Open AccessRAD18 contributes to the migration and invasion of human cervical cancer cells via the interleukin‑1β pathway
Author(s) -
Pengrong Lou,
Shitao Zou,
Zhiguo Shang,
Chao He,
Aidi Gao,
Shunyu Hou,
Jundong Zhou
Publication year - 2019
Publication title -
molecular medicine reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.727
H-Index - 56
eISSN - 1791-3004
pISSN - 1791-2997
DOI - 10.3892/mmr.2019.10564
Subject(s) - oncogene , gene silencing , ubiquitin ligase , gene knockdown , biology , cancer research , ubiquitin , cell cycle , cancer , motility , proinflammatory cytokine , apoptosis , immunology , microbiology and biotechnology , inflammation , gene , biochemistry , genetics
The E3 ubiquitin ligase RAD18 has been identified as an oncoprotein that exhibits prometastatic properties in various types of cancer; however, the role of RAD18 in cervical cancer (CC) remains unclear. In the present study, it was revealed that increased expression of RAD18 was associated with worse prognosis of patients with CC. Knockdown of endogenous RAD18 suppressed the motility and invasiveness of CC cells, as evaluated by Transwell assays. mRNA sequencing revealed that silencing RAD18 altered the expression profile of proinflammatory mediators, such as interleukin‑1β (IL‑1β). Furthermore, exogenous IL‑1β treatment rescued RAD18‑mediated CC cell invasion. These findings indicated an underlying mechanism via which RAD18 promotes CC progression, suggesting that RAD18 may be a potential biomarker and therapeutic target for malignant CC.