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Unraveling the prevalence of various signalling pathways in non-small-cell lung cancer: a review

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Abstract

Cancer has become a huge public health issue all around the world. The focus of research is on innovative cancer therapy techniques that include the disease's unique targets. Among the cancer-related deaths that occur, lung cancer is considered to be one of the major, accounting for about 1.6 million fatalities globally in 2012, or nearly 20% of all cancer deaths. Non-small-cell lung cancer, a type of lung cancer comprises upto 84% of lung cancer cases, demonstrating the need for a more effective treatment. A novel category of cancer management, known as targeted cancer medicines, has risen to prominence in recent years. Targeted cancer treatments, like traditional chemotherapy, employ pharmacological drugs to slow cancer development, enhance cell death, and prevent it from spreading. Targeted treatments, as the name implies, work by interfering with particular proteins implicated in cancer. Numerous research conducted in the last several decades have led to the conclusion that signalling pathways are involved in the growth of lung cancer. All malignant tumours are produced, spread, invade, and behave in various abnormal ways due to abnormal pathways. Numerous significant signalling pathways, including the RTK/RAS/MAP-Kinase pathway (hence often referred to as RTK-RAS for simplicity), PI3K/Akt signalling, and others, have been discovered as commonly genetically changed. The current developments in research on various signalling pathways, as well as the underlying mechanisms of the molecules implicated in these pathways, are innovatively summarised in this review. To give a good sense of the study that has been done so far, many routes are placed together. Thus, this review includes the detailed description regarding each pathways, the mutations formed, and the present treatment strategy to overcome the resistance.

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Abbreviations

NSCLC:

Non-small-cell lung cancer

SCLC:

Small-cell lung cancer

RTK:

Receptor tyrosine kinase

EGFR:

Epidermal growth factor receptor

EGF:

Epidermal growth factor

TKI:

Tyrosine kinase inhibitor

PFS:

Progression-free survival

VEGF:

Vascular endothelial growth factor

VEGFR:

Vascular endothelial growth factor receptor

ALK:

Anaplastic lymphoma kinase

MET:

Mesenchymal–epithelial transition

KRAS:

Kirsten rat sarcoma 2 viral oncogene

PDGF:

Platelet-derived growth factor

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Acknowledgements

We are thankful to Dr. Sabitha M., Principal, Amrita School of Pharmacy, Amrita Vishwa Vidyapeetham, AIMS Health Sciences Campus, Kochi-682041, Kerala, India, for providing assistance for this work.

Funding

This work did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.

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Authors and Affiliations

  1. Department of Pharmaceutical Chemistry & Analysis, Amrita School of Pharmacy, Amrita Vishwa Vidyapeetham, Kochi, Kerala, India

    Aathira Sujathan Nair, Ajay P. Jayan, K R Anandu, V N Saiprabha & Leena K. Pappachen

Authors
  1. Aathira Sujathan Nair
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  2. Ajay P. Jayan
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  3. K R Anandu
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  4. V N Saiprabha
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  5. Leena K. Pappachen
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Contributions

Aathira Sujathan Nair, Ajay P Jayan and Anandu K R performed the literature search, data analysis and drafted the manuscript and Dr. Saiprabha V N and Dr. Leena K Pappachen critically revised the work.

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Correspondence to V N Saiprabha or Leena K. Pappachen.

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Aathira Sujathan Nair, Ajay P Jayan, Anandu K R, Dr Leena K Pappachen, and Dr Saiprabha V N have no conflict of interest to declare.

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Nair, A.S., Jayan, A.P., Anandu, K.R. et al. Unraveling the prevalence of various signalling pathways in non-small-cell lung cancer: a review. Mol Cell Biochem 478, 2875–2890 (2023). https://doi.org/10.1007/s11010-023-04704-4

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  • DOI: https://doi.org/10.1007/s11010-023-04704-4

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