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Mechanistic Insights of hsa-mir-301a Regulation by Tobacco Smoke in Lung Squamous Cell Carcinoma: Evidence From Bioinformatics Analysis. / Pustylnyak, Vladimir O.; Perevalova, Alina M.; Gulyaeva, Lyudmila F.

In: Bioinformatics and Biology Insights, Vol. 18, 05.12.2024, p. 1-8.

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@article{eb2cbf73c714448a963ed3a1089b3e7a,
title = "Mechanistic Insights of hsa-mir-301a Regulation by Tobacco Smoke in Lung Squamous Cell Carcinoma: Evidence From Bioinformatics Analysis",
abstract = "MicroRNAs play a significant role in the development of cancers, including lung cancer. A recent study revealed that smoking, a key risk factor for lung cancer, increased the levels of hsa-mir-301a in the tumor tissues of patients with lung squamous cell carcinoma (LUSC). The aim of the current study is to investigate the mechanism by which tobacco smoke increases hsa-mir-301a levels in LUSC tumor tissues using bioinformatics analysis. Bioinformatics tools and online databases, including The Cancer Genome Atlas (TCGA), LinkedOmics, and Encyclopedia of RNA Interactomes (ENCORI), were applied in this study. Our results showed a correlation between the upregulation of hsa-mir-301a in LUSC tissues and smoking exposure. However, no correlation was discovered between patients{\textquoteright} smoking status and the expression level of the hsa-mir-301a host gene, SKA2, prompting us to investigate possible changes in microRNA processing under tobacco smoke exposure. In silico results using online platforms suggest that post-transcriptional processes, which involve the RNA-binding proteins DGCR8 and FUS, contribute to the elevation of mature hsa-mir-301a levels in smoking patients with LUSC. Our findings suggest that RNA-binding proteins play a key role in controlling the processing of hsa-mir-301a, indicating a complex regulation of hsa-mir-301a in the LUSC tissues of smokers.",
keywords = "DGCR8, DICER1, FUS, lung cancer, microRNA, mir-301a, tobacco smoke",
author = "Pustylnyak, {Vladimir O.} and Perevalova, {Alina M.} and Gulyaeva, {Lyudmila F.}",
note = "The author(s) disclosed receipt of the following financial support for the research, authorship, and/or publication of this article: This research was funded by RUSSIAN SCIENCE FOUNDATION (grant no. 22-15-00065).",
year = "2024",
month = dec,
day = "5",
doi = "10.1177/11779322241302168",
language = "English",
volume = "18",
pages = "1--8",
journal = "Bioinformatics and Biology Insights",
issn = "1177-9322",
publisher = "Libertas Academica Ltd.",

}

RIS

TY - JOUR

T1 - Mechanistic Insights of hsa-mir-301a Regulation by Tobacco Smoke in Lung Squamous Cell Carcinoma: Evidence From Bioinformatics Analysis

AU - Pustylnyak, Vladimir O.

AU - Perevalova, Alina M.

AU - Gulyaeva, Lyudmila F.

N1 - The author(s) disclosed receipt of the following financial support for the research, authorship, and/or publication of this article: This research was funded by RUSSIAN SCIENCE FOUNDATION (grant no. 22-15-00065).

PY - 2024/12/5

Y1 - 2024/12/5

N2 - MicroRNAs play a significant role in the development of cancers, including lung cancer. A recent study revealed that smoking, a key risk factor for lung cancer, increased the levels of hsa-mir-301a in the tumor tissues of patients with lung squamous cell carcinoma (LUSC). The aim of the current study is to investigate the mechanism by which tobacco smoke increases hsa-mir-301a levels in LUSC tumor tissues using bioinformatics analysis. Bioinformatics tools and online databases, including The Cancer Genome Atlas (TCGA), LinkedOmics, and Encyclopedia of RNA Interactomes (ENCORI), were applied in this study. Our results showed a correlation between the upregulation of hsa-mir-301a in LUSC tissues and smoking exposure. However, no correlation was discovered between patients’ smoking status and the expression level of the hsa-mir-301a host gene, SKA2, prompting us to investigate possible changes in microRNA processing under tobacco smoke exposure. In silico results using online platforms suggest that post-transcriptional processes, which involve the RNA-binding proteins DGCR8 and FUS, contribute to the elevation of mature hsa-mir-301a levels in smoking patients with LUSC. Our findings suggest that RNA-binding proteins play a key role in controlling the processing of hsa-mir-301a, indicating a complex regulation of hsa-mir-301a in the LUSC tissues of smokers.

AB - MicroRNAs play a significant role in the development of cancers, including lung cancer. A recent study revealed that smoking, a key risk factor for lung cancer, increased the levels of hsa-mir-301a in the tumor tissues of patients with lung squamous cell carcinoma (LUSC). The aim of the current study is to investigate the mechanism by which tobacco smoke increases hsa-mir-301a levels in LUSC tumor tissues using bioinformatics analysis. Bioinformatics tools and online databases, including The Cancer Genome Atlas (TCGA), LinkedOmics, and Encyclopedia of RNA Interactomes (ENCORI), were applied in this study. Our results showed a correlation between the upregulation of hsa-mir-301a in LUSC tissues and smoking exposure. However, no correlation was discovered between patients’ smoking status and the expression level of the hsa-mir-301a host gene, SKA2, prompting us to investigate possible changes in microRNA processing under tobacco smoke exposure. In silico results using online platforms suggest that post-transcriptional processes, which involve the RNA-binding proteins DGCR8 and FUS, contribute to the elevation of mature hsa-mir-301a levels in smoking patients with LUSC. Our findings suggest that RNA-binding proteins play a key role in controlling the processing of hsa-mir-301a, indicating a complex regulation of hsa-mir-301a in the LUSC tissues of smokers.

KW - DGCR8

KW - DICER1

KW - FUS

KW - lung cancer

KW - microRNA

KW - mir-301a

KW - tobacco smoke

UR - https://www.scopus.com/record/display.uri?eid=2-s2.0-85210745892&origin=inward&txGid=9379484c70d5d7d939e44b0d8ad4aefd

UR - https://www.webofscience.com/wos/woscc/full-record/WOS:001366379200001

UR - https://www.mendeley.com/catalogue/09e1f020-ec84-32a7-8ed8-d98289029556/

U2 - 10.1177/11779322241302168

DO - 10.1177/11779322241302168

M3 - Article

C2 - 39619736

VL - 18

SP - 1

EP - 8

JO - Bioinformatics and Biology Insights

JF - Bioinformatics and Biology Insights

SN - 1177-9322

ER -

ID: 61161960