Background: The microenvironment of various tumor tissues is acidic. Acid-sensing ion channels (ASICs) are a class of ligand-gated ion channels which are sensitive to extracellular protons and are often highly expressed in tumor tissues. Breast cancer, whose extracellular microenvironment is thought to be acidic, is the most common cancer type among females in the world. Methods: Thirty breast cancer tissues and adjacent normal tissues of patients were collected from 2009 to 2015 at the Xinhua hospital affiliated to Shanghai Jiao Tong University School of Medicine. The expression of acid-sensing ion channel 1a (ASIC1a), a subtype of ASICs family, was detected by immunohistochemistry in breast cancer tissues, and the effect of ASIC1a on the physiological activity of tumor cells was analyzed in vitro and in vivo experiments.Results: In this study, it was found that ASIC1a is highly expressed in the tissues of breast cancer patients.In vitro experiments revealed that down-regulation of ASIC1a by its antagonist PcTx-1 or ASIC1a siRNA could significantly weaken the migration, proliferation and invasion of tumor cells. In vivo studies, downregulation or inhibition of the ASIC1a could inhibit breast tumor growth. Conclusions:The high expression of ASIC1a might be related to the enhanced biological activity of breast cancer cells. Whether ASIC1a is a potential therapeutic target for some types of breast cancer deserves further study.
Background In a previous study, persistent pain was suggested to be a risk factor for tumor patients. However, the mechanism underlying this phenomenon is still unclear. Substance P (SP), a pain-related neuropeptide secreted by the neural system and the immune system, plays an important role in the induction and maintenance of persistent pain. Methods In this study, in order to explore whether SP participates in the influence of pain on tumor progression, the serum samples of lung cancer and breast cancer patients were collected and tested. An elevated expression of SP was found in patients with pain. Results Cell pharmacological experiments revealed that SP can upregulate the expression of Toll-like receptor-4 (TLR-4) in tumor cells and increase the proliferation, migration, and invasive activity of tumor cells. As high expression of TLR-4 has the ability to enhance the biological activity of tumor cells, TLR-4 is thought to be involved in SP-induced tumor proliferation, migration, and invasion. Treatment of tumor cells with Aprepitant, a specific blocker of the NK-1 receptor, could reduce the expression of TLR-4 and reduce the proliferation, invasion, and migration activities of tumor cells; further proof of the influence of SP on TLR-4 expression depends on the NK-1 receptor located in tumor cells. Conclusions Based on the results above, we proposed a possible mechanism underlying pain affecting tumor progression: The presence of pain increases the content of SP in patients’ blood, and elevated SP increases the expression of tumor TLR-4 by acting on the NK-1 receptor, which ultimately affects the biological activity of the tumor.
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