Investigation into drug resistance to cisplatin in cancer stem cell-enriched population in non-small cell lung cancer

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Dere E., Akgün O., Aztopal N., Ulukaya E.

TURKISH JOURNAL OF BIOCHEMISTRY, cilt.50, sa.2, ss.1-7, 2025 (SCI-Expanded)

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 50 Sayı: 2
  • Basım Tarihi: 2025
  • Doi Numarası: 10.1515/tjb-2024-0181
  • Dergi Adı: TURKISH JOURNAL OF BIOCHEMISTRY
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, Academic Search Premier, Food Science & Technology Abstracts, Directory of Open Access Journals
  • Sayfa Sayıları: ss.1-7
  • Bursa Uludağ Üniversitesi Adresli: Evet

Özet

Objectives

understanding drug resistance in cancer is of importance in treatment. Cancer stem cells are main factor for drug resistance. Therefore, the possible gene/gene interactions/proteins were explored in our study using a cancer stem cell-enriched population (H1299/S) derived from a parental non-small cell lung cancer cell line (H1299/P).

Methods

response to cisplatin, which is the main drug for the treatment of lung cancer, was evaluated with the Adenosine triphosphate (ATP) viability test. As a result of the gene expression analysis, while 14 genes were not evaluated, expression profiles were obtained for 37 genes out of 51 genes. By the drug-protein interaction analyses, Topoisomerase I (TOPI), Topoisomerase 2 alpha (TOP2A), Topoisomerase 2 beta (TOP2B), Cyclin-dependent kinases 4 (CDK4), Cyclin-dependent kinases 6 (CDK6), ATP binding cassette subfamily B member 1 (ABCB1), ATP binding cassette subfamily C member 1 (ABCC1), ATP binding cassette subfamily C member 3 (ABCC3), B-cell leukemia/lymphoma 2 (BCL2), Poly (ADP-ribose) polymerase 1 (PARP1), Breast cancer gene 1 (BRCA1) and Cyclin dependent kinase inhibitor 1A (CDKN1A) genes and protein products were statistically significantly found to be in association with drug resistance.

Results and discussion

in bioinformatics analyses, it was observed that 13 pathways were affected due to expression changes and 12 genes related to these pathways were determined to activate multidrug resistance mechanisms.

Conclusions

platinum-based drugs, as well as a broad range of other agents including topoisomerase and PARP1 inhibitors, and anthracyclines, have been shown to potentially possess multiple drug resistance.