ArticleClinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico2022
Effect of PPP1R14D gene high expression in lung adenocarcinoma knocked out on proliferation and apoptosis of DMS53 cell.
Article in Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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- Comprehensive analysis to identify GNG7 as a prognostic biomarker in lung adenocarcinoma correlating with immune infiltrates.Frontiers in genetics · 2022Article
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5 authors at 1 institution in 1 country.
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Abstract
purposeGlobally, lung cancer remains the most commonly diagnosed cancer and the leading cause of cancer-related mortality. Lung adenocarcinoma (LUAD) is a common subtype of lung cancer and carries a poor prognosis. Treatment outcomes biomarkers in LUAD are critical, and there is currently a paucity of data; therefore, there is a need for novel biomarkers and newer therapeutic targets.
methodsBayesian analysis was used to obtain the whole-genome t value of LUAD. Gene set enrichment analysis (GSEA) was conducted to obtain the normalized enrichment scores (NES) of the whole genome, and the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway was analyzed using the Gene Set Analysis Toolkit. Herein, we investigated the PPP1R14D expression level at the protein level in LUAD and the impact of PPP1R14D knockdown on the proliferation and apoptosis of LUAD cells in vitro.
resultsA total of 483 LUAD samples and 59 normal control samples were included, and 904 differentially expressed genes (DEGs) and 504 LUAD-related genes reported in the literature were obtained. The DEGs showed that PPP1R14D was the most significantly up-regulated gene. Western blot of 30 cases of LUAD tissue and adjacent normal tissue also found that PPP1R14D was significantly highly expressed in cancer tissues. Lentivirus-mediated shRNA strategy effectively inhibited PPP1R14D expression in human LUAD cells DMS53, while PPP1R14D knockdown induced apoptosis and cell proliferation in DMS53 cells.
conclusionAbnormally up-regulated PPP1R14D promotes the survival and proliferation of tumor cells in human LUAD and may serve as a therapeutic and diagnostic target for LUAD.
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