Yu Chen1, Lihong Li1, Jinfan Zhang1. 1. Department of Breast Surgery, The Affiliated Hospital of Putian University, Putian City, Fujian Province, China.
Abstract
PURPOSE: This paper aims to assess the role of CEMIP in human breast cancer, and explore the potential mechanisms of CEMIP in the progression of breast cancer. METHODS: We examined the expression levels of CEMIP in breast cancer tissues and cell lines by quantitative PCR and immunohistochemical assays. The effects of CEMIP on the proliferation, migration and invasion of breast cancer cells were determined through colony formation assay, flow cytometry (FCM) assay, wound healing assay and transwell assay, respectively. Additionally, the downstream targets of CEMIP were examined by Immunoblot assays. RESULTS: CEMIP expression was upregulated in both breast cancer tissues and cell lines. Patients with higher CEMIP expression displayed shorter survival time than those with lower expression. In addition, CEMIP knockdown inhibited breast cancer cell proliferation, migration, and invasion in vitro. Our data further confirmed that CEMIP promoted the proliferation and migration of breast cancer cells via GRP78-STAT3 axis. CONCLUSION: Our data demonstrated the role of CEMIP in breast cancer was associated with STAT3 signaling pathway. Therefore, CEMIP might act as a possible therapeutic target for breast cancer.
PURPOSE: This paper aims to assess the role of CEMIP in humanbreast cancer, and explore the potential mechanisms of CEMIP in the progression of breast cancer. METHODS: We examined the expression levels of CEMIP in breast cancer tissues and cell lines by quantitative PCR and immunohistochemical assays. The effects of CEMIP on the proliferation, migration and invasion of breast cancer cells were determined through colony formation assay, flow cytometry (FCM) assay, wound healing assay and transwell assay, respectively. Additionally, the downstream targets of CEMIP were examined by Immunoblot assays. RESULTS:CEMIP expression was upregulated in both breast cancer tissues and cell lines. Patients with higher CEMIP expression displayed shorter survival time than those with lower expression. In addition, CEMIP knockdown inhibited breast cancer cell proliferation, migration, and invasion in vitro. Our data further confirmed that CEMIP promoted the proliferation and migration of breast cancer cells via GRP78-STAT3 axis. CONCLUSION: Our data demonstrated the role of CEMIP in breast cancer was associated with STAT3 signaling pathway. Therefore, CEMIP might act as a possible therapeutic target for breast cancer.
Entities:
Keywords:
Breast cancer; CEMIP; GRP78; STAT3 signaling pathway; migration; proliferation