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LncRNA MEG3 promotes endoplasmic reticulum stress and suppresses proliferation and invasion of colorectal carcinoma cells through the MEG3/miR-103a-3p/PDHB ceRNA pathway.

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机构: [1]Cancer Biotherapy Center, The Third Affiliated Hospital of Kunming Medical University, Yunnan Cancer Hospital, Kunming, China. [2]Department of Hepatobiliary and Pancreatic Surgery, The Third Affiliated Hospital of Kunming Medical University, Yunnan Cancer Hospital, Kunming, China. [3]Department of Rehabilitation Medicine, The Third People's Hospital of Yunnan Province, Kunming, China. [4]Department of Breast Surgery, The Third Affiliated Hospital of Kunming Medical University, Yunnan Cancer Hospital, Kunming, China. [5]Cadre Medical Division, The Third Affiliated Hospital of Kunming Medical University, Yunnan Cancer Hospital, Kunming, China. [6]Department of Palliative Medicine, The Third Affiliated Hospital of Kunming Medical University, Yunnan Cancer Hospital, Kunming, China. [7]Cancer Institute, The Third Affiliated Hospital of Kunming Medical University, Yunnan Cancer Hospital, Kunming, China. [8]Department of Gastrointestinal Surgery, First Affiliated Hospital of Kunming Medical University, Kunming, China. [9]Department of General Surgery, The Fifth Affiliated Hospital of Kunming Medical University, Kunming, China. [10]Integrated Traditional Chinese and Western Medicine, The Third Affiliated Hospital of Kunming Medical University, Yunnan Cancer Hospital, Kunming, China.
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LncRNA maternally expressed gene 3 (MEG3) is a potential prognostic and diagnostic biomarker in colorectal carcinoma (CC). However, its cellular functions and mechanism remain not fully uncovered. Relative expression of MEG3, miRNA (miR)-103a-3p, and pyruvate dehydrogenase E1 subunit beta (PDHB) was detected by RT-qPCR and western blotting. Cell proliferation was measured by CCK-8 assay, colony formation assay, and flow cytometry, as well as xenograft tumor assay. Transwell assay examined cell invasion. Endoplasmic reticulum (ER) stress was evaluated by western blotting. Dual-luciferase reporter assay and RNA immunoprecipitation determined the relationship between miR-103a-3p and MEG3 or PDHB. Expression of MEG3 was downregulated in human CC tumor tissues and cells (SW620 and HCT116), accompanied by higher miR-103a-3p and lower PDHB. Restoring MEG3 suppressed cell viability, colony formation ability, and invasion, arrested cell cycle, and induced apoptosis rate in SW620 and HCT116 cells, as well as promoted expression of ER stress-related proteins (GRP78, ATF6, CHOP, caspase-3, and caspase-9). Furthermore, MEG3 overexpression hindered tumor growth and facilitated ER stress in vivo. Molecularly, miR-103a-3p was a target of MEG3, and further targeted PDHB. Similarly, in function, blocking miR-103a-3p suppressed CC in vitro by affecting proliferation, invasion, and ER stress; in addition, restoring miR-103a-3p partially counteracted the suppressive role of MEG3 in CC cells. MEG3 sponged miR-103a-3p to suppress CC malignancy by inducing ER stress and inhibiting cell proliferation and invasion via upregulating PDHB, suggesting a novel MEG3/miR-103a-3p/PDHB ceRNA pathway.

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出版当年[2022]版:
大类 | 4 区 医学
小类 | 4 区 肿瘤学
最新[2023]版:
大类 | 4 区 医学
小类 | 4 区 肿瘤学
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Q3 ONCOLOGY
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Q3 ONCOLOGY

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第一作者机构: [1]Cancer Biotherapy Center, The Third Affiliated Hospital of Kunming Medical University, Yunnan Cancer Hospital, Kunming, China.
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