The Investigation of the Association Between the Bcl-2 3’-UTR rs1564483 Polymorphism and miR-296-3p in the Development of Breast and Gastric Cancers
Background: B-cell leukemia/lymphoma 2 (Bcl-2) gene regulates carcinogenesis by inhibiting apoptosis. This study evaluated the association of Bcl-2 3′-untranslated regions (3′ UTR) rs1564483 polymorphism and miR-296-3p with the development of breast and gastric cancers. Methods: A microarray analysi...
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description | Background:
B-cell leukemia/lymphoma 2 (Bcl-2) gene regulates carcinogenesis by inhibiting apoptosis. This study evaluated the association of Bcl-2 3′-untranslated regions (3′ UTR) rs1564483 polymorphism and miR-296-3p with the development of breast and gastric cancers.
Methods:
A microarray analysis was performed on the Genomic Spatial Event (GSE)29431 and GSE161533 datasets for breast and gastric cancers. Blood samples were taken from 222 (111 patients and 111 controls) and 210 (84 patients and 126 controls) individuals for breast and gastric cancers, respectively. Genomic DNA was extracted from the blood samples and genotyping was performed using real-time polymerase chain reaction (RT-PCR), followed by examining the high-temperature melting curve. Statistical analysis was conducted to examine the potential correlation between the rs1564483 polymorphism and the risk of breast and gastric cancers concerning pathological characteristics.
Results:
The results of the microarray showed that the Bcl-2 gene was up-regulated in gastric cancer (logFC [log fold change]: 0.65, adjusted P |
doi_str_mv | 10.1177/11795549231207835 |
format | Article |
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B-cell leukemia/lymphoma 2 (Bcl-2) gene regulates carcinogenesis by inhibiting apoptosis. This study evaluated the association of Bcl-2 3′-untranslated regions (3′ UTR) rs1564483 polymorphism and miR-296-3p with the development of breast and gastric cancers.
Methods:
A microarray analysis was performed on the Genomic Spatial Event (GSE)29431 and GSE161533 datasets for breast and gastric cancers. Blood samples were taken from 222 (111 patients and 111 controls) and 210 (84 patients and 126 controls) individuals for breast and gastric cancers, respectively. Genomic DNA was extracted from the blood samples and genotyping was performed using real-time polymerase chain reaction (RT-PCR), followed by examining the high-temperature melting curve. Statistical analysis was conducted to examine the potential correlation between the rs1564483 polymorphism and the risk of breast and gastric cancers concerning pathological characteristics.
Results:
The results of the microarray showed that the Bcl-2 gene was up-regulated in gastric cancer (logFC [log fold change]: 0.65, adjusted P < .05). Clinical outcome showed no notable relationship between the rs1564483 polymorphism and breast cancer risk; however, for gastric cancer, it identified a large difference between healthy controls and patients for an allelic frequency of rs1564483 (P ⩽ .001). Moreover, an assay of different models (dominant, recessive, and co-dominant) showed a significant association between the AG genotype between control and gastric cases (Pearson chi-square test, P = .046). In addition, the prevalence of the AG genotype was greater in persons under the age of 45 and in patients with H. pylori infection (P ⩽ .001). The AG genotype was not related to smoking, although the AA genotype was associated with increased cancer incidence in smokers (P ⩽ .001).
Conclusions:
In silico studies and calculations of the ΔG binding of micro ribonucleic acid (miRNA) hsa-miR-296-3p to the mutant and wild alleles of the rs15644833 single nucleotide polymorphism (SNP) have revealed that Bcl-2 mRNA expression in gastric cancer decreases, thus confirming the tumor suppressor role of the Bcl-2 gene.</description><identifier>ISSN: 1179-5549</identifier><identifier>EISSN: 1179-5549</identifier><identifier>DOI: 10.1177/11795549231207835</identifier><language>eng</language><publisher>London, England: SAGE Publications</publisher><subject>Breast cancer ; Gastric cancer ; Genotype & phenotype ; Original ; Polymorphism</subject><ispartof>Clinical Medicine Insights. Oncology, 2023-01, Vol.17, p.11795549231207835-11795549231207835</ispartof><rights>The Author(s) 2023</rights><rights>The Author(s) 2023. This work is licensed under the Creative Commons Attribution – Non-Commercial License https://creativecommons.org/licenses/by-nc/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 2023 SAGE Publications Ltd unless otherwise noted. Manuscript content on this site is licensed under Creative Commons Licenses</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c396t-9a423f0d0ada23de986d3347ac53b5fd94ce4ee517fe7b70e77133f501b979623</cites><orcidid>0000-0002-1131-107X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC10625176/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC10625176/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,21945,27830,27901,27902,44921,45309,53766,53768</link.rule.ids></links><search><creatorcontrib>Azadeh Jouneghani, Mehrnoush</creatorcontrib><creatorcontrib>Keshavarzi, Fatemeh</creatorcontrib><creatorcontrib>Haghnazari, Nahid</creatorcontrib><creatorcontrib>Hooshmandi, Zahra</creatorcontrib><creatorcontrib>Amini, Sabrieh</creatorcontrib><title>The Investigation of the Association Between the Bcl-2 3’-UTR rs1564483 Polymorphism and miR-296-3p in the Development of Breast and Gastric Cancers</title><title>Clinical Medicine Insights. Oncology</title><description>Background:
B-cell leukemia/lymphoma 2 (Bcl-2) gene regulates carcinogenesis by inhibiting apoptosis. This study evaluated the association of Bcl-2 3′-untranslated regions (3′ UTR) rs1564483 polymorphism and miR-296-3p with the development of breast and gastric cancers.
Methods:
A microarray analysis was performed on the Genomic Spatial Event (GSE)29431 and GSE161533 datasets for breast and gastric cancers. Blood samples were taken from 222 (111 patients and 111 controls) and 210 (84 patients and 126 controls) individuals for breast and gastric cancers, respectively. Genomic DNA was extracted from the blood samples and genotyping was performed using real-time polymerase chain reaction (RT-PCR), followed by examining the high-temperature melting curve. Statistical analysis was conducted to examine the potential correlation between the rs1564483 polymorphism and the risk of breast and gastric cancers concerning pathological characteristics.
Results:
The results of the microarray showed that the Bcl-2 gene was up-regulated in gastric cancer (logFC [log fold change]: 0.65, adjusted P < .05). Clinical outcome showed no notable relationship between the rs1564483 polymorphism and breast cancer risk; however, for gastric cancer, it identified a large difference between healthy controls and patients for an allelic frequency of rs1564483 (P ⩽ .001). Moreover, an assay of different models (dominant, recessive, and co-dominant) showed a significant association between the AG genotype between control and gastric cases (Pearson chi-square test, P = .046). In addition, the prevalence of the AG genotype was greater in persons under the age of 45 and in patients with H. pylori infection (P ⩽ .001). The AG genotype was not related to smoking, although the AA genotype was associated with increased cancer incidence in smokers (P ⩽ .001).
Conclusions:
In silico studies and calculations of the ΔG binding of micro ribonucleic acid (miRNA) hsa-miR-296-3p to the mutant and wild alleles of the rs15644833 single nucleotide polymorphism (SNP) have revealed that Bcl-2 mRNA expression in gastric cancer decreases, thus confirming the tumor suppressor role of the Bcl-2 gene.</description><subject>Breast cancer</subject><subject>Gastric cancer</subject><subject>Genotype & phenotype</subject><subject>Original</subject><subject>Polymorphism</subject><issn>1179-5549</issn><issn>1179-5549</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>AFRWT</sourceid><sourceid>BENPR</sourceid><recordid>eNp1UU1v1DAQjRBIVKU_gJslLlxS_BHb8Ql1FyiVKoGq7dnyOpNdV4kd7Oyi3vgVSP17_SU4TVWgVefgGT2_92bsKYq3BB8TIuWHfCjOK0UZoVjWjL8oDiasnMCX_9Svi6OUrnAOxjDm8qD4vdoCOvN7SKPbmNEFj0KLxgyepBSsm6EFjD8B_B2-sF1JEbv9dVNeri5QTISLqqoZ-h666z7EYetSj4xvUO8uSqpEyQbkZu0n2EMXhh78OLVZRDBpvOOe5iI6i5bGW4jpTfGqNV2Co_t8WFx--bxafi3Pv52eLU_OS8uUGEtlKspa3GDTGMoaULVoGKuksZyteduoykIFwIlsQa4lBikJYy3HZK2kEpQdFh9n32G37qGxebBoOj1E15t4rYNx-v8b77Z6E_aaYEGzrcgO7-8dYvixy9-oe5csdJ3xEHZJ07oWAhNKpmbvHlGvwi76_D5NFcVEUlWrzCIzy8aQUoT2YRqC9bRu_WTdWXM8a5LZwF_X5wV_ALyaqao</recordid><startdate>20230101</startdate><enddate>20230101</enddate><creator>Azadeh Jouneghani, Mehrnoush</creator><creator>Keshavarzi, Fatemeh</creator><creator>Haghnazari, Nahid</creator><creator>Hooshmandi, Zahra</creator><creator>Amini, Sabrieh</creator><general>SAGE Publications</general><general>Sage Publications Ltd</general><scope>AFRWT</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AYAGU</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-1131-107X</orcidid></search><sort><creationdate>20230101</creationdate><title>The Investigation of the Association Between the Bcl-2 3’-UTR rs1564483 Polymorphism and miR-296-3p in the Development of Breast and Gastric Cancers</title><author>Azadeh Jouneghani, Mehrnoush ; Keshavarzi, Fatemeh ; Haghnazari, Nahid ; Hooshmandi, Zahra ; Amini, Sabrieh</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c396t-9a423f0d0ada23de986d3347ac53b5fd94ce4ee517fe7b70e77133f501b979623</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Breast cancer</topic><topic>Gastric cancer</topic><topic>Genotype & phenotype</topic><topic>Original</topic><topic>Polymorphism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Azadeh Jouneghani, Mehrnoush</creatorcontrib><creatorcontrib>Keshavarzi, Fatemeh</creatorcontrib><creatorcontrib>Haghnazari, Nahid</creatorcontrib><creatorcontrib>Hooshmandi, Zahra</creatorcontrib><creatorcontrib>Amini, Sabrieh</creatorcontrib><collection>Sage Journals GOLD Open Access 2024</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</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 Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>Australia & New Zealand Database</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</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>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Clinical Medicine Insights. Oncology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Azadeh Jouneghani, Mehrnoush</au><au>Keshavarzi, Fatemeh</au><au>Haghnazari, Nahid</au><au>Hooshmandi, Zahra</au><au>Amini, Sabrieh</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The Investigation of the Association Between the Bcl-2 3’-UTR rs1564483 Polymorphism and miR-296-3p in the Development of Breast and Gastric Cancers</atitle><jtitle>Clinical Medicine Insights. Oncology</jtitle><date>2023-01-01</date><risdate>2023</risdate><volume>17</volume><spage>11795549231207835</spage><epage>11795549231207835</epage><pages>11795549231207835-11795549231207835</pages><issn>1179-5549</issn><eissn>1179-5549</eissn><abstract>Background:
B-cell leukemia/lymphoma 2 (Bcl-2) gene regulates carcinogenesis by inhibiting apoptosis. This study evaluated the association of Bcl-2 3′-untranslated regions (3′ UTR) rs1564483 polymorphism and miR-296-3p with the development of breast and gastric cancers.
Methods:
A microarray analysis was performed on the Genomic Spatial Event (GSE)29431 and GSE161533 datasets for breast and gastric cancers. Blood samples were taken from 222 (111 patients and 111 controls) and 210 (84 patients and 126 controls) individuals for breast and gastric cancers, respectively. Genomic DNA was extracted from the blood samples and genotyping was performed using real-time polymerase chain reaction (RT-PCR), followed by examining the high-temperature melting curve. Statistical analysis was conducted to examine the potential correlation between the rs1564483 polymorphism and the risk of breast and gastric cancers concerning pathological characteristics.
Results:
The results of the microarray showed that the Bcl-2 gene was up-regulated in gastric cancer (logFC [log fold change]: 0.65, adjusted P < .05). Clinical outcome showed no notable relationship between the rs1564483 polymorphism and breast cancer risk; however, for gastric cancer, it identified a large difference between healthy controls and patients for an allelic frequency of rs1564483 (P ⩽ .001). Moreover, an assay of different models (dominant, recessive, and co-dominant) showed a significant association between the AG genotype between control and gastric cases (Pearson chi-square test, P = .046). In addition, the prevalence of the AG genotype was greater in persons under the age of 45 and in patients with H. pylori infection (P ⩽ .001). The AG genotype was not related to smoking, although the AA genotype was associated with increased cancer incidence in smokers (P ⩽ .001).
Conclusions:
In silico studies and calculations of the ΔG binding of micro ribonucleic acid (miRNA) hsa-miR-296-3p to the mutant and wild alleles of the rs15644833 single nucleotide polymorphism (SNP) have revealed that Bcl-2 mRNA expression in gastric cancer decreases, thus confirming the tumor suppressor role of the Bcl-2 gene.</abstract><cop>London, England</cop><pub>SAGE Publications</pub><doi>10.1177/11795549231207835</doi><orcidid>https://orcid.org/0000-0002-1131-107X</orcidid><oa>free_for_read</oa></addata></record> |
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source | DOAJ Directory of Open Access Journals; Sage Journals GOLD Open Access 2024; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; PubMed Central Open Access |
subjects | Breast cancer Gastric cancer Genotype & phenotype Original Polymorphism |
title | The Investigation of the Association Between the Bcl-2 3’-UTR rs1564483 Polymorphism and miR-296-3p in the Development of Breast and Gastric Cancers |
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