Journal
JOURNAL OF CELLULAR AND MOLECULAR MEDICINE
Volume 26, Issue 8, Pages 2363-2376Publisher
WILEY
DOI: 10.1111/jcmm.17257
Keywords
bladder cancer; IL8; OCLN; tumour angiogenesis
Categories
Funding
- Fundamental Research Funds for the Central Universities, Sun Yat-sen University [2021qntd35]
- Shenzhen Science and Technology Innovation Commission, China [JCYJ20190807160209294, JCYJ20190807160813467]
- National Natural Science Foundation of China [32100564, 32170789, 81970191]
Ask authors/readers for more resources
According to recent studies, the tight junction protein occludin (OCLN) is highly expressed in bladder cancer tissues and is associated with a poor prognosis. Downregulation of OCLN inhibits tumor angiogenesis, while overexpression of OCLN has the opposite effect. Mechanistically, OCLN increases levels of interleukin-8 (IL8) and phosphorylated Signal Transducer and Activator of Transcription 3 (p-STAT3) to promote bladder cancer angiogenesis. OCLN regulates IL8 transcriptional activity through the transcription factor STAT4.
Bladder cancer (BLCA) is a common genitourinary cancer in patients, and tumour angiogenesis is indispensable for its occurrence and development. However, the indepth mechanism of tumour angiogenesis in BLCA remains elusive. According to recent studies, the tight junction protein family member occludin (OCLN) is expressed at high levels in BLCA tissues and correlates with a poor prognosis. Downregulation of OCLN inhibits tumour angiogenesis in BLCA cells and murine xenografts, whereas OCLN overexpression exerts the opposite effect. Mechanistically, the RT-qPCR analysis and Western blotting results showed that OCLN increased interleukin-8 (IL8) and p-signal transducer and activator of transcription 3 (STAT3) levels to promote BLCA angiogenesis. RNA sequencing analysis and dual-luciferase reporter assays indicated that OCLN regulated IL8 transcriptional activity via the transcription factor STAT4. In summary, our results provide new perspectives on OCLN, as this protein participates in the development of BLCA angiogenesis by activating the IL8/STAT3 pathway via STAT4 and may serve as a novel and unique therapeutic target.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available