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Elucidating the role of missense SNP of protein kinase C epsilon in HCV-induced hepatocellular carcinoma
The protein kinase C (PKC) family of serine/threonine kinases contains more than ten isozymes that are involved in multiple signaling pathways, including cell cycle regulation and carcinogenesis. The PKCε isozyme is an oncogene known to be upregulated in various signaling pathways involved in hepati...
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Published in: | BMC cancer 2023-02, Vol.23 (1), p.147-147, Article 147 |
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creator | Rehman, Areeba Shabbir, Maria Badshah, Yasmin Khan, Khushbukhat Trembley, Janeen H Ashraf, Naeem Mahmood Afsar, Tayyaba Almajwal, Ali Alruwaili, Nawaf W Alshamari, Ali Alanezi, Tariq Nahar Razak, Suhail |
description | The protein kinase C (PKC) family of serine/threonine kinases contains more than ten isozymes that are involved in multiple signaling pathways, including cell cycle regulation and carcinogenesis. The PKCε isozyme is an oncogene known to be upregulated in various signaling pathways involved in hepatitis C virus (HCV)-induced hepatocellular carcinoma (HCC). However, there is no known association of missense SNPs in PKCε with this disease, which can be a potential biomarker for early diagnosis and treatment. This research reveals a novel missense SNP in PKCε that is associated with HCV-induced HCC in the Pakistani population.
The PKCε SNP with amino acid substitution of E14K was chosen for wet lab analysis. Tetra ARMS-PCR was employed for the identification of high-risk SNP in PKCε of HCV-induced HCC patients. Liver function testing was also performed for comparison between the liver condition of the HCC patient and control group, and the viral load of HCC patient samples was evaluated to determine any alteration in the viral infectivity between different genotypes of the selected high-risk PKCε variant SNP.
Frequency distribution of the homozygous GG genotype was found to be highest among HCV-induced HCC patients and was also found to be significantly associated with disease development and progression. The p values of comparative data obtained for the other two genotypes, heterozygous AG and homozygous AA, of the SNP also showed the significance of the data for these alleles. Still, their odds ratio and relative risk analysis did not indicate their association with HCV-induced HCC.
The distribution of a genotype GG of PKCε has been found in HCV- induced HCC patients. Therefore, these PKCε SNP have the potential to be biomarkers for HCV-induced HCC. Further investigation using a larger sample size would provide additional insight into these initial data and open a new avenue for a better prognosis of this disease. |
doi_str_mv | 10.1186/s12885-023-10618-7 |
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The PKCε SNP with amino acid substitution of E14K was chosen for wet lab analysis. Tetra ARMS-PCR was employed for the identification of high-risk SNP in PKCε of HCV-induced HCC patients. Liver function testing was also performed for comparison between the liver condition of the HCC patient and control group, and the viral load of HCC patient samples was evaluated to determine any alteration in the viral infectivity between different genotypes of the selected high-risk PKCε variant SNP.
Frequency distribution of the homozygous GG genotype was found to be highest among HCV-induced HCC patients and was also found to be significantly associated with disease development and progression. The p values of comparative data obtained for the other two genotypes, heterozygous AG and homozygous AA, of the SNP also showed the significance of the data for these alleles. Still, their odds ratio and relative risk analysis did not indicate their association with HCV-induced HCC.
