RESUMO
Breast cancer is the malignant tumor with the highest incidence rate at present, and its incidence rate ranks first in the female population. COL11A1 is an important component of collagen XI and is considered to play an important role in a variety of connective tissue diseases. Recent studies have shown that COL11A1 is associated with the occurrence and development of many kinds of malignant tumors. However, its prognostic value in breast cancer and its correlation with immune cell infiltration in tumor tissue are not clear. In this paper, we reveal the prognostic value of COL11A1 in breast cancer and its tumor immune-related function through in-depth bioinformatics analysis. The expression of COL11A1 is abnormally upregulated in breast cancer and is significantly related to the poor prognosis of breast cancer. In the analysis of the clinical characteristics of the patients, we found that the expression level of COLL11A1 was closely related to lymph node metastasis, PAM50 (Prediction Analysis of Microarray 50) expression, clinical stage and so on. Gene Ontology (GO) and Kyoto Encyclopedia of Gene and Genome (KEGG) all suggest that COL11A1 is related to tumor immunity. Further study found that the COL11A1 expression was significantly correlated with the degree of immune infiltration and the expression of a variety of immune cell markers in tumor tissue. More importantly, COL11A1 can affect the prognosis of breast cancer patients by participating in the regulation of tumor immune infiltration. Therefore, we believe that COL11A1 is a very potential target for diagnosis and treatment of breast cancer.
RESUMO
Breast cancer is one of the major challenges for women's health. However, the role and mechanisms of interleukins (ILs) on the progression of breast cancer are not well illustrated. Our present study revealed that the expressions of IL-6 and IL-8 were significantly increased in oestrogen receptor-negative (ER-) breast cancer cells. Increased expression of IL-6 was observed in 83.9% (26/31) ER- breast cancer tissues as compared with their matched adjacent normal tissues. In vitro studies indicated that IL-6 can significantly promote the migration and invasion of ER- breast cancer cells via increasing the dephosphorylation, nuclear translocation and transcriptional activities of YAP in breast cancer cells. Knockdown of YAP can attenuate IL-6-induced migration and invasion of cancer cells, suggesting that YAP plays an essential role in IL-6-induced malignancy of breast cancer cells. Furthermore, IL-6 treatment also decreased the phosphorylation of LATS1/2. The knockdown of LATS1/2 synergistically suppressed si-IL-6-induced deactivation of YAP. Targeted inhibition of IL-6/YAP can significantly suppress the invasion of ER- breast cancer cells. Collectively, our study revealed that IL-6 can trigger the malignancy of breast cancer cells via activation of YAP signals. Targeted inhibition of IL-6/YAP might be a novel therapeutic approach for the treatment of ER- breast cancer.
