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Review

Molecular Mechanisms of Chemoresistance Induced by Cisplatin in NSCLC Cancer Therapy

1
Department of Biomedicine and Genetics, Medical University of Lodz, 92-213 Lodz, Poland
2
Institute of Medical Biology, Polish Academy of Sciences, 93-232 Lodz, Poland
*
Author to whom correspondence should be addressed.
Academic Editors: Alexander Schramm and Marcel Wiesweg
Int. J. Mol. Sci. 2021, 22(16), 8885; https://doi.org/10.3390/ijms22168885
Received: 13 July 2021 / Revised: 12 August 2021 / Accepted: 13 August 2021 / Published: 18 August 2021
(This article belongs to the Special Issue Precision Oncology in Non-small Cell Lung Cancer)
Cancer cells utilise several mechanisms to increase their survival and progression as well as their resistance to anticancer therapy: deregulation of growth regulatory pathways by acquiring grow factor independence, immune system suppression, reducing the expression of antigens activating T lymphocyte cells (mimicry), induction of anti-apoptotic signals to counter the action of drugs, activation of several DNA repair mechanisms and driving the active efflux of drugs from the cell cytoplasm, and epigenetic regulation by microRNAs (miRNAs). Because it is commonly diagnosed late, lung cancer remains a major malignancy with a low five-year survival rate; when diagnosed, the cancer is often highly advanced, and the cancer cells may have acquired drug resistance. This review summarises the main mechanisms involved in cisplatin resistance and interactions between cisplatin-resistant cancer cells and the tumour microenvironment. It also analyses changes in the gene expression profile of cisplatin sensitive vs. cisplatin-resistant non-small cell lung cancer (NSCLC) cellular model using the GSE108214 Gene Expression Omnibus database. It describes a protein-protein interaction network that indicates highly dysregulated TP53, MDM2, and CDKN1A genes as they encode the top networking proteins that may be involved in cisplatin tolerance, these all being upregulated in cisplatin-resistant cells. Furthermore, it illustrates the multifactorial nature of cisplatin resistance by examining the diversity of dysregulated pathways present in cisplatin-resistant NSCLC cells based on KEGG pathway analysis. View Full-Text
Keywords: non-small cell lung cancer; cisplatin; chemoresistance molecular mechanisms; tumour microenvironment; DNA repair mechanisms non-small cell lung cancer; cisplatin; chemoresistance molecular mechanisms; tumour microenvironment; DNA repair mechanisms
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MDPI and ACS Style

Kryczka, J.; Kryczka, J.; Czarnecka-Chrebelska, K.H.; Brzeziańska-Lasota, E. Molecular Mechanisms of Chemoresistance Induced by Cisplatin in NSCLC Cancer Therapy. Int. J. Mol. Sci. 2021, 22, 8885. https://doi.org/10.3390/ijms22168885

AMA Style

Kryczka J, Kryczka J, Czarnecka-Chrebelska KH, Brzeziańska-Lasota E. Molecular Mechanisms of Chemoresistance Induced by Cisplatin in NSCLC Cancer Therapy. International Journal of Molecular Sciences. 2021; 22(16):8885. https://doi.org/10.3390/ijms22168885

Chicago/Turabian Style

Kryczka, Jolanta, Jakub Kryczka, Karolina H. Czarnecka-Chrebelska, and Ewa Brzeziańska-Lasota. 2021. "Molecular Mechanisms of Chemoresistance Induced by Cisplatin in NSCLC Cancer Therapy" International Journal of Molecular Sciences 22, no. 16: 8885. https://doi.org/10.3390/ijms22168885

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