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Effect of silencing the T‑Box transcription factor TBX2 in prostate cancer PC3 and LNCaP cells.

Molecular medicine reports (2017-08-30)
Wen-Liang Du, Qian Fang, Yue Chen, Jing-Wei Teng, Yong-Shuang Xiao, Ping Xie, Bo Jin, Jun-Qi Wang
RESUMO

T‑Box (TBX)‑2 is a member of the T‑box gene family, which is aberrantly expressed in numerous types of malignant tumors, and has previously been demonstrated to be conducive to tumor progression by acting as a transcription factor. However, specific information regarding the expression and function of TBX2 in prostate cancer cells remains to be elucidated. The present study demonstrated that silencing of TBX2 by TBX2 small interfering RNA inhibited cell proliferation and promoted cell senescence. It was demonstrated that knockdown of TBX2 inhibited cell metastatic abilities by upregulating E‑cadherin and downregulating N‑cadherin, Vimentin and fibronectin. In addition, the expression of TBX2 in prostate cancer tissues and tumor adjacent tissues was detected by immunohistochemistry. The results indicated that the expression rates of TBX2 were significantly increased in the cancerous tissues, compared with the healthy tumor adjacent tissue, and TBX2 increased staining was associated with the clinical stage and pathological grade. The findings of the present study therefore suggest that TBX2 expression is markedly increased in prostate cancer and TBX2 may act as a potential beneficial therapeutic target for the future treatment of prostate cancer.

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Sigma-Aldrich
(Tyr[SO3H]27)Cholecystokinin fragment 26-33 Amide, ≥97% (HPLC), powder
Sigma-Aldrich
MISSION® esiRNA, targeting human TBX2