The distribution of a genotype GG of PKCε has been found in HCV- induced HCC patients. Therefore, these PKCε SNP have the potential to be biomarkers for HCV-induced HCC. Further investigation using a larger sample size would provide additional insight into these initial data and open a new avenue for a better prognosis of this disease.</description><identifier>ISSN: 1471-2407</identifier><identifier>EISSN: 1471-2407</identifier><identifier>DOI: 10.1186/s12885-023-10618-7</identifier><identifier>PMID: 36782184</identifier><language>eng</language><publisher>England: BioMed Central Ltd</publisher><subject>Amino acid substitution ; Bioinformatics ; Biomarkers ; Cancer ; Carcinogenesis ; Carcinoma, Hepatocellular - pathology ; Carcinoma, Hepatocellular - virology ; Case-Control Studies ; Cell cycle ; Development and progression ; Gene expression ; Genetic aspects ; Genetic Predisposition to Disease ; Genotype ; Genotype & phenotype ; Genotypes ; Hepacivirus ; Hepatitis C ; Hepatitis C - complications ; Hepatitis C - genetics ; Hepatitis C virus ; Hepatitis C virus (HCV) ; Hepatocellular carcinoma ; Hepatocellular carcinoma (HCC) ; Hepatoma ; Humans ; Infections ; Infectivity ; Isoenzymes ; Kinases ; Liver ; Liver cancer ; Liver Neoplasms - pathology ; Liver Neoplasms - virology ; Mutation, Missense ; Oncology, Experimental ; Phenols ; Polymorphism, Single Nucleotide ; Protein kinase C ; Protein kinase C (PKC) ; Protein Kinase C-epsilon - genetics ; Proteins ; Risk factors ; Signal transduction ; Single nucleotide polymorphism (SNP) ; Single nucleotide polymorphisms ; Statistical analysis ; Threonine ; Viruses</subject><ispartof>BMC cancer, 2023-02, Vol.23 (1), p.147-147, Article 147</ispartof><rights>2023. The Author(s).</rights><rights>COPYRIGHT 2023 BioMed Central Ltd.</rights><rights>2023. This work is licensed under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>The Author(s) 2023</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c628t-27cfaa88421c7c60ca85844add8616315b442f4ef4acd08c9c854f771fd76ec33</citedby><cites>FETCH-LOGICAL-c628t-27cfaa88421c7c60ca85844add8616315b442f4ef4acd08c9c854f771fd76ec33</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9926771/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2777771398?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,25753,27924,27925,37012,37013,44590,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/36782184$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Rehman, Areeba</creatorcontrib><creatorcontrib>Shabbir, Maria</creatorcontrib><creatorcontrib>Badshah, Yasmin</creatorcontrib><creatorcontrib>Khan, Khushbukhat</creatorcontrib><creatorcontrib>Trembley, Janeen H</creatorcontrib><creatorcontrib>Ashraf, Naeem Mahmood</creatorcontrib><creatorcontrib>Afsar, Tayyaba</creatorcontrib><creatorcontrib>Almajwal, Ali</creatorcontrib><creatorcontrib>Alruwaili, Nawaf W</creatorcontrib><creatorcontrib>Alshamari, Ali</creatorcontrib><creatorcontrib>Alanezi, Tariq Nahar</creatorcontrib><creatorcontrib>Razak, Suhail</creatorcontrib><title>Elucidating the role of missense SNP of protein kinase C epsilon in HCV-induced hepatocellular carcinoma</title><title>BMC cancer</title><addtitle>BMC Cancer</addtitle><description>The protein kinase C (PKC) family of serine/threonine kinases contains more than ten isozymes that are involved in multiple signaling pathways, including cell cycle regulation and carcinogenesis. The PKCε isozyme is an oncogene known to be upregulated in various signaling pathways involved in hepatitis C virus (HCV)-induced hepatocellular carcinoma (HCC). However, there is no known association of missense SNPs in PKCε with this disease, which can be a potential biomarker for early diagnosis and treatment. This research reveals a novel missense SNP in PKCε that is associated with HCV-induced HCC in the Pakistani population.
The PKCε SNP with amino acid substitution of E14K was chosen for wet lab analysis. Tetra ARMS-PCR was employed for the identification of high-risk SNP in PKCε of HCV-induced HCC patients. Liver function testing was also performed for comparison between the liver condition of the HCC patient and control group, and the viral load of HCC patient samples was evaluated to determine any alteration in the viral infectivity between different genotypes of the selected high-risk PKCε variant SNP.
Frequency distribution of the homozygous GG genotype was found to be highest among HCV-induced HCC patients and was also found to be significantly associated with disease development and progression. The p values of comparative data obtained for the other two genotypes, heterozygous AG and homozygous AA, of the SNP also showed the significance of the data for these alleles. Still, their odds ratio and relative risk analysis did not indicate their association with HCV-induced HCC.
