Mechanistic analysis of endothelial lipase G promotion of the occurrence and development of cervical carcinoma by activating the phosphatidylinositol-4,5-bisphosphate 3-kinase/protein kinase B/mechanistic target of rapamycin kinase signalling pathway
Lipase G, endothelial type (LIPG) is expressed abundantly in tissues with a high metabolic rate and vascularisation. Research on LIPG has focussed on metabolic syndromes. However, the role of LIPG in providing lipid precursors suggests that it might function in the metabolism of carcinoma cells. Ana...
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| Veröffentlicht in: | Journal of obstetrics and gynaecology 2023-12, Vol.43 (1), p.2151353-2151353 |
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| description | Lipase G, endothelial type (LIPG) is expressed abundantly in tissues with a high metabolic rate and vascularisation. Research on LIPG has focussed on metabolic syndromes. However, the role of LIPG in providing lipid precursors suggests that it might function in the metabolism of carcinoma cells. Analysis in The Cancer Genome Atlas indicated that patients with cervical carcinoma with high LIPG expression had a lower survival prognosis compared with patients with low LIPG expression. The mechanism underlying the effects of LIPG in cervical carcinoma is unclear. The present study aimed to determine the role of LIPG in cervical carcinoma and its mechanism. The results showed that the LIPG expression level was higher in cervical cancer. Downregulation of LIPG expression inhibited cell migration, invasion, proliferation, and the formation of cell colonies, but increased the rate of apoptosis. The Human papillomavirus E6 protein might reduce the expression of miR-148a-3p, relieve the inhibitory effect of miR-148a-3p on LIPG expression, and promote the progression of cervical cancer through the phosphatidylinositol-4,5-bisphosphate 3-kinase/protein kinase B/mechanistic target of rapamycin kinase signalling pathway.
IMPACT STATEMENT
What is already known on this subject? LIPG provides lipid precursors, suggesting that it might function in the metabolism of carcinoma cells
What do the results of this study add? LIPG might be regulated by HPV16 E6/miR-148a-3p and promote cervical carcinoma progression via the PI3K/AKT/mTOR signalling pathway.
What are the implications of these finding for clinical practice and/or further research? The results indicated that novel treatment and diagnosis strategies for cervical carcinoma could be developed related to LIPG. However, the detailed relationship between LIPG and cervical carcinoma remains to be fully determined. |
| doi_str_mv | 10.1080/01443615.2022.2151353 |
| format | Article |
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IMPACT STATEMENT
What is already known on this subject? LIPG provides lipid precursors, suggesting that it might function in the metabolism of carcinoma cells
What do the results of this study add? LIPG might be regulated by HPV16 E6/miR-148a-3p and promote cervical carcinoma progression via the PI3K/AKT/mTOR signalling pathway.
What are the implications of these finding for clinical practice and/or further research? The results indicated that novel treatment and diagnosis strategies for cervical carcinoma could be developed related to LIPG. However, the detailed relationship between LIPG and cervical carcinoma remains to be fully determined.</description><identifier>ISSN: 0144-3615</identifier><identifier>EISSN: 1364-6893</identifier><identifier>DOI: 10.1080/01443615.2022.2151353</identifier><identifier>PMID: 36606668</identifier><language>eng</language><publisher>England: Taylor & Francis</publisher><subject>AKT ; Cell Line, Tumor ; Cervical cancer ; cervical carcinoma ; Female ; Gene Expression Regulation, Neoplastic ; HPV ; Humans ; Kinases ; Lipase - genetics ; Lipase - metabolism ; LIPG ; Lipids ; Medical prognosis ; Metabolism ; MicroRNAs ; miR-148a-3p ; mTOR ; Phosphatidylinositol 3-Kinases - genetics ; Phosphatidylinositol 3-Kinases - metabolism ; PI3K ; Proteins ; Proto-Oncogene Proteins c-akt - genetics ; Proto-Oncogene Proteins c-akt - metabolism ; Uterine Cervical Neoplasms - pathology</subject><ispartof>Journal of obstetrics and gynaecology, 2023-12, Vol.43 (1), p.2151353-2151353</ispartof><rights>2023 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group. 2023</rights><rights>2023 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group. This work is licensed under the Creative Commons Attribution License 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><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c507t-567fb1cda516f46fa5575212f3e8256e1319be19c1bd384e1ac92bd497f4fe343</citedby><cites>FETCH-LOGICAL-c507t-567fb1cda516f46fa5575212f3e8256e1319be19c1bd384e1ac92bd497f4fe343</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.tandfonline.com/doi/pdf/10.1080/01443615.2022.2151353$$EPDF$$P50$$Ginformaworld$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.tandfonline.com/doi/full/10.1080/01443615.2022.2151353$$EHTML$$P50$$Ginformaworld$$Hfree_for_read</linktohtml><link.rule.ids>314,776,780,860,2095,27481,27903,27904,59119,59120</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/36606668$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Huang, Jing</creatorcontrib><creatorcontrib>Liu, Renci</creatorcontrib><creatorcontrib>Zhang, Yiwen</creatorcontrib><creatorcontrib>Sheng, Xiujie</creatorcontrib><title>Mechanistic analysis of endothelial lipase G promotion of the occurrence and development of cervical carcinoma by activating the phosphatidylinositol-4,5-bisphosphate 3-kinase/protein kinase B/mechanistic target of rapamycin kinase signalling pathway</title><title>Journal of obstetrics and gynaecology</title><addtitle>J Obstet Gynaecol</addtitle><description>Lipase G, endothelial type (LIPG) is expressed abundantly in tissues with a high metabolic rate and vascularisation. Research on LIPG has focussed on metabolic syndromes. However, the role of LIPG in providing lipid precursors suggests that it might function in the metabolism of carcinoma cells. Analysis in The Cancer Genome Atlas indicated that patients with cervical carcinoma with high LIPG expression had a lower survival prognosis compared with patients with low LIPG expression. The mechanism underlying the effects of LIPG in cervical carcinoma is unclear. The present study aimed to determine the role of LIPG in cervical carcinoma and its mechanism. The results showed that the LIPG expression level was higher in cervical cancer. Downregulation of LIPG expression inhibited cell migration, invasion, proliferation, and the formation of cell colonies, but increased the rate of apoptosis. The Human papillomavirus E6 protein might reduce the expression of miR-148a-3p, relieve the inhibitory effect of miR-148a-3p on LIPG expression, and promote the progression of cervical cancer through the phosphatidylinositol-4,5-bisphosphate 3-kinase/protein kinase B/mechanistic target of rapamycin kinase signalling pathway.
IMPACT STATEMENT
What is already known on this subject? LIPG provides lipid precursors, suggesting that it might function in the metabolism of carcinoma cells
What do the results of this study add? LIPG might be regulated by HPV16 E6/miR-148a-3p and promote cervical carcinoma progression via the PI3K/AKT/mTOR signalling pathway.
What are the implications of these finding for clinical practice and/or further research? The results indicated that novel treatment and diagnosis strategies for cervical carcinoma could be developed related to LIPG. However, the detailed relationship between LIPG and cervical carcinoma remains to be fully determined.</description><subject>AKT</subject><subject>Cell Line, Tumor</subject><subject>Cervical cancer</subject><subject>cervical carcinoma</subject><subject>Female</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>HPV</subject><subject>Humans</subject><subject>Kinases</subject><subject>Lipase - genetics</subject><subject>Lipase - metabolism</subject><subject>LIPG</subject><subject>Lipids</subject><subject>Medical prognosis</subject><subject>Metabolism</subject><subject>MicroRNAs</subject><subject>miR-148a-3p</subject><subject>mTOR</subject><subject>Phosphatidylinositol 3-Kinases - genetics</subject><subject>Phosphatidylinositol 3-Kinases - metabolism</subject><subject>PI3K</subject><subject>Proteins</subject><subject>Proto-Oncogene Proteins c-akt - genetics</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Uterine Cervical Neoplasms - pathology</subject><issn>0144-3615</issn><issn>1364-6893</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>0YH</sourceid><sourceid>EIF</sourceid><sourceid>DOA</sourceid><recordid>eNp9kk9v1DAQxSMEoqXwEUCWuHAgrR3_SXIDKiiVirjAOZo4410XJw62t1W-Oiec3bYgDpyssX_z5nn0iuIlo6eMNvSMMiG4YvK0olV1WjHJuOSPimPGlShV0_LHxfHKlCt0VDyL8ZpSyqgUT4sjrhRVSjXHxa8vqLcw2ZisJjCBW6KNxBuC0-DTFp0FR5ydISK5IHPwo0_WTyuRX4nXehcCThpz80AGvEHn5xGntBIaw43VWUBD0HbyI5B-IaCTvYFkp81eYt76OG9zPSwuM9Em70rxVpa9jfdvSHj5w07ZxFm2kNBO5FCSD2fjXx9IEDa4Hx1ghnHRf8BoN_l3bp06Q9rewvK8eGLARXxxd54U3z99_Hb-ubz6enF5_v6q1JLWqZSqNj3TA0imjFAGpKxlxSrDsamkQsZZ2yNrNesH3ghkoNuqH0RbG2GQC35SXB50Bw_X3RzsCGHpPNhuf-HDpoOQ3TvssDW1UE1fGSFEXddQAwpVDY3WtJWostabg1Zew88dxtSNNmp0Dib0u9hVtWJtoyRdx77-B732u5B3EDtOm1ryhrE2U_JA6eBjDGgeDDLarUHr7oPWrUHr7oKW-17dqe_6EYeHrvtkZeDdAbCT8WGEWx_c0CVYnA8mwKRt9vH_Gb8BggfoWw</recordid><startdate>202312</startdate><enddate>202312</enddate><creator>Huang, Jing</creator><creator>Liu, Renci</creator><creator>Zhang, Yiwen</creator><creator>Sheng, Xiujie</creator><general>Taylor & Francis</general><general>Taylor & Francis Ltd</general><general>Taylor & Francis Group</general><scope>0YH</scope><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>K9.