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Title: MiR-361-5p acts as a tumor suppressor in prostate cancer by targeting signal transducer and activator of transcription-6(STAT6)

Journal Article · · Biochemical and Biophysical Research Communications
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  1. Department of Urology, Zhongda Hospital, Medical School, Southeast University, Nanjing, Jiangsu Province 210009 (China)
  2. Surgery Central Laboratory of Southeast University, Nanjing, Jiangsu Province 210009 (China)
  3. Department of Pathology, Zhongda Hospital Affiliated with Southeast University, Nanjing, Jiangsu Province 210009 (China)
  4. Department of Urology, Xuzhou Central Hospital Affiliated with Southeast University, Xuzhou, Jiangsu Province 221009 (China)

Highlights: • The role of miR-361-5p in prostate cancer (PCa) has not been evaluated until date. • We found that the expression of miR-361-5p in CRPC was lower than in ADPC. • MiR-361-5p suppressed DU145 cell proliferation and triggered apoptosis. • STAT6 is a direct target of miR-361-5p. • STAT6 enhances the expression of Bcl-xL at the transcriptional level. - Abstract: Castration-resistant prostate cancer (CRPC), whose pathogenesis is known to be regulated by microRNAs (miRNAs), has a poor prognosis. In our present study, we found that the expression of miR-361-5p in CRPC was lower than in androgen-dependent prostate cancer (ADPC), indicating that miR-361-5p may play an important role in the progression of ADPC to CRPC. The role of miR-361-5p in prostate cancer (PCa) has not been evaluated until date. Our findings suggest that miR-361-5p is a suppressor in CRPC. Signal transducer and activator of transcription-6 (STAT6), a direct target of miR-361-5p, enhances the expression of B-cell lymphoma-extra large (Bcl-xL), while miR-361-5p inhibits its expression through STAT6. Therefore, miR-361-5p has great clinical significance in preventing the malignant progression of PCa.

OSTI ID:
22416293
Journal Information:
Biochemical and Biophysical Research Communications, Vol. 445, Issue 1; Other Information: Copyright (c) 2014 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
Country of Publication:
United States
Language:
English

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