Tumor suppressor PTEN regulation by tobacco smoke in lung squamous-cell carcinoma based on bioinformatics analysis

Vladimir O Pustylnyak; Efim Y Alekseenok; Alina M Perevalova; Vadim V Kozlov; Lyudmila F Gulyaeva

doi:10.1016/j.heliyon.2023.e19044

Tumor suppressor PTEN regulation by tobacco smoke in lung squamous-cell carcinoma based on bioinformatics analysis

Heliyon. 2023 Aug 9;9(8):e19044. doi: 10.1016/j.heliyon.2023.e19044. eCollection 2023 Aug.

Authors

Vladimir O Pustylnyak^{1

2}, Efim Y Alekseenok², Alina M Perevalova¹, Vadim V Kozlov^{2

3}, Lyudmila F Gulyaeva^{1

2}

Affiliations

¹ Novosibirsk State University, 630090, Novosibirsk, Russia.
² Federal Research Center of Fundamental and Translational Medicine, 630117, Novosibirsk, Russia.
³ Novosibirsk Regional Oncology Center, 630108, Novosibirsk, Russia.

Abstract

Phosphatase and tensin homolog deleted on chromosome 10 (PTEN), is a tumor suppressor inactivated in a variety of human cancers. PTEN alteration correlates with lung squamous-cell carcinoma (LUSC) histology. However, it is still unclear how tobacco smoke regulates PTEN in LUSC tissues. In this study, we used free online databases and online tools to analyze PTEN expression and the role of smoking on PTEN alteration in patients with LUSC. We validated bioinformatics data by performing RT-PCR analysis using LUSC patient samples. Our results showed a correlation between the downregulation of PTEN in LUSC tissues compared to normal tissues and smoking exposure. In silico results using online platforms suggest that hsa-mir-301a down-regulates PTEN expression level in smoking patients with LUSC. RT-PCR analysis demonstrated that the PTEN expression was significantly decreased, whereas expression of hsa-mir-301a was up-regulated in the smoker cohort of LUSC tissue compared to adjacent non-cancerous tissues. A significant negative correlation between PTEN and hsa-mir-301a levels was observed in tumour tissues in our cohort of LUSC patients. Our results suggest that the downregulation PTEN gene caused by tobacco smoke-mediated increase of hsa-mir-301a may play an important role in LUSC tumorigenesis.

Keywords: Lung cancer; PTEN; Tobacco smoke; microRNA; mir-301a.