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Tumor suppressor PTEN regulation by tobacco smoke in lung squamous-cell carcinoma based on bioinformatics analysis. / Pustylnyak, Vladimir O; Alekseenok, Efim Y; Perevalova, Alina M et al.

In: Heliyon, Vol. 9, No. 8, e19044, 08.2023.

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Pustylnyak VO, Alekseenok EY, Perevalova AM, Kozlov VV, Gulyaeva LF. Tumor suppressor PTEN regulation by tobacco smoke in lung squamous-cell carcinoma based on bioinformatics analysis. Heliyon. 2023 Aug;9(8):e19044. doi: 10.1016/j.heliyon.2023.e19044

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BibTeX

@article{3256a473ae574c7d9177cf6681cb0af0,
title = "Tumor suppressor PTEN regulation by tobacco smoke in lung squamous-cell carcinoma based on bioinformatics analysis",
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.",
author = "Pustylnyak, {Vladimir O} and Alekseenok, {Efim Y} and Perevalova, {Alina M} and Kozlov, {Vadim V} and Gulyaeva, {Lyudmila F}",
note = "This work was financially supported by the Russian Science Foundation , grant No. 22-15-00065 . The authors acknowledge the Center for Collective Use “Proteomic Analysis” (supported by funding from the Ministry of Science and Higher Education of the Russian Federation , agreement No. 075-15-2021-691 ) for providing the necessary equipment to perform this study. {\textcopyright} 2023 The Authors.",
year = "2023",
month = aug,
doi = "10.1016/j.heliyon.2023.e19044",
language = "English",
volume = "9",
journal = "Heliyon",
issn = "2405-8440",
publisher = "Elsevier",
number = "8",

}

RIS

TY - JOUR

T1 - Tumor suppressor PTEN regulation by tobacco smoke in lung squamous-cell carcinoma based on bioinformatics analysis

AU - Pustylnyak, Vladimir O

AU - Alekseenok, Efim Y

AU - Perevalova, Alina M

AU - Kozlov, Vadim V

AU - Gulyaeva, Lyudmila F

N1 - This work was financially supported by the Russian Science Foundation , grant No. 22-15-00065 . The authors acknowledge the Center for Collective Use “Proteomic Analysis” (supported by funding from the Ministry of Science and Higher Education of the Russian Federation , agreement No. 075-15-2021-691 ) for providing the necessary equipment to perform this study. © 2023 The Authors.

PY - 2023/8

Y1 - 2023/8

N2 - 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.

AB - 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.

UR - https://www.scopus.com/record/display.uri?eid=2-s2.0-85169035309&origin=inward&txGid=c0c0059b2f149ff7b95ef19d45bd94ba

U2 - 10.1016/j.heliyon.2023.e19044

DO - 10.1016/j.heliyon.2023.e19044

M3 - Article

C2 - 37609416

VL - 9

JO - Heliyon

JF - Heliyon

SN - 2405-8440

IS - 8

M1 - e19044

ER -

ID: 55299830