Yanchen Liu1, Mengyun Li1, Danping Shi1, Yuguang Zhu2. 1. Department of Ophthalmology, Yidu Central Hospital of Weifang, Qingzhou, 262500, People's Republic of China. 2. Department of Ophthalmology, The Affiliated Hospital of Weifang Medical University, Weifang, 261031, People's Republic of China. zhuyug0419@sina.com.
Abstract
OBJECTIVE: The purpose of our present study was to investigate the expression of cation transport regulator-like protein 1 (CHAC1) in uveal melanoma (UM) tissues and its function in UM progression. METHODS: The mRNA expression of CHAC1 in UM tissues and its prognostic value were investigated based on Gene Expression Omnibus database and The Cancer Genome Atlas database. SP6.5 and M23 UM cell lines with depleted CHAC1 were constructed using small interfering RNA. The viability and migration ability of SP6.5 and M23 UM cells were determined by MTT and wound healing assays, respectively. Western blot was conducted to test the influences of CHAC1 depletion on PI3K signaling pathway. RESULTS: Higher expression of CHAC1 was observed in the UM tissues from patients with liver metastases compared to that from patients without metastases. High CHAC1 expression was correlated with poor prognostic and was an independent predictor for UM patients. Depletion of CHAC1 remarkably inhibited the proliferation and motility of SP6.5 and M23 UM cells. Moreover, the ratios of p-AKT/AKT and p-mTOR/mTOR were reduced notably after silencing CHAC1. CONCLUSIONS: Our results suggested that CHAC1 functioned as a facilitator in UM cell proliferation and migration and possessed the potential to be a predictor as well as a therapeutic target for UM patients.
OBJECTIVE: The purpose of our present study was to investigate the expression of cation transport regulator-like protein 1 (CHAC1) in uveal melanoma (UM) tissues and its function in UM progression. METHODS: The mRNA expression of CHAC1 in UM tissues and its prognostic value were investigated based on Gene Expression Omnibus database and The Cancer Genome Atlas database. SP6.5 and M23 UM cell lines with depleted CHAC1 were constructed using small interfering RNA. The viability and migration ability of SP6.5 and M23 UM cells were determined by MTT and wound healing assays, respectively. Western blot was conducted to test the influences of CHAC1 depletion on PI3K signaling pathway. RESULTS: Higher expression of CHAC1 was observed in the UM tissues from patients with liver metastases compared to that from patients without metastases. High CHAC1 expression was correlated with poor prognostic and was an independent predictor for UM patients. Depletion of CHAC1 remarkably inhibited the proliferation and motility of SP6.5 and M23 UM cells. Moreover, the ratios of p-AKT/AKT and p-mTOR/mTOR were reduced notably after silencing CHAC1. CONCLUSIONS: Our results suggested that CHAC1 functioned as a facilitator in UM cell proliferation and migration and possessed the potential to be a predictor as well as a therapeutic target for UM patients.
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