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pmid:38601452

Regulatory role of the miR-142-3p/CDC25C axis in modulating autophagy in non-small cell lung cancer.

Jing Meng · Zongchang Song · Shuxian Cong · Qiong Sun · Qinyun Ma · Weiwei Shi · Linxuan Wang

Translational lung cancer research · 2024 doi:10.21037/tlcr-24-82

Paper

complete

Experiment

complete

Data

partial

Analysis

complete

Execution

absent

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title
Regulatory role of the miR-142-3p/CDC25C axis in modulating autophagy in non-small cell lung cancer.
doi
10.21037/tlcr-24-82
pmid
38601452
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[0]
Jing Meng
[1]
Zongchang Song
[2]
Shuxian Cong
[3]
Qiong Sun
[4]
Qinyun Ma
[5]
Weiwei Shi
[6]
Linxuan Wang
journal
Translational lung cancer research
year
2024
abstract
Background: With its diverse genetic foundation and heterogeneous nature, non-small cell lung cancer (NSCLC) needs a better comprehension of prognostic evaluation and efficient treatment targeting. Methods: Bioinformatics analysis was performed of The Cancer Genome Atlas (TCGA)-NSCLC and GSE68571 dataset. Overlapping differentially expressed genes (DEGs) were used for functional enrichment analysis and constructing the protein-protein interaction (PPI) network. In addition, key prognostic genes were identified through prognostic risk models, and their expression levels were verified. The phenotypic effects of cell division cycle 25C (CDC25C) regulation on NSCLC cell lines were assessed by in vitro experiments using various techniques such as flow cytometry, Transwell, and colony formation. Protein levels related to autophagy and apoptosis were assessed, specifically examining the impact of autophagy inhibition [3-methyladenine (3-MA)] and the miR-142-3p/CDC25C axis on this regulatory system. Results: CDC25C was identified as a key prognostic marker in NSCLC, showing high expression in tumor samples. In vitro experiments showed that CDC25C knockdown markedly reduced the capacity of cells to proliferate, migrate, invade, trigger apoptosis, and initiate cell cycle arrest. CDC25C and miR-142-3p displayed a reciprocal regulatory relationship. CDC25C reversed the inhibitory impacts of miR-142-3p on NSCLC cell cycle proliferation and progression. The synergy of miR-142-3p inhibition, CDC25C silencing, and 3-MA treatment was shown to regulate NSCLC cell processes including proliferation, apoptosis, and autophagy. Conclusions: MiR-142-3p emerged as a key player in governing autophagy and apoptosis by directly targeting CDC25C expression. This emphasizes the pivotal role of the miR-142-3p/CDC25C axis as a critical regulatory pathway in NSCLC.
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We used LASSO Cox regression analysis on 42 genes in the PPI network to look for possible predictive biomarkers.
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Data Sharing Statement: Available at https://tlcr.amegroups.com/article/view/10.21037/tlcr-24-82/dss
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CDC25C was identified as a key prognostic marker in NSCLC, showing high expression in tumor samples.
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CDC25C was identified as a key prognostic marker in NSCLC, showing high expression in tumor samples.
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caArray_beer-00153: Gene-expression profiles predict survival of patients with lung adenocarcinoma
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experiments using various techniques such as flow cytometry, Transwell, and colony formation. Protein le
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ion. Protein levels related to autophagy and apoptosis were assessed, specifically examining the im
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SCLC cell processes including proliferation, apoptosis, and autophagy. Conclusions: MiR-142-3p emer
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Complete file
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Overlapping differentially expressed genes (DEGs) were used for functional enrichment analysis and constructing the protein-protein interaction (PPI) network. In addition, key prognostic genes were identified through prognostic risk models, and their expression levels were verified. The phenotypic effects of cell division cycle 25C (CDC25C) regulation on NSCLC cell lines were assessed by in vitro experiments using various techniques such as flow cytometry, Transwell, and colony formation. Protein levels related to autophagy and apoptosis were assessed, specifically examining the impact of autophagy inhibition [3-methyladenine (3-MA)] and the miR-142-3p/CDC25C axis on this regulatory system.\nResults: CDC25C was identified as a key prognostic marker in NSCLC, showing high expression in tumor samples. In vitro experiments showed that CDC25C knockdown markedly reduced the capacity of cells to proliferate, migrate, invade, trigger apoptosis, and initiate cell cycle arrest. CDC25C and miR-142-3p displayed a reciprocal regulatory relationship. CDC25C reversed the inhibitory impacts of miR-142-3p on NSCLC cell cycle proliferation and progression. The synergy of miR-142-3p inhibition, CDC25C silencing, and 3-MA treatment was shown to regulate NSCLC cell processes including proliferation, apoptosis, and autophagy.\nConclusions: MiR-142-3p emerged as a key player in governing autophagy and apoptosis by directly targeting CDC25C expression. 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Thi"], "order_basis": "paper_text_order:897", "id": "assay:2"}, {"role": "data_generation", "definition_id": "transfection", "definition_version": "99e1195c7d6f", "definition_digest": null, "required_operations": [], "support_state": "partial", "source_hashes": {"assay_lexicon": "99e1195c7d6f"}, "confidence": 0.85, "evidence": ["les. 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