Identification of prognostic hub genes and therapeutic targets for selenium deficiency in chicks model through transcriptome profiling

Abstract Selenium deficiency is a prevalent micronutrient deficiency that poses a major health concern worldwide. This study aimed to shed light on the molecular mechanisms underlying selenium deficiency using a chick model. Chickens were divided into control and selenium deficient groups. Plasma sa...

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Main Authors: Lakshman Kumar Lingamgunta, Bindu Prasuna Aloor, Sreenivasulu Dasari, Ranjani Ramakrishnan, Mahendran Botlagunta, Ashok Kumar Madikonda, Shankar Gopal, Ankanna Sade
Format: Article
Language:English
Published: Nature Portfolio 2023-05-01
Series:Scientific Reports
Online Access:https://doi.org/10.1038/s41598-023-34955-6
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author Lakshman Kumar Lingamgunta
Bindu Prasuna Aloor
Sreenivasulu Dasari
Ranjani Ramakrishnan
Mahendran Botlagunta
Ashok Kumar Madikonda
Shankar Gopal
Ankanna Sade
author_facet Lakshman Kumar Lingamgunta
Bindu Prasuna Aloor
Sreenivasulu Dasari
Ranjani Ramakrishnan
Mahendran Botlagunta
Ashok Kumar Madikonda
Shankar Gopal
Ankanna Sade
author_sort Lakshman Kumar Lingamgunta
collection DOAJ
description Abstract Selenium deficiency is a prevalent micronutrient deficiency that poses a major health concern worldwide. This study aimed to shed light on the molecular mechanisms underlying selenium deficiency using a chick model. Chickens were divided into control and selenium deficient groups. Plasma samples were collected to measure selenium concentration and transcriptome analyse were performed on oviduct samples. The results showed that selenium deficiency led to a significant reduction in plasma selenium levels and altered the expression of 10,266 differentially expressed genes (DEGs). These DEGs primarily regulated signal transduction and cell motility. The molecular function includes GTPase regulatory activity, and KEGG pathway analysis showed that they were mainly involved in the signal transduction. By using Cytoscape and CancerGeneNet tool, we identified 8 modules and 10 hub genes (FRK, JUN, PTPRC, ACTA2, MST1R, SDC4, SDC1, CXCL12, MX1 and EZR) associated with receptor tyrosine kinase pathway, Wnt and mTOR signaling pathways that may be closely related to cancer. These hub genes could be served as precise diagnostic and prognostic candidate biomarkers of selenium deficiency and potential targets for treatment strategies in both animals and humans. This study sheds light on the molecular basis of selenium deficiency and its potential impact on public health.
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spelling doaj.art-46a59d29422c4f27be4e00647d2771f62023-06-04T11:28:51ZengNature PortfolioScientific Reports2045-23222023-05-0113111610.1038/s41598-023-34955-6Identification of prognostic hub genes and therapeutic targets for selenium deficiency in chicks model through transcriptome profilingLakshman Kumar Lingamgunta0Bindu Prasuna Aloor1Sreenivasulu Dasari2Ranjani Ramakrishnan3Mahendran Botlagunta4Ashok Kumar Madikonda5Shankar Gopal6Ankanna Sade7Department of Biochemistry, Sri Venkateswara UniversityDepartment of Botany, Rayalaseema UniversityDepartment of Biochemistry, Sri Venkateswara UniversityDepartment of Virology, Sri Venkateswara UniversitySchool of Biosciences, Engineering and Technology, Vellore Institute of Technology (VIT)Department of Biochemistry & Molecular Biology, Central University of KeralaDepartment of Biochemistry, Sri Venkateswara UniversityDepartment of Botany, Sri Venkateswara UniversityAbstract Selenium deficiency is a prevalent micronutrient deficiency that poses a major health concern worldwide. This study aimed to shed light on the molecular mechanisms underlying selenium deficiency using a chick model. Chickens were divided into control and selenium deficient groups. Plasma samples were collected to measure selenium concentration and transcriptome analyse were performed on oviduct samples. The results showed that selenium deficiency led to a significant reduction in plasma selenium levels and altered the expression of 10,266 differentially expressed genes (DEGs). These DEGs primarily regulated signal transduction and cell motility. The molecular function includes GTPase regulatory activity, and KEGG pathway analysis showed that they were mainly involved in the signal transduction. By using Cytoscape and CancerGeneNet tool, we identified 8 modules and 10 hub genes (FRK, JUN, PTPRC, ACTA2, MST1R, SDC4, SDC1, CXCL12, MX1 and EZR) associated with receptor tyrosine kinase pathway, Wnt and mTOR signaling pathways that may be closely related to cancer. These hub genes could be served as precise diagnostic and prognostic candidate biomarkers of selenium deficiency and potential targets for treatment strategies in both animals and humans. This study sheds light on the molecular basis of selenium deficiency and its potential impact on public health.https://doi.org/10.1038/s41598-023-34955-6
spellingShingle Lakshman Kumar Lingamgunta
Bindu Prasuna Aloor
Sreenivasulu Dasari
Ranjani Ramakrishnan
Mahendran Botlagunta
Ashok Kumar Madikonda
Shankar Gopal
Ankanna Sade
Identification of prognostic hub genes and therapeutic targets for selenium deficiency in chicks model through transcriptome profiling
Scientific Reports
title Identification of prognostic hub genes and therapeutic targets for selenium deficiency in chicks model through transcriptome profiling
title_full Identification of prognostic hub genes and therapeutic targets for selenium deficiency in chicks model through transcriptome profiling
title_fullStr Identification of prognostic hub genes and therapeutic targets for selenium deficiency in chicks model through transcriptome profiling
title_full_unstemmed Identification of prognostic hub genes and therapeutic targets for selenium deficiency in chicks model through transcriptome profiling
title_short Identification of prognostic hub genes and therapeutic targets for selenium deficiency in chicks model through transcriptome profiling
title_sort identification of prognostic hub genes and therapeutic targets for selenium deficiency in chicks model through transcriptome profiling
url https://doi.org/10.1038/s41598-023-34955-6
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