Background <p>As the leading cause of cancer-related deaths worldwide, lung cancer (LC) continues to be a significant public health concern. These microscopic non-coding RNAs (ncRNA), also known as microRNAs (miRNAs), are essential for controlling gene expression following transcription. Cellular processes such as metastasis, differentiation, apoptosis, and proliferation all depend on them. Abnormal expression of miRNAs impacts key oncogenic signaling pathways, which in turn plays a significant role in the onset and progression of both small cell lung cancer (SCLC) and non-small cell lung cancer (NSCLC).</p> Results <p>Certain miRNAs are essential for controlling a number of significant signaling pathways in lung cancer. In the TGF-β pathway, for example, miR-93 and 9 promote processes such as metastasis and epithelial-mesenchymal transition (EMT), whereas miR-145 and 124 act as inhibitors. Regarding the Wnt/β-catenin pathway, miR-20b activates it while miR-577 and miR-33b inhibit it. MiR-124 inhibits the NF-κB pathway, whereas oncogenic miR-196b-5p and miR-1307-5p enhance it. MiR-21 and miR-125b also activate the PI3K/AKT/mTOR pathway, but the lack of miR-410 and miR-153 destabilizes this pathway, which increases tumor growth and treatment resistance. Through YAP/TAZ, miR-135b and miR-762 stimulate oncogenic activity in the Hippo signaling pathway, whereas miR-188 and miR-582-5p aid in the restoration of tumor-suppressive properties and encourage apoptosis.</p> Conclusion <p>This review highlights how important miRNAs are to the development and spread of lung cancer. It highlights their potential as useful therapeutic targets and diagnostic indicators. Gaining a deeper understanding of how miRNA-mediated signaling works could greatly enhance early detection efforts and encourage the development of more individualized and efficient lung cancer treatment plans.</p> Graphical abstract <p></p>

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MicroRNA-mediated modulation of signalling pathways in lung cancer: implications for diagnosis and treatment

  • Mogeshwaran Appasamy,
  • Prakavi Kirubaharan,
  • Vijayalakshmi Sulluru,
  • Thirunavukkarasu Palaniyandi,
  • Gomathy Baskar,
  • Mugip Rahaman Abdul Wahab

摘要

Background

As the leading cause of cancer-related deaths worldwide, lung cancer (LC) continues to be a significant public health concern. These microscopic non-coding RNAs (ncRNA), also known as microRNAs (miRNAs), are essential for controlling gene expression following transcription. Cellular processes such as metastasis, differentiation, apoptosis, and proliferation all depend on them. Abnormal expression of miRNAs impacts key oncogenic signaling pathways, which in turn plays a significant role in the onset and progression of both small cell lung cancer (SCLC) and non-small cell lung cancer (NSCLC).

Results

Certain miRNAs are essential for controlling a number of significant signaling pathways in lung cancer. In the TGF-β pathway, for example, miR-93 and 9 promote processes such as metastasis and epithelial-mesenchymal transition (EMT), whereas miR-145 and 124 act as inhibitors. Regarding the Wnt/β-catenin pathway, miR-20b activates it while miR-577 and miR-33b inhibit it. MiR-124 inhibits the NF-κB pathway, whereas oncogenic miR-196b-5p and miR-1307-5p enhance it. MiR-21 and miR-125b also activate the PI3K/AKT/mTOR pathway, but the lack of miR-410 and miR-153 destabilizes this pathway, which increases tumor growth and treatment resistance. Through YAP/TAZ, miR-135b and miR-762 stimulate oncogenic activity in the Hippo signaling pathway, whereas miR-188 and miR-582-5p aid in the restoration of tumor-suppressive properties and encourage apoptosis.

Conclusion

This review highlights how important miRNAs are to the development and spread of lung cancer. It highlights their potential as useful therapeutic targets and diagnostic indicators. Gaining a deeper understanding of how miRNA-mediated signaling works could greatly enhance early detection efforts and encourage the development of more individualized and efficient lung cancer treatment plans.

Graphical abstract