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Silencing LINC00504 inhibits cell proliferation, invasion as well as migration and promotes cell apoptosis in lung cancer cells via upregulating miR-876-3p

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Abstract

LINC00504 acts as an oncogene and associates with unfavorable prognosis in patients with lung cancer. Silencing LINC00504 may be a promising strategy for treatment of lung cancer and its effects were firstly investigated in lung cancer cells this study. The gene expression level of miR-876-3p as well as LINC00504 were measured via PCR assay. The cell proliferation was investigated through Cell Counting Kit-8 (CCK-8) assay and colony formation assay. Flow cytometry was applied for detection of cell apoptosis. Wound healing and transwell assay were performed for measurement of cell migration and invasion respectively. The apoptosis related protein expressions were measured by western blot. Luciferase report assay was conducted for verification the target gene. LINC00504 was higher expressed in five types of lung cancer cells studied herein when compared with the control normal cells. LINC00504 knockdown exerted inhibitory effects on cell apoptosis, cell migration as well as cell invasion and promoted cell apoptosis. All the effects mentioned above were counteracted by miR-876-3p inhibitor. Silencing LINC00504 possessed anti-proliferation, repression of cell invasion as well as migration and pro-apoptosis effects via targeting up-regulation of miR-876-3p in lung cancer cells, proving the new therapeutic targets and highlighting the potential application in future diagnosis and treatment in lung cancer.

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The datasets used and/or analyzed during the current study are available from the corresponding author on reasonable request.

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The code used during the current study are available from the corresponding author.

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Correspondence to Zhen Zhang.

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The experiment was approved by the ethics committee Fu Yang People’s Hospital.

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Zhang, Z. Silencing LINC00504 inhibits cell proliferation, invasion as well as migration and promotes cell apoptosis in lung cancer cells via upregulating miR-876-3p. Cytotechnology 72, 807–817 (2020). https://doi.org/10.1007/s10616-020-00424-5

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  • DOI: https://doi.org/10.1007/s10616-020-00424-5

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