Journal
ONCOLOGY RESEARCH
Volume 24, Issue 4, Pages 271-277Publisher
COGNIZANT COMMUNICATION CORP
DOI: 10.3727/096504016X14666990347473
Keywords
Cullin 4B (CUL4B); Non-small cell lung cancer (NSCLC); Invasion; Wnt/beta-catenin pathway
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Funding
- Crossing Research Projects of Zhengzhou University [340700532007]
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Cullin 4B (CUL4B), a scaffold protein that assembles CRL4B ubiquitin ligase complexes, was found to be overexpressed in many types of tumors. However, the expression pattern and role of CUL4B in non-small cell lung cancer (NSCLC) remain largely unknown. Therefore, in the present study, we investigated the role of CUL4B in NSCLC, and the underlying mechanism was also explored. Our results showed that CUL4B was highly expressed in NSCLC cell lines. Silencing CUL4B obviously inhibited proliferation and migration/invasion of NSCLC cells, and it also suppressed the epithelial mesenchymal transition (EMT) progress in NSCLC cells. Furthermore, knockdown of CUL4B significantly inhibited the expression of beta-catenin, cyclin D1, and c-Myc in NSCLC cells. Taken together, these results suggest that knockdown of CUL4B inhibited the proliferation and invasion through suppressing the Wnt/beta-catenin signaling pathway in NSCLC cells. Therefore, CUL4B may represent a novel therapeutic target for the treatment of NSCLC.
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