Journal of cellular biochemistry · 2018
Upregulation of lncRNA FER1L4 suppresses the proliferation and migration of the hepatocellular carcinoma via regulating PI3K/AKT signal pathway.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Wang Xu, Dong Ke, Jin Qizhi, Ma Yujing, Yin Shujun, Wang Shan
Аннотация
BACKGROUND AND OBJECTIVES: This study aimed to investigate the potential function of FER1L4 in the progression of hepatocellular carcinoma and uncover its underlying molecular mechanism.
METHODS: In the current study, quantitative real-time polymerase chain reaction (qRT-PCR) was conducted to determine the expression profile of FER1L4 in normal liver tissues and hepatocellular carcinoma tissues of human, as well as hepatocellular carcinoma (HCC) cell lines including HL-7702[L-02], HepG-2, Hep3b, and SMMC-7721. Then, HepG-2 cells were transfected with pcDNA3.1-FER1L4 (pcDNA3.1-empty as negative control) for gain-of-function analysis, followed with cell functional abnormality tests. Specifically, colony formation analysis and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide experiment were taken advantage to measure the cell proliferation, while cell migration and invasion were evaluated by wound healing assay and transwell experiment respectively. Additionally, cell apoptosis was detected by flow cytometry. Moreover, the effect of FER1L4 on PI3K/AKT signal pathway activation was investigated through analyzing phosphorylation of related proteins, p-AKT/AKT and p-PI3K/PI3K, via Western blot assay.
RESULTS: Downregulation of FER1L4 in hepatocellular carcinoma tissues and cells was demonstrated by qRT-PCR analysis. Besides, FER1L4 overexpression evidently attenuated the cell proliferation, migration and invasion, but prompted cell apoptosis. Importantly, Western blot assays revealed that PII3K/AKT signal pathway were involved in mediating the progression regulation role of FER1L4 in HCC cells.
CONCLUSIONS: Our study suggested that FER1L4 might alleviate progression of hepatocellular carcinoma via blocking PI3K/AKT pathway, which encourages a better understanding of the pathogenesis of HCC and may provide a novel potential therapeutic target for clinical treatment.
METHODS: In the current study, quantitative real-time polymerase chain reaction (qRT-PCR) was conducted to determine the expression profile of FER1L4 in normal liver tissues and hepatocellular carcinoma tissues of human, as well as hepatocellular carcinoma (HCC) cell lines including HL-7702[L-02], HepG-2, Hep3b, and SMMC-7721. Then, HepG-2 cells were transfected with pcDNA3.1-FER1L4 (pcDNA3.1-empty as negative control) for gain-of-function analysis, followed with cell functional abnormality tests. Specifically, colony formation analysis and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide experiment were taken advantage to measure the cell proliferation, while cell migration and invasion were evaluated by wound healing assay and transwell experiment respectively. Additionally, cell apoptosis was detected by flow cytometry. Moreover, the effect of FER1L4 on PI3K/AKT signal pathway activation was investigated through analyzing phosphorylation of related proteins, p-AKT/AKT and p-PI3K/PI3K, via Western blot assay.
RESULTS: Downregulation of FER1L4 in hepatocellular carcinoma tissues and cells was demonstrated by qRT-PCR analysis. Besides, FER1L4 overexpression evidently attenuated the cell proliferation, migration and invasion, but prompted cell apoptosis. Importantly, Western blot assays revealed that PII3K/AKT signal pathway were involved in mediating the progression regulation role of FER1L4 in HCC cells.
CONCLUSIONS: Our study suggested that FER1L4 might alleviate progression of hepatocellular carcinoma via blocking PI3K/AKT pathway, which encourages a better understanding of the pathogenesis of HCC and may provide a novel potential therapeutic target for clinical treatment.