The distribution of a genotype GG of PKCε has been found in HCV- induced HCC patients. Therefore, these PKCε SNP have the potential to be biomarkers for HCV-induced HCC. Further investigation using a larger sample size would provide additional insight into these initial data and open a new avenue for a better prognosis of this disease.</description><subject>Amino acid substitution</subject><subject>Bioinformatics</subject><subject>Biomarkers</subject><subject>Cancer</subject><subject>Carcinogenesis</subject><subject>Carcinoma, Hepatocellular - pathology</subject><subject>Carcinoma, Hepatocellular - virology</subject><subject>Case-Control Studies</subject><subject>Cell cycle</subject><subject>Development and progression</subject><subject>Gene expression</subject><subject>Genetic aspects</subject><subject>Genetic Predisposition to Disease</subject><subject>Genotype</subject><subject>Genotype & phenotype</subject><subject>Genotypes</subject><subject>Hepacivirus</subject><subject>Hepatitis C</subject><subject>Hepatitis C - complications</subject><subject>Hepatitis C - genetics</subject><subject>Hepatitis C virus</subject><subject>Hepatitis C virus (HCV)</subject><subject>Hepatocellular carcinoma</subject><subject>Hepatocellular carcinoma (HCC)</subject><subject>Hepatoma</subject><subject>Humans</subject><subject>Infections</subject><subject>Infectivity</subject><subject>Isoenzymes</subject><subject>Kinases</subject><subject>Liver</subject><subject>Liver cancer</subject><subject>Liver Neoplasms - pathology</subject><subject>Liver Neoplasms - virology</subject><subject>Mutation, Missense</subject><subject>Oncology, Experimental</subject><subject>Phenols</subject><subject>Polymorphism, Single Nucleotide</subject><subject>Protein kinase C</subject><subject>Protein kinase C (PKC)</subject><subject>Protein Kinase C-epsilon - genetics</subject><subject>Proteins</subject><subject>Risk factors</subject><subject>Signal transduction</subject><subject>Single nucleotide polymorphism (SNP)</subject><subject>Single nucleotide polymorphisms</subject><subject>Statistical analysis</subject><subject>Threonine</subject><subject>Viruses</subject><issn>1471-2407</issn><issn>1471-2407</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNptkl2P1CAUhhujcT_0D3hhmpiY9aIrUFrojclmsrqTbNS46i05w8eUsQMjUKP_XrqzrlNjuAAOz3mBN29RPMPoHGPevo6YcN5UiNQVRi3mFXtQHGPKcEUoYg8P1kfFSYwbhDDjiD8ujuqWcYI5PS76y2GUVkGybl2mXpfBD7r0ptzaGLWLurx5_3Ha74JP2rrym3WQq4tS76IdvCtz7WrxtbJOjVKrstc7SF7qYRgHCKWEIK3zW3hSPDIwRP30bj4tvry9_Ly4qq4_vFsuLq4r2RKeKsKkAeCcEiyZbJEE3nBKQSne4rbGzYpSYqg2FKRCXHaSN9Qwho1irZZ1fVos97rKw0bsgt1C-CU8WHFb8GEtICQrBy2ydr0yyEBjOkpWvGtUY1ZE1Q3i0HCUtd7stXbjaquV1C4FGGai8xNne7H2P0TXkTa_KQuc3QkE_33UMYls6-QNOO3HKAhjbYM5wtO7X_yDbvwYXLZqotik1vG_1BryB6wzPt8rJ1FxwWqWU8C6JlPn_6HyUHprpXfa2FyfNbyaNWQm6Z9pDWOMYnnzac6-PGB7DUPqox_GZL2Lc5DsQRl8jEGbe-MwElOAxT7AIgdY3AZYsNz0_NDy-5Y_ia1_A01p6Rc</recordid><startdate>20230213</startdate><enddate>20230213</enddate><creator>Rehman, Areeba</creator><creator>Shabbir, Maria</creator><creator>Badshah, Yasmin</creator><creator>Khan, Khushbukhat</creator><creator>Trembley, Janeen H</creator><creator>Ashraf, Naeem Mahmood</creator><creator>Afsar, Tayyaba</creator><creator>Almajwal, Ali</creator><creator>Alruwaili, Nawaf W</creator><creator>Alshamari, Ali</creator><creator>Alanezi, Tariq Nahar</creator><creator>Razak, Suhail</creator><general>BioMed Central Ltd</general><general>BioMed Central</general><general>BMC</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>ISR</scope><scope>3V.