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Background <p>MicroRNAs (miRNAs) exert pivotal regulatory functions in cancer initiation, progression, and metastasis by regulating cell proliferation-cycle related genes. However, tumor-associated miRNAs in lung adenocarcinoma (LUAD) remains incompletely characterized.</p> Results and findings <p>By interrogating TCGA mRNA-Seq datasets, we identified 1672 differentially expressed genes (DEGs) implicated in proliferation-cycle regulation in LUAD. A significant overrepresentation of transmembrane signal receptors, kinases, and TFs was observed among the DEGs, with primary enrichment in signaling pathways such as chemokine/cytokine, Wnt, EGF, Cadherin, and p53 cascades. Remarkably, <i>CDK1</i> and <i>E2F2</i> were characterized as key proliferation-cycle regulatory genes, demonstrating &gt; fivefold transcriptional up-regulation in LUAD specimens compared to normal lung tissues (p &lt; 0.001). Mechanistically, pharmacological CDK1 inhibition using fostamatinib or alsterpaullone reversed aberrant proliferative phenotypes in LUAD cells, demonstrating therapeutic reversibility in vitro. Concurrently, DEmiRNA and target analysis identified miR-31 as a critical regulator of CDK1/E2F2, showing elevated expression in LUAD.</p> Clinical implications <p>Collectively, our study establishes miR-31 as a novel biomarker for LUAD proliferative potential and implicates the miR-31/CDK1-E2F2 network as a promising target for disrupting LUAD progression. These findings establish a miRNA-centric precision therapeutic paradigm for effectively suppressing oncogenic proliferation in LUAD.</p>

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MiR-31 suppresses lung adenocarcinoma cell proliferation through CDK1 and E2F2-mediated cell cycle arrest

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年1月9日

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  • Pan Sun,
  • Man Zhang,
  • Shanshan Wang,
  • Yulin He,
  • Chenjing Lin,
  • Yi Tian,
  • Jizhuang Luo,
  • Kai Wang

摘要

Background

MicroRNAs (miRNAs) exert pivotal regulatory functions in cancer initiation, progression, and metastasis by regulating cell proliferation-cycle related genes. However, tumor-associated miRNAs in lung adenocarcinoma (LUAD) remains incompletely characterized.

Results and findings

By interrogating TCGA mRNA-Seq datasets, we identified 1672 differentially expressed genes (DEGs) implicated in proliferation-cycle regulation in LUAD. A significant overrepresentation of transmembrane signal receptors, kinases, and TFs was observed among the DEGs, with primary enrichment in signaling pathways such as chemokine/cytokine, Wnt, EGF, Cadherin, and p53 cascades. Remarkably, CDK1 and E2F2 were characterized as key proliferation-cycle regulatory genes, demonstrating > fivefold transcriptional up-regulation in LUAD specimens compared to normal lung tissues (p < 0.001). Mechanistically, pharmacological CDK1 inhibition using fostamatinib or alsterpaullone reversed aberrant proliferative phenotypes in LUAD cells, demonstrating therapeutic reversibility in vitro. Concurrently, DEmiRNA and target analysis identified miR-31 as a critical regulator of CDK1/E2F2, showing elevated expression in LUAD.

Clinical implications

Collectively, our study establishes miR-31 as a novel biomarker for LUAD proliferative potential and implicates the miR-31/CDK1-E2F2 network as a promising target for disrupting LUAD progression. These findings establish a miRNA-centric precision therapeutic paradigm for effectively suppressing oncogenic proliferation in LUAD.