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MicroRNAs modulation in lung cancer: exploring dual mechanisms and clinical prospects

SHAHID HUSSAIN1,*, HABIB BOKHARI1, XINGXING FAN2, SHAUKAT IQBAL MALIK3, SUNDAS IJAZ1, MUHAMMAD ADNAN SHEREEN4, AIMAN FATIMA3

1 Department of Biotechnology, Kohsar University Murree, Murree, Pakistan
2 Macau University of Science and Technology State Key Laboratory of Quality Research in Chinese Medicines, Taipa, Macau
3 Department of Bioinformatics and Biosciences, Capital University of Science and Technology, Islamabad, Pakistan
4 Department of Microbiology, Kohsar University Murree, Murree, Pakistan

* Corresponding Author: SHAHID HUSSAIN. Email: email

(This article belongs to the Special Issue: Advances in Biomarker Research: Unveiling the Pathways to Precision Medicine)

BIOCELL 2024, 48(3), 403-413. https://doi.org/10.32604/biocell.2024.044801

Abstract

The global incidence of lung cancer is marked by a considerably elevated mortality rate. MicroRNAs (miRNAs) exert pivotal influence in the intricate orchestration of gene regulation, and their dysregulation can precipitate dire consequences, notably cancer. Within this context, miRNAs encapsulated in exosomes manifest a diversified impact on the landscape of lung cancer, wherein their actions may either foster angiogenesis, cell proliferation, and metastasis, or counteract these processes. This comprehensive review article discerns potential targets for the prospective development of therapeutic agents tailored for lung cancer. Tumor-suppressive miRNAs, such as miR-204, miR-192, miR-30a, miR-34a, miR-34b, miR-203, and miR-212, exhibit heightened expression and demonstrate the capacity to inhibit cellular proliferation and invasiveness. Conversely, the deleterious effects of tumor-promoting miRNAs like miR-21, miR-106a, miR-155, miR-205, and miR-210 can be attenuated through the application of their respective inhibitors. Distinct miRNAs selectively target various oncogenes, including NUAK Family Kinase 1 (NUAK1), Snail Family Transcriptional Repressor 1 (Snai1), Astrocyte elevated gene-1 (AEG-1), Vimentin, Proliferation and apoptosis adaptor protein 15 (PEA-15/PED), Hypoxia-inducible factor 1-alpha (HIF1), as well as tumor suppressor genes such as phosphatase and tensin homolog (PTEN), Suppressor of cytokine signaling 1 (SOCS1), Tumor protein P53 binding protein 1 (TP53BP1), and PH Domain and Leucine Rich Repeat Protein Phosphatase 2 (PHLP22). This investigative approach proves invaluable in elucidating the specific miRNAs implicated in the deregulation of crucial genes pivotal to the pathogenesis of cancer.

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APA Style
HUSSAIN, S., BOKHARI, H., FAN, X., MALIK, S.I., IJAZ, S. et al. (2024). Micrornas modulation in lung cancer: exploring dual mechanisms and clinical prospects. BIOCELL, 48(3), 403-413. https://doi.org/10.32604/biocell.2024.044801
Vancouver Style
HUSSAIN S, BOKHARI H, FAN X, MALIK SI, IJAZ S, SHEREEN MA, et al. Micrornas modulation in lung cancer: exploring dual mechanisms and clinical prospects. BIOCELL . 2024;48(3):403-413 https://doi.org/10.32604/biocell.2024.044801
IEEE Style
S. HUSSAIN et al., "MicroRNAs modulation in lung cancer: exploring dual mechanisms and clinical prospects," BIOCELL , vol. 48, no. 3, pp. 403-413. 2024. https://doi.org/10.32604/biocell.2024.044801



cc Copyright © 2024 The Author(s). Published by Tech Science Press.
This work is licensed under a Creative Commons Attribution 4.0 International License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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