</scope><scope>7TO</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20230213</creationdate><title>Elucidating the role of missense SNP of protein kinase C epsilon in HCV-induced hepatocellular carcinoma</title><author>Rehman, Areeba ; Shabbir, Maria ; Badshah, Yasmin ; Khan, Khushbukhat ; Trembley, Janeen H ; Ashraf, Naeem Mahmood ; Afsar, Tayyaba ; Almajwal, Ali ; Alruwaili, Nawaf W ; Alshamari, Ali ; Alanezi, Tariq Nahar ; Razak, Suhail</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c628t-27cfaa88421c7c60ca85844add8616315b442f4ef4acd08c9c854f771fd76ec33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Amino acid substitution</topic><topic>Bioinformatics</topic><topic>Biomarkers</topic><topic>Cancer</topic><topic>Carcinogenesis</topic><topic>Carcinoma, Hepatocellular - pathology</topic><topic>Carcinoma, Hepatocellular - virology</topic><topic>Case-Control Studies</topic><topic>Cell cycle</topic><topic>Development and progression</topic><topic>Gene expression</topic><topic>Genetic aspects</topic><topic>Genetic Predisposition to Disease</topic><topic>Genotype</topic><topic>Genotype & phenotype</topic><topic>Genotypes</topic><topic>Hepacivirus</topic><topic>Hepatitis C</topic><topic>Hepatitis C - complications</topic><topic>Hepatitis C - genetics</topic><topic>Hepatitis C virus</topic><topic>Hepatitis C virus (HCV)</topic><topic>Hepatocellular carcinoma</topic><topic>Hepatocellular carcinoma (HCC)</topic><topic>Hepatoma</topic><topic>Humans</topic><topic>Infections</topic><topic>Infectivity</topic><topic>Isoenzymes</topic><topic>Kinases</topic><topic>Liver</topic><topic>Liver cancer</topic><topic>Liver Neoplasms - pathology</topic><topic>Liver Neoplasms - virology</topic><topic>Mutation, Missense</topic><topic>Oncology, Experimental</topic><topic>Phenols</topic><topic>Polymorphism, Single Nucleotide</topic><topic>Protein kinase C</topic><topic>Protein kinase C (PKC)</topic><topic>Protein Kinase C-epsilon - genetics</topic><topic>Proteins</topic><topic>Risk factors</topic><topic>Signal transduction</topic><topic>Single nucleotide polymorphism (SNP)</topic><topic>Single nucleotide polymorphisms</topic><topic>Statistical analysis</topic><topic>Threonine</topic><topic>Viruses</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Rehman, Areeba</creatorcontrib><creatorcontrib>Shabbir, Maria</creatorcontrib><creatorcontrib>Badshah, Yasmin</creatorcontrib><creatorcontrib>Khan, Khushbukhat</creatorcontrib><creatorcontrib>Trembley, Janeen H</creatorcontrib><creatorcontrib>Ashraf, Naeem Mahmood</creatorcontrib><creatorcontrib>Afsar, Tayyaba</creatorcontrib><creatorcontrib>Almajwal, Ali</creatorcontrib><creatorcontrib>Alruwaili, Nawaf W</creatorcontrib><creatorcontrib>Alshamari, Ali</creatorcontrib><creatorcontrib>Alanezi, Tariq Nahar</creatorcontrib><creatorcontrib>Razak, Suhail</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Science (Gale in Context)</collection><collection>ProQuest Central (Corporate)</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Health & Medical Complete (ProQuest Database)</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>BMC cancer</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Rehman, Areeba</au><au>Shabbir, Maria</au><au>Badshah, Yasmin</au><au>Khan, Khushbukhat</au><au>Trembley, Janeen H</au><au>Ashraf, Naeem Mahmood</au><au>Afsar, Tayyaba</au><au>Almajwal, Ali</au><au>Alruwaili, Nawaf W</au><au>Alshamari, Ali</au><au>Alanezi, Tariq Nahar</au><au>Razak, Suhail</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Elucidating the role of missense SNP of protein kinase C epsilon in HCV-induced hepatocellular carcinoma</atitle><jtitle>BMC cancer</jtitle><addtitle>BMC Cancer</addtitle><date>2023-02-13</date><risdate>2023</risdate><volume>23</volume><issue>1</issue><spage>147</spage><epage>147</epage><pages>147-147</pages><artnum>147</artnum><issn>1471-2407</issn><eissn>1471-2407</eissn><abstract>The protein kinase C (PKC) family of serine/threonine kinases contains more than ten isozymes that are involved in multiple signaling pathways, including cell cycle regulation and carcinogenesis. The PKCε isozyme is an oncogene known to be upregulated in various signaling pathways involved in hepatitis C virus (HCV)-induced hepatocellular carcinoma (HCC). However, there is no known association of missense SNPs in PKCε with this disease, which can be a potential biomarker for early diagnosis and treatment. This research reveals a novel missense SNP in PKCε that is associated with HCV-induced HCC in the Pakistani population.
The PKCε SNP with amino acid substitution of E14K was chosen for wet lab analysis. Tetra ARMS-PCR was employed for the identification of high-risk SNP in PKCε of HCV-induced HCC patients. Liver function testing was also performed for comparison between the liver condition of the HCC patient and control group, and the viral load of HCC patient samples was evaluated to determine any alteration in the viral infectivity between different genotypes of the selected high-risk PKCε variant SNP.
Frequency distribution of the homozygous GG genotype was found to be highest among HCV-induced HCC patients and was also found to be significantly associated with disease development and progression. The p values of comparative data obtained for the other two genotypes, heterozygous AG and homozygous AA, of the SNP also showed the significance of the data for these alleles. Still, their odds ratio and relative risk analysis did not indicate their association with HCV-induced HCC.
The distribution of a genotype GG of PKCε has been found in HCV- induced HCC patients. Therefore, these PKCε SNP have the potential to be biomarkers for HCV-induced HCC. Further investigation using a larger sample size would provide additional insight into these initial data and open a new avenue for a better prognosis of this disease.</abstract><cop>England</cop><pub>BioMed Central Ltd</pub><pmid>36782184</pmid><doi>10.1186/s12885-023-10618-7</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Amino acid substitution Bioinformatics Biomarkers Cancer Carcinogenesis Carcinoma, Hepatocellular - pathology Carcinoma, Hepatocellular - virology Case-Control Studies Cell cycle Development and progression Gene expression Genetic aspects Genetic Predisposition to Disease Genotype Genotype & phenotype Genotypes Hepacivirus Hepatitis C Hepatitis C - complications Hepatitis C - genetics Hepatitis C virus Hepatitis C virus (HCV) Hepatocellular carcinoma Hepatocellular carcinoma (HCC) Hepatoma Humans Infections Infectivity Isoenzymes Kinases Liver Liver cancer Liver Neoplasms - pathology Liver Neoplasms - virology Mutation, Missense Oncology, Experimental Phenols Polymorphism, Single Nucleotide Protein kinase C Protein kinase C (PKC) Protein Kinase C-epsilon - genetics Proteins Risk factors Signal transduction Single nucleotide polymorphism (SNP) Single nucleotide polymorphisms Statistical analysis Threonine Viruses |
title | Elucidating the role of missense SNP of protein kinase C epsilon in HCV-induced hepatocellular carcinoma |
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