Mast Cell Chymase Can Disrupt the Human Bronchial Epithelium and Stimulate the Loss of Adhesion Molecules

Zhou, Xiaoying; Cox, Christopher W.; Rajenthirar, S.; Mahrous, A.A.; Masters, Bettie Sue Siler; Walls, Andrew F.

doi:10.1016/j.jaci.2007.12.439

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“…Treating cells with the lowest concentration of MCC (5 mU/ml) resulted in increased cell viability, whereas the higher doses of MCC (25 and 50 mU/ml) caused decreased viability of A549 and H520 cell lines. Similar results were observed with MCC treated human epithelial cells (26). The duration and the activity of MCC also influenced the cell cycle where p53 and p21 are involved.…”

Section: Discussionsupporting

confidence: 84%

Mast cell chymase affects the proliferation and metastasis of lung carcinoma cells in vitro

Jiang

Hardie

et al. 2017

Oncology Letters

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Abstract. Metastasis of lung carcinoma cells is a major cause of organ failure and mortality of patients with lung cancer. Lung mast cells are a type of immune cell which reside in the respiratory mucosa. High numbers of mast cells are associated with the majority of common types of cancer; however, the effects of mast cells on cancer remain unclear. In the present study, the effects of mast cell chymase (MCC) on the proliferation and adhesion of the lung carcinoma cell lines A549 and H520 was investigated. After 24 h of treatment, the highest dose of MCC (50 mU/ml) decreased the proliferation rate of A549 and H520 cells, whereas the lowest dose of MCC (5 mU/ml) resulted in a small increase in the viability. A549 cells treated with MCC lost adhesion ability in a MCC dose-dependent manner; however, these detached cells were able to regrow when transferred to a fresh culture. The protein expression of epithelial (E-) cadherin, p53 and p21 in A549 lung carcinoma cells were detected by western blot analysis. The results of the present study revealed that, following 24 h of treatment, the expression level of E-cadherin was decreased, the p53 tumor suppressor protein was expressed in limited quantities and the expression of p21 was decreased. Zymography was used to examine the effects of MCC on the expression and activation of matrix metalloproteinase-9 (MMP-9) in A549 and H520 cells. The expression of MMP-9 in the two cell lines was time-and MCC dose-dependent. The results of the present study demonstrated that MCC stimulated lung carcinoma cell proliferation and adhesion, as well as regulated E-cadherin expression and the cell cycle, all of which are associated with cancer metastasis. Therefore, MCC may be a potential candidate for lung carcinoma therapy.

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Section: Discussionsupporting

confidence: 84%