SNHG15 promotes gallbladder cancer progression by enhancing the autophagy of tumor cell under nutrition stress
Gallbladder cancer (GBC) is a major malignant carcinoma of the biliary tract with extremely poor prognosis. Currently, there is no useful therapy strategies for GBC treatment, indicating the unmet mechanism researches for GBC. In this study, our data showed that SNHG15 expression significantly up-re...
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| Veröffentlicht in: | Cell cycle (Georgetown, Tex.) Tex.), 2023-10, Vol.22 (19), p.2130-2141 |
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| creator | Min, He Yang, Linhua Xu, Xinsen Geng, Yajun Liu, Fatao