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LINC02466 promotes the progression of hepatocellular carcinoma through the mTOR pathway
Objective Long non-coding RNAs (lncRNAs) LINC02466 is an lncRNA newly linked to the adverse outcomes in primary liver cancer patients, and its crucial involvement in the disease's escalation. Decoding the specific role of LINC02466 in HCC progression is of great significance to provide a potent...
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Published in: | Discover. Oncology 2024-11, Vol.15 (1), p.623-15, Article 623 |
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container_title | Discover. Oncology |
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creator | Liu, Shiqian Quan, Zhipeng Liang, Jiaming Wang, Fuqiang Yan, Hao Wang, Zhenran Tang, Bo Qin, Xuebin |
description | Objective
Long non-coding RNAs (lncRNAs) LINC02466 is an lncRNA newly linked to the adverse outcomes in primary liver cancer patients, and its crucial involvement in the disease's escalation. Decoding the specific role of LINC02466 in HCC progression is of great significance to provide a potential therapeutic target for HCC.
Methods
RT-qPCR and Western Blot techniques was used to analyze the expression levels of LINC02466 in both malignant and surrounding healthy liver tissues. CCK8 assays and colony formation experiments indicates the LINC02466's effect on the proliferation rates of liver cancer cells. Flow cytometry was pivotal in revealing its significant influence on the cell cycle of these cells. Kaplan–Meier survival analysis with log-rank tests were employed.
Results
The suppression of LINC02466 markedly reduces the stemness attributes of liver cancer cells, indicating a potential therapeutic target. LINC02466 overexpression significantly increased tumor growth rates and final volumes. Further research indicated that LINC02466 significantly influences liver cancer progression through regulating the mTOR signaling pathway.
Conclusion
LINC02466 regulating cell proliferation, the cell cycle, and stemness characteristics via the mTOR pathway, suggesting LINC02466 as a potential therapeutic target for primary liver cancer. |
doi_str_mv | 10.1007/s12672-024-00999-x |
format | article |
fullrecord | <record><control><sourceid>proquest_doaj_</sourceid><recordid>TN_cdi_doaj_primary_oai_doaj_org_article_2c3f417f059443dfbe767ccd9ef08f05</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><doaj_id>oai_doaj_org_article_2c3f417f059443dfbe767ccd9ef08f05</doaj_id><sourcerecordid>3124692395</sourcerecordid><originalsourceid>FETCH-LOGICAL-c394t-5e56cf1512f9e1e031690938befac740780d83826c882fcca7bd3372536683af3</originalsourceid><addsrcrecordid>eNp9kUFv1DAQhaMKRKvSP8ChypFL6NiO7fiE0AroSisqoVY9Wl5nnGSVxIudQPvv8W5K1V442Z5583n0XpZ9IPCJAMirSKiQtABaFgBKqeLhJDujkkEhgJA3L-6n2UWMOwCgnDAG_F12yhQHplh1lt1v1j9WCSJEvg9-8BPGfGrx8GgCxtj5Mfcub3FvJm-x7-fehNyaYLvRDyZpg5-b9jgz3N78zJOu_WMe32dvnekjXjyd59ndt6-3q-tic_N9vfqyKSxT5VRw5MI6wgl1CgkCI0JBWmyLzlhZgqygrlhFha0q6qw1clszJilnQlTMOHaerRdu7c1O70M3mPCoven0seBDo02YOtujppa5kkgHXJUlq90WpZDW1godVKmaWJ8X1n7eDlhbHKdg-lfQ152xa3Xjf2tCeEmUFInw8YkQ_K8Z46SHLh5cMyP6OWpGktOKJvuTlC5SG3yMAd3zPwT0IWG9JKxTOPqYsH5IQ5cvN3we-ZdnErBFEFNrbDDonZ_DmBL4H_YvQ06x1A</addsrcrecordid><sourcetype>Open Website</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>3124692395</pqid></control><display><type>article</type><title>LINC02466 promotes the progression of hepatocellular carcinoma through the mTOR pathway</title><source>Publicly Available Content Database</source><source>PubMed Central</source><creator>Liu, Shiqian ; Quan, Zhipeng ; Liang, Jiaming ; Wang, Fuqiang ; Yan, Hao ; Wang, Zhenran ; Tang, Bo ; Qin, Xuebin</creator><creatorcontrib>Liu, Shiqian ; Quan, Zhipeng ; Liang, Jiaming ; Wang, Fuqiang ; Yan, Hao ; Wang, Zhenran ; Tang, Bo ; Qin, Xuebin</creatorcontrib><description>Objective
Long non-coding RNAs (lncRNAs) LINC02466 is an lncRNA newly linked to the adverse outcomes in primary liver cancer patients, and its crucial involvement in the disease's escalation. Decoding the specific role of LINC02466 in HCC progression is of great significance to provide a potential therapeutic target for HCC.
Methods
RT-qPCR and Western Blot techniques was used to analyze the expression levels of LINC02466 in both malignant and surrounding healthy liver tissues. CCK8 assays and colony formation experiments indicates the LINC02466's effect on the proliferation rates of liver cancer cells. Flow cytometry was pivotal in revealing its significant influence on the cell cycle of these cells. Kaplan–Meier survival analysis with log-rank tests were employed.
Results
The suppression of LINC02466 markedly reduces the stemness attributes of liver cancer cells, indicating a potential therapeutic target. LINC02466 overexpression significantly increased tumor growth rates and final volumes. Further research indicated that LINC02466 significantly influences liver cancer progression through regulating the mTOR signaling pathway.
Conclusion
LINC02466 regulating cell proliferation, the cell cycle, and stemness characteristics via the mTOR pathway, suggesting LINC02466 as a potential therapeutic target for primary liver cancer.</description><identifier>ISSN: 2730-6011</identifier><identifier>EISSN: 2730-6011</identifier><identifier>DOI: 10.1007/s12672-024-00999-x</identifier><identifier>PMID: 39503938</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Cancer Research ; HCC ; Internal Medicine ; LINC02466 ; Medicine ; Medicine & Public Health ; Molecular Medicine ; mTOR ; Oncology ; Proliferation ; Radiotherapy ; Stem cell ; Surgical Oncology</subject><ispartof>Discover. Oncology, 2024-11, Vol.15 (1), p.623-15, Article 623</ispartof><rights>The Author(s) 2024</rights><rights>2024. The Author(s).</rights><rights>The Author(s) 2024 2024</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c394t-5e56cf1512f9e1e031690938befac740780d83826c882fcca7bd3372536683af3</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/PMC11541976/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC11541976/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27903,27904,36992,53769,53771</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/39503938$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Liu, Shiqian</creatorcontrib><creatorcontrib>Quan, Zhipeng</creatorcontrib><creatorcontrib>Liang, Jiaming</creatorcontrib><creatorcontrib>Wang, Fuqiang</creatorcontrib><creatorcontrib>Yan, Hao</creatorcontrib><creatorcontrib>Wang, Zhenran</creatorcontrib><creatorcontrib>Tang, Bo</creatorcontrib><creatorcontrib>Qin, Xuebin</creatorcontrib><title>LINC02466 promotes the progression of hepatocellular carcinoma through the mTOR pathway</title><title>Discover. Oncology</title><addtitle>Discov Onc</addtitle><addtitle>Discov Oncol</addtitle><description>Objective
Long non-coding RNAs (lncRNAs) LINC02466 is an lncRNA newly linked to the adverse outcomes in primary liver cancer patients, and its crucial involvement in the disease's escalation. Decoding the specific role of LINC02466 in HCC progression is of great significance to provide a potential therapeutic target for HCC.
Methods
RT-qPCR and Western Blot techniques was used to analyze the expression levels of LINC02466 in both malignant and surrounding healthy liver tissues. CCK8 assays and colony formation experiments indicates the LINC02466's effect on the proliferation rates of liver cancer cells. Flow cytometry was pivotal in revealing its significant influence on the cell cycle of these cells. Kaplan–Meier survival analysis with log-rank tests were employed.
Results
The suppression of LINC02466 markedly reduces the stemness attributes of liver cancer cells, indicating a potential therapeutic target. LINC02466 overexpression significantly increased tumor growth rates and final volumes. Further research indicated that LINC02466 significantly influences liver cancer progression through regulating the mTOR signaling pathway.
Conclusion
LINC02466 regulating cell proliferation, the cell cycle, and stemness characteristics via the mTOR pathway, suggesting LINC02466 as a potential therapeutic target for primary liver cancer.</description><subject>Cancer Research</subject><subject>HCC</subject><subject>Internal Medicine</subject><subject>LINC02466</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Molecular Medicine</subject><subject>mTOR</subject><subject>Oncology</subject><subject>Proliferation</subject><subject>Radiotherapy</subject><subject>Stem cell</subject><subject>Surgical Oncology</subject><issn>2730-6011</issn><issn>2730-6011</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>DOA</sourceid><recordid>eNp9kUFv1DAQhaMKRKvSP8ChypFL6NiO7fiE0AroSisqoVY9Wl5nnGSVxIudQPvv8W5K1V442Z5583n0XpZ9IPCJAMirSKiQtABaFgBKqeLhJDujkkEhgJA3L-6n2UWMOwCgnDAG_F12yhQHplh1lt1v1j9WCSJEvg9-8BPGfGrx8GgCxtj5Mfcub3FvJm-x7-fehNyaYLvRDyZpg5-b9jgz3N78zJOu_WMe32dvnekjXjyd59ndt6-3q-tic_N9vfqyKSxT5VRw5MI6wgl1CgkCI0JBWmyLzlhZgqygrlhFha0q6qw1clszJilnQlTMOHaerRdu7c1O70M3mPCoven0seBDo02YOtujppa5kkgHXJUlq90WpZDW1godVKmaWJ8X1n7eDlhbHKdg-lfQ152xa3Xjf2tCeEmUFInw8YkQ_K8Z46SHLh5cMyP6OWpGktOKJvuTlC5SG3yMAd3zPwT0IWG9JKxTOPqYsH5IQ5cvN3we-ZdnErBFEFNrbDDonZ_DmBL4H_YvQ06x1A</recordid><startdate>20241106</startdate><enddate>20241106</enddate><creator>Liu, Shiqian</creator><creator>Quan, Zhipeng</creator><creator>Liang, Jiaming</creator><creator>Wang, Fuqiang</creator><creator>Yan, Hao</creator><creator>Wang, Zhenran</creator><creator>Tang, Bo</creator><creator>Qin, Xuebin</creator><general>Springer US</general><general>Springer</general><scope>C6C</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20241106</creationdate><title>LINC02466 promotes the progression of hepatocellular carcinoma through the mTOR pathway</title><author>Liu, Shiqian ; Quan, Zhipeng ; Liang, Jiaming ; Wang, Fuqiang ; Yan, Hao ; Wang, Zhenran ; Tang, Bo ; Qin, Xuebin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c394t-5e56cf1512f9e1e031690938befac740780d83826c882fcca7bd3372536683af3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Cancer Research</topic><topic>HCC</topic><topic>Internal Medicine</topic><topic>LINC02466</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Molecular Medicine</topic><topic>mTOR</topic><topic>Oncology</topic><topic>Proliferation</topic><topic>Radiotherapy</topic><topic>Stem cell</topic><topic>Surgical Oncology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Liu, Shiqian</creatorcontrib><creatorcontrib>Quan, Zhipeng</creatorcontrib><creatorcontrib>Liang, Jiaming</creatorcontrib><creatorcontrib>Wang, Fuqiang</creatorcontrib><creatorcontrib>Yan, Hao</creatorcontrib><creatorcontrib>Wang, Zhenran</creatorcontrib><creatorcontrib>Tang, Bo</creatorcontrib><creatorcontrib>Qin, Xuebin</creatorcontrib><collection>Springer Nature OA Free Journals</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>Open Access: DOAJ - Directory of Open Access Journals</collection><jtitle>Discover. Oncology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Liu, Shiqian</au><au>Quan, Zhipeng</au><au>Liang, Jiaming</au><au>Wang, Fuqiang</au><au>Yan, Hao</au><au>Wang, Zhenran</au><au>Tang, Bo</au><au>Qin, Xuebin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>LINC02466 promotes the progression of hepatocellular carcinoma through the mTOR pathway</atitle><jtitle>Discover. Oncology</jtitle><stitle>Discov Onc</stitle><addtitle>Discov Oncol</addtitle><date>2024-11-06</date><risdate>2024</risdate><volume>15</volume><issue>1</issue><spage>623</spage><epage>15</epage><pages>623-15</pages><artnum>623</artnum><issn>2730-6011</issn><eissn>2730-6011</eissn><abstract>Objective
Long non-coding RNAs (lncRNAs) LINC02466 is an lncRNA newly linked to the adverse outcomes in primary liver cancer patients, and its crucial involvement in the disease's escalation. Decoding the specific role of LINC02466 in HCC progression is of great significance to provide a potential therapeutic target for HCC.
Methods
RT-qPCR and Western Blot techniques was used to analyze the expression levels of LINC02466 in both malignant and surrounding healthy liver tissues. CCK8 assays and colony formation experiments indicates the LINC02466's effect on the proliferation rates of liver cancer cells. Flow cytometry was pivotal in revealing its significant influence on the cell cycle of these cells. Kaplan–Meier survival analysis with log-rank tests were employed.
Results
The suppression of LINC02466 markedly reduces the stemness attributes of liver cancer cells, indicating a potential therapeutic target. LINC02466 overexpression significantly increased tumor growth rates and final volumes. Further research indicated that LINC02466 significantly influences liver cancer progression through regulating the mTOR signaling pathway.
Conclusion
LINC02466 regulating cell proliferation, the cell cycle, and stemness characteristics via the mTOR pathway, suggesting LINC02466 as a potential therapeutic target for primary liver cancer.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>39503938</pmid><doi>10.1007/s12672-024-00999-x</doi><tpages>15</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Cancer Research HCC Internal Medicine LINC02466 Medicine Medicine & Public Health Molecular Medicine mTOR Oncology Proliferation Radiotherapy Stem cell Surgical Oncology |
title | LINC02466 promotes the progression of hepatocellular carcinoma through the mTOR pathway |
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