We found a match
Your institution may have rights to this item. Sign in to continue.
- Title
Tumor-associated macrophages correlate with the clinicopathological features and poor outcomes via inducing epithelial to mesenchymal transition in oral squamous cell carcinoma.
- Authors
Yong Hu; Meng-Ying He; Li-Fang Zhu; Cong-Chong Yang; Mei-Ling Zhou; Qiong Wang; Wei Zhang; Yang-Yu Zheng; Dong-Miao Wang; Zeng-Qi Xu; Yu-Nong Wu; Lai-Kui Liu
- Abstract
Background: Both tumor-associated macrophages (TAMs) and the epithelial to mesenchymal transition (EMT) of cancer cells play key roles in promoting tumor progression. However, whether TAMs could induce EMT in the progression of oral squamous cell carcinoma (OSCC) remains undefined. Results: Here we detected the expression of macrophages markers CD68 and CD163, epithelial marker E-cadherin and mesenchymal marker vimentin in 127 OSCC patients by using semi-quantitative immunohistochemistry. CD68 and CD163 expression was not confined to the infiltrating TAMs, but also detected in cancer cells. The high number of CD68-positive macrophages was correlated with poor overall survival. Meanwhile, the expression of CD163 both in macrophages and in cancer cells was associated with poor overall survival and had a significant prognostic impact in OSCC. Importantly, the expression of CD163 in cancer cells had a significant relationship with E-cadherin and vimentin. Furthermore, the incubation of TAMs conditioned medium resulted in a fibroblast-like appearance of cancer cells (HN4, HN6 and SCC9) together with the decreased/increased expression of E-cadherin/ vimentin, which were correlated with the enhanced ability of migration and invasion. Conclusions: Our results indicate that TAMs could promote the EMT of cancer cells, thereby leading to the progression of oral cancer.
- Subjects
MACROPHAGES; SQUAMOUS cell carcinoma; ORAL cancer; CANCER cells; CANCER invasiveness; TUMOR markers; HEMATOPOIETIC stem cells; TUMOR necrosis factors; PROGNOSIS
- Publication
Journal of Experimental & Clinical Cancer Research (17569966), 2016, Vol 35, p1
- ISSN
1756-9966
- Publication type
Article
- DOI
10.1186/s13046-015-0281-z