Abstract
Abstract Hormonal-receptor positive (HRP) breast cancer patients with positive metastatic axillary lymph nodes (LNs) are characterized by poor prognosis and increase the mortality rate. The mechanisms by which cancer cells invade lymph node have not been fully explored yet. Studies showed that the expression of interleukin-6 (IL-6) cytokine and the proteolytic enzyme cathepsin B (CTSB) are associated with breast cancer poor prognosis. In the present study, we tested the effect of different concentration of IL-6 on invasiveness capacity of HRP breast cancer cell lines MCF-7 cells using in vitro invasion chamber assay. Moreover, we investigated the impact of IL-6 on expression and activity of CTSB. Our findings indicates that IL-6 fosters invasion potential of MCF-7 cells in a dose-dependent manner. Furthermore, MCF-7 cells displayed increased CTSB expression and activity with acquisition of fibroblastic morphology upon IL-6 induction. To validate our results in vivo we assessed the level of expression of IL-6 and CTSB in the carcinoma tissues of positive and negative axillary metastatic lymph-nodes in HRP breast cancer patients., Western blot and immunohistochemistry showed that the expression of IL-6 and CTSB were higher in carcinoma tissues with positive lymph node compared to carcinoma tissues of patients with negative lymph node. Collectively, our findings suggest that IL-6 and CTSB may play a role in lymph node in HRP breast cancer patients. Targeting IL-6-CTSB axis may emerge as a therapeutic approach for hormonal-receptor positive with positive lymph node breast cancer patients. Note: This abstract was not presented at the conference. Citation Format: Ahmed Osama Hassan, Sherif A. Ibrahim, Eslam A. El-Ghonaimy, Hebatallah Hassan, Tahani El-Mamlouk, Mohamed El-Shinawi, Mona M. Mohamed. Hormonal-receptor positive breast cancer: IL-6 augments invasion and lymph node metastasis via stimulating cathepsin B expression. [abstract]. In: Proceedings of the AACR Special Conference on Advances in Breast Cancer Research; Oct 17-20, 2015; Bellevue, WA. Philadelphia (PA): AACR; Mol Cancer Res 2016;14(2_Suppl):Abstract nr A41.
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