Original Article
FHL2 Antagonizes Id1-Promoted Proliferation and Invasive Capacity of Human MCF-7 Breast Cancer Cells
Abstract
Objective: FHL2 was previously identified to be a novel interacting factor of Id family proteins. The aim of this study was to investigate, the effects of FHL2 on Id1-mediated transcriptional regulation activity and its oncogenic activity in human breast cancer cells.
Methods: Cell transfection was performed by Superfect reagent. Id1 stably overexpressed MCF-7 cells was cloned by G418 screening. The protein level of Id1 was detected by western blot analysis. Dual relative luciferase assays were used to measure the effect of E47-mediated transcriptional activity in MCF-7 human breast cancer cells. MTT assay was used to measure cell proliferation. Transwell assay was used to measure the invasive capacity of MCF-7 cancer cells.
Results: The basic helix-loop-helix (bHLH) factor E47-mediated transcription activity was markedly repressed by Id1 in MCF-7 cells. This Id1-mediated repression was effectively antagonized by FHL2 transduction. Overexpression of Id1 markedly promoted the proliferation rate and invasive capacity of MCF-7 cells; however, these effects induced by Id1 were significantly suppressed by overexpression of FHL2 in cells.
Conclusion: FHL2 can inhibit the proliferation and invasiveness of human breast cancer cells by repressing the functional activity of Id1. These findings provide the basis for further investigating the functional roles of FHL2-Id1 signaling in the carcinogenesis and development of human breast cancer.
Methods: Cell transfection was performed by Superfect reagent. Id1 stably overexpressed MCF-7 cells was cloned by G418 screening. The protein level of Id1 was detected by western blot analysis. Dual relative luciferase assays were used to measure the effect of E47-mediated transcriptional activity in MCF-7 human breast cancer cells. MTT assay was used to measure cell proliferation. Transwell assay was used to measure the invasive capacity of MCF-7 cancer cells.
Results: The basic helix-loop-helix (bHLH) factor E47-mediated transcription activity was markedly repressed by Id1 in MCF-7 cells. This Id1-mediated repression was effectively antagonized by FHL2 transduction. Overexpression of Id1 markedly promoted the proliferation rate and invasive capacity of MCF-7 cells; however, these effects induced by Id1 were significantly suppressed by overexpression of FHL2 in cells.
Conclusion: FHL2 can inhibit the proliferation and invasiveness of human breast cancer cells by repressing the functional activity of Id1. These findings provide the basis for further investigating the functional roles of FHL2-Id1 signaling in the carcinogenesis and development of human breast cancer.