</scope><scope>7X8</scope><scope>DOA</scope></search><sort><creationdate>202312</creationdate><title>Mechanistic analysis of endothelial lipase G promotion of the occurrence and development of cervical carcinoma by activating the phosphatidylinositol-4,5-bisphosphate 3-kinase/protein kinase B/mechanistic target of rapamycin kinase signalling pathway</title><author>Huang, Jing ; Liu, Renci ; Zhang, Yiwen ; Sheng, Xiujie</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c507t-567fb1cda516f46fa5575212f3e8256e1319be19c1bd384e1ac92bd497f4fe343</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>AKT</topic><topic>Cell Line, Tumor</topic><topic>Cervical cancer</topic><topic>cervical carcinoma</topic><topic>Female</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>HPV</topic><topic>Humans</topic><topic>Kinases</topic><topic>Lipase - genetics</topic><topic>Lipase - metabolism</topic><topic>LIPG</topic><topic>Lipids</topic><topic>Medical prognosis</topic><topic>Metabolism</topic><topic>MicroRNAs</topic><topic>miR-148a-3p</topic><topic>mTOR</topic><topic>Phosphatidylinositol 3-Kinases - genetics</topic><topic>Phosphatidylinositol 3-Kinases - metabolism</topic><topic>PI3K</topic><topic>Proteins</topic><topic>Proto-Oncogene Proteins c-akt - genetics</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>Uterine Cervical Neoplasms - pathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Huang, Jing</creatorcontrib><creatorcontrib>Liu, Renci</creatorcontrib><creatorcontrib>Zhang, Yiwen</creatorcontrib><creatorcontrib>Sheng, Xiujie</creatorcontrib><collection>Taylor & Francis Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Journal of obstetrics and gynaecology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Huang, Jing</au><au>Liu, Renci</au><au>Zhang, Yiwen</au><au>Sheng, Xiujie</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Mechanistic analysis of endothelial lipase G promotion of the occurrence and development of cervical carcinoma by activating the phosphatidylinositol-4,5-bisphosphate 3-kinase/protein kinase B/mechanistic target of rapamycin kinase signalling pathway</atitle><jtitle>Journal of obstetrics and gynaecology</jtitle><addtitle>J Obstet Gynaecol</addtitle><date>2023-12</date><risdate>2023</risdate><volume>43</volume><issue>1</issue><spage>2151353</spage><epage>2151353</epage><pages>2151353-2151353</pages><issn>0144-3615</issn><eissn>1364-6893</eissn><abstract>Lipase G, endothelial type (LIPG) is expressed abundantly in tissues with a high metabolic rate and vascularisation. Research on LIPG has focussed on metabolic syndromes. However, the role of LIPG in providing lipid precursors suggests that it might function in the metabolism of carcinoma cells. Analysis in The Cancer Genome Atlas indicated that patients with cervical carcinoma with high LIPG expression had a lower survival prognosis compared with patients with low LIPG expression. The mechanism underlying the effects of LIPG in cervical carcinoma is unclear. The present study aimed to determine the role of LIPG in cervical carcinoma and its mechanism. The results showed that the LIPG expression level was higher in cervical cancer. Downregulation of LIPG expression inhibited cell migration, invasion, proliferation, and the formation of cell colonies, but increased the rate of apoptosis. The Human papillomavirus E6 protein might reduce the expression of miR-148a-3p, relieve the inhibitory effect of miR-148a-3p on LIPG expression, and promote the progression of cervical cancer through the phosphatidylinositol-4,5-bisphosphate 3-kinase/protein kinase B/mechanistic target of rapamycin kinase signalling pathway.
IMPACT STATEMENT
What is already known on this subject? LIPG provides lipid precursors, suggesting that it might function in the metabolism of carcinoma cells
What do the results of this study add? LIPG might be regulated by HPV16 E6/miR-148a-3p and promote cervical carcinoma progression via the PI3K/AKT/mTOR signalling pathway.
What are the implications of these finding for clinical practice and/or further research? The results indicated that novel treatment and diagnosis strategies for cervical carcinoma could be developed related to LIPG. However, the detailed relationship between LIPG and cervical carcinoma remains to be fully determined.</abstract><cop>England</cop><pub>Taylor & Francis</pub><pmid>36606668</pmid><doi>10.1080/01443615.2022.2151353</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | AKT Cell Line, Tumor Cervical cancer cervical carcinoma Female Gene Expression Regulation, Neoplastic HPV Humans Kinases Lipase - genetics Lipase - metabolism LIPG Lipids Medical prognosis Metabolism MicroRNAs miR-148a-3p mTOR Phosphatidylinositol 3-Kinases - genetics Phosphatidylinositol 3-Kinases - metabolism PI3K Proteins Proto-Oncogene Proteins c-akt - genetics Proto-Oncogene Proteins c-akt - metabolism Uterine Cervical Neoplasms - pathology |
| title | Mechanistic analysis of endothelial lipase G promotion of the occurrence and development of cervical carcinoma by activating the phosphatidylinositol-4,5-bisphosphate 3-kinase/protein kinase B/mechanistic target of rapamycin kinase signalling pathway |
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