology of prostate cancer.
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