Effects of Helicobacter pylori on the expression of the FTO gene and its biological role in gastric cancer
( ) is a primary risk factor for gastric cancer. The fat mass and obesity-associated (FTO) gene is associated with the development and progression of various cancer types such as glioma, leukemia, breast cancer and colorectal cancer. The aim of the present study was to investigate the effect of infe...
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| Veröffentlicht in: | Oncology letters 2023-04, Vol.25 (4), p.143, Article 143 |
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| description | (
) is a primary risk factor for gastric cancer. The fat mass and obesity-associated (FTO) gene is associated with the development and progression of various cancer types such as glioma, leukemia, breast cancer and colorectal cancer. The aim of the present study was to investigate the effect of
infection on the expression of FTO and its roles in gastric cancer. It was found that the expression levels of both FTO mRNA and protein were significantly increased in
-infected human gastric mucosal epithelial cells and Mongolian gerbil gastric tissues. The expression of FTO in gastric cancer tissues was higher than that in para-cancer tissues. Data from The Cancer Genome Atlas demonstrated that FTO expression in gastric cancer tissues was significantly higher than that in normal tissues. Patient survival rate was significantly decreased in patients with high expression levels of FTO. It was also demonstrated that FTO expression was associated with several pathological parameters, such as tumor stage, metastasis stage and the American Joint Committee on Cancer stage. The FTO gene was positively correlated with 16,601 genes in gastric cancer and negatively correlated with 3,623 genes. Gene Ontology enrichment analysis demonstrated that FTO was significantly enriched in the regulation of gene expression and oxidative RNA demethylase activity, and it was associated with components such as the RNA N6-methyladenosine methyltransferase complex and nuclear speckle. In addition, knockdown of the FTO gene inhibited the migration and invasion of
-infected cells. In conclusion, the data suggests that
infection leads to upregulation of the FTO gene, which may be related to patient survival rate, tumor staging and other pathological parameters of patients with gastric cancer. It also suggests that FTO promotes proliferation and migration of gastric cancer cells, which may be involved in the pathogenesis of
-induced gastric cancer. |
| doi_str_mv | 10.3892/ol.2023.13729 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_9996366</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A744137632</galeid><sourcerecordid>A744137632</sourcerecordid><originalsourceid>FETCH-LOGICAL-c513t-4e62755741514299ecf0403e9e0ea117e4324d1a223422e6cc5b806378026b6e3</originalsourceid><addsrcrecordid>eNptks9uVCEUxonR2KZ26daQmLi7I_8uXDYmTdNakybd1DXhMufeoTIwAmPat_FZfDIZW8dOIiw4HH7nCxw-hN5SsuCDZh9TWDDC-IJyxfQLdEyVZh0lA3u5j5U4Qqel3JE2ekmHQb5GR1xqolvNMfp2MU3gasFpwlcQvEujdRXyr5-bh5CyxyniugIM95sMpfi2beQuc3l7g2eIgG1cYt8URp9Cmr2zAecUAPuIZ1tq9g47Gx3kN-jVZEOB06f1BH29vLg9v-qubz5_OT-77lxPee0ESKb6XgnaU8G0BjcRQThoIGApVSA4E0tqGeOCMZDO9eNAJFcDYXKUwE_Qp0fdzXZcw9JBrNkGs8l-bfODSdabw5PoV2ZOP4zWWnIpm8D7J4Gcvm-hVHOXtjm2OxumhsboQah_1GwDGB-n1MTc2hdnzpQQ7U8kZ41a_Idqcwnr1u0Ik2_5g4IPzwpWYENdlRS2tfW-HILdI-hyKiXDtH8hJWZnD5OC2dnD_LFH4989b8ue_msG_hsTdbOo</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2789639847</pqid></control><display><type>article</type><title>Effects of Helicobacter pylori on the expression of the FTO gene and its biological role in gastric cancer</title><source>Spandidos Publications Journals</source><source>EZB-FREE-00999 freely available EZB journals</source><source>PubMed Central</source><creator>Gui, Shuqin ; Wang, Qinrong ; Bao, Liya ; He, Xiaofeng ; Wang, Zhengrong ; Liu, Linlin ; Wu, Lixia ; Zhao, Yan ; Zhou, Jianjiang ; Xie, Yuan</creator><creatorcontrib>Gui, Shuqin ; Wang, Qinrong ; Bao, Liya ; He, Xiaofeng ; Wang, Zhengrong ; Liu, Linlin ; Wu, Lixia ; Zhao, Yan ; Zhou, Jianjiang ; Xie, Yuan</creatorcontrib><description>(
) is a primary risk factor for gastric cancer. The fat mass and obesity-associated (FTO) gene is associated with the development and progression of various cancer types such as glioma, leukemia, breast cancer and colorectal cancer. The aim of the present study was to investigate the effect of
infection on the expression of FTO and its roles in gastric cancer. It was found that the expression levels of both FTO mRNA and protein were significantly increased in
-infected human gastric mucosal epithelial cells and Mongolian gerbil gastric tissues. The expression of FTO in gastric cancer tissues was higher than that in para-cancer tissues. Data from The Cancer Genome Atlas demonstrated that FTO expression in gastric cancer tissues was significantly higher than that in normal tissues. Patient survival rate was significantly decreased in patients with high expression levels of FTO. It was also demonstrated that FTO expression was associated with several pathological parameters, such as tumor stage, metastasis stage and the American Joint Committee on Cancer stage. The FTO gene was positively correlated with 16,601 genes in gastric cancer and negatively correlated with 3,623 genes. Gene Ontology enrichment analysis demonstrated that FTO was significantly enriched in the regulation of gene expression and oxidative RNA demethylase activity, and it was associated with components such as the RNA N6-methyladenosine methyltransferase complex and nuclear speckle. In addition, knockdown of the FTO gene inhibited the migration and invasion of
-infected cells. In conclusion, the data suggests that
infection leads to upregulation of the FTO gene, which may be related to patient survival rate, tumor staging and other pathological parameters of patients with gastric cancer. It also suggests that FTO promotes proliferation and migration of gastric cancer cells, which may be involved in the pathogenesis of
-induced gastric cancer.</description><identifier>ISSN: 1792-1074</identifier><identifier>EISSN: 1792-1082</identifier><identifier>DOI: 10.3892/ol.2023.13729</identifier><identifier>PMID: 36909372</identifier><language>eng</language><publisher>Greece: Spandidos Publications</publisher><subject>Breast cancer ; Cancer ; Cells ; Colorectal cancer ; Ethanol ; Gastric cancer ; Gene expression ; Genes ; Genetic aspects ; Genomics ; Health aspects ; Helicobacter pylori ; Infection ; Infections ; Medical prognosis ; Medical research ; Medicine, Experimental ; Mortality ; Oncology ; Plasmids ; Reagents ; RNA ; Scientific equipment and supplies industry ; Stomach cancer ; Tumor staging</subject><ispartof>Oncology letters, 2023-04, Vol.25 (4), p.143, Article 143</ispartof><rights>Copyright: © Gui et al.</rights><rights>COPYRIGHT 2023 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2023</rights><rights>Copyright: © Gui et al. 2023</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c513t-4e62755741514299ecf0403e9e0ea117e4324d1a223422e6cc5b806378026b6e3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9996366/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9996366/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/36909372$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Gui, Shuqin</creatorcontrib><creatorcontrib>Wang, Qinrong</creatorcontrib><creatorcontrib>Bao, Liya</creatorcontrib><creatorcontrib>He, Xiaofeng</creatorcontrib><creatorcontrib>Wang, Zhengrong</creatorcontrib><creatorcontrib>Liu, Linlin</creatorcontrib><creatorcontrib>Wu, Lixia</creatorcontrib><creatorcontrib>Zhao, Yan</creatorcontrib><creatorcontrib>Zhou, Jianjiang</creatorcontrib><creatorcontrib>Xie, Yuan</creatorcontrib><title>Effects of Helicobacter pylori on the expression of the FTO gene and its biological role in gastric cancer</title><title>Oncology letters</title><addtitle>Oncol Lett</addtitle><description>(
) is a primary risk factor for gastric cancer. The fat mass and obesity-associated (FTO) gene is associated with the development and progression of various cancer types such as glioma, leukemia, breast cancer and colorectal cancer. The aim of the present study was to investigate the effect of
infection on the expression of FTO and its roles in gastric cancer. It was found that the expression levels of both FTO mRNA and protein were significantly increased in
-infected human gastric mucosal epithelial cells and Mongolian gerbil gastric tissues. The expression of FTO in gastric cancer tissues was higher than that in para-cancer tissues. Data from The Cancer Genome Atlas demonstrated that FTO expression in gastric cancer tissues was significantly higher than that in normal tissues. Patient survival rate was significantly decreased in patients with high expression levels of FTO. It was also demonstrated that FTO expression was associated with several pathological parameters, such as tumor stage, metastasis stage and the American Joint Committee on Cancer stage. The FTO gene was positively correlated with 16,601 genes in gastric cancer and negatively correlated with 3,623 genes. Gene Ontology enrichment analysis demonstrated that FTO was significantly enriched in the regulation of gene expression and oxidative RNA demethylase activity, and it was associated with components such as the RNA N6-methyladenosine methyltransferase complex and nuclear speckle. In addition, knockdown of the FTO gene inhibited the migration and invasion of
-infected cells. In conclusion, the data suggests that
infection leads to upregulation of the FTO gene, which may be related to patient survival rate, tumor staging and other pathological parameters of patients with gastric cancer. It also suggests that FTO promotes proliferation and migration of gastric cancer cells, which may be involved in the pathogenesis of
-induced gastric cancer.</description><subject>Breast cancer</subject><subject>Cancer</subject><subject>Cells</subject><subject>Colorectal cancer</subject><subject>Ethanol</subject><subject>Gastric cancer</subject><subject>Gene expression</subject><subject>Genes</subject><subject>Genetic aspects</subject><subject>Genomics</subject><subject>Health aspects</subject><subject>Helicobacter pylori</subject><subject>Infection</subject><subject>Infections</subject><subject>Medical prognosis</subject><subject>Medical research</subject><subject>Medicine, Experimental</subject><subject>Mortality</subject><subject>Oncology</subject><subject>Plasmids</subject><subject>Reagents</subject><subject>RNA</subject><subject>Scientific equipment and supplies industry</subject><subject>Stomach cancer</subject><subject>Tumor staging</subject><issn>1792-1074</issn><issn>1792-1082</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNptks9uVCEUxonR2KZ26daQmLi7I_8uXDYmTdNakybd1DXhMufeoTIwAmPat_FZfDIZW8dOIiw4HH7nCxw-hN5SsuCDZh9TWDDC-IJyxfQLdEyVZh0lA3u5j5U4Qqel3JE2ekmHQb5GR1xqolvNMfp2MU3gasFpwlcQvEujdRXyr5-bh5CyxyniugIM95sMpfi2beQuc3l7g2eIgG1cYt8URp9Cmr2zAecUAPuIZ1tq9g47Gx3kN-jVZEOB06f1BH29vLg9v-qubz5_OT-77lxPee0ESKb6XgnaU8G0BjcRQThoIGApVSA4E0tqGeOCMZDO9eNAJFcDYXKUwE_Qp0fdzXZcw9JBrNkGs8l-bfODSdabw5PoV2ZOP4zWWnIpm8D7J4Gcvm-hVHOXtjm2OxumhsboQah_1GwDGB-n1MTc2hdnzpQQ7U8kZ41a_Idqcwnr1u0Ik2_5g4IPzwpWYENdlRS2tfW-HILdI-hyKiXDtH8hJWZnD5OC2dnD_LFH4989b8ue_msG_hsTdbOo</recordid><startdate>20230401</startdate><enddate>20230401</enddate><creator>Gui, Shuqin</creator><creator>Wang, Qinrong</creator><creator>Bao, Liya</creator><creator>He, Xiaofeng</creator><creator>Wang, Zhengrong</creator><creator>Liu, Linlin</creator><creator>Wu, Lixia</creator><creator>Zhao, Yan</creator><creator>Zhou, Jianjiang</creator><creator>Xie, Yuan</creator><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</general><general>D.A. 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) is a primary risk factor for gastric cancer. The fat mass and obesity-associated (FTO) gene is associated with the development and progression of various cancer types such as glioma, leukemia, breast cancer and colorectal cancer. The aim of the present study was to investigate the effect of
infection on the expression of FTO and its roles in gastric cancer. It was found that the expression levels of both FTO mRNA and protein were significantly increased in
-infected human gastric mucosal epithelial cells and Mongolian gerbil gastric tissues. The expression of FTO in gastric cancer tissues was higher than that in para-cancer tissues. Data from The Cancer Genome Atlas demonstrated that FTO expression in gastric cancer tissues was significantly higher than that in normal tissues. Patient survival rate was significantly decreased in patients with high expression levels of FTO. It was also demonstrated that FTO expression was associated with several pathological parameters, such as tumor stage, metastasis stage and the American Joint Committee on Cancer stage. The FTO gene was positively correlated with 16,601 genes in gastric cancer and negatively correlated with 3,623 genes. Gene Ontology enrichment analysis demonstrated that FTO was significantly enriched in the regulation of gene expression and oxidative RNA demethylase activity, and it was associated with components such as the RNA N6-methyladenosine methyltransferase complex and nuclear speckle. In addition, knockdown of the FTO gene inhibited the migration and invasion of
-infected cells. In conclusion, the data suggests that
infection leads to upregulation of the FTO gene, which may be related to patient survival rate, tumor staging and other pathological parameters of patients with gastric cancer. It also suggests that FTO promotes proliferation and migration of gastric cancer cells, which may be involved in the pathogenesis of
-induced gastric cancer.</abstract><cop>Greece</cop><pub>Spandidos Publications</pub><pmid>36909372</pmid><doi>10.3892/ol.2023.13729</doi><oa>free_for_read</oa></addata></record> |
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| source | Spandidos Publications Journals; EZB-FREE-00999 freely available EZB journals; PubMed Central |
| subjects | Breast cancer Cancer Cells Colorectal cancer Ethanol Gastric cancer Gene expression Genes Genetic aspects Genomics Health aspects Helicobacter pylori Infection Infections Medical prognosis Medical research Medicine, Experimental Mortality Oncology Plasmids Reagents RNA Scientific equipment and supplies industry Stomach cancer Tumor staging |
| title | Effects of Helicobacter pylori on the expression of the FTO gene and its biological role in gastric cancer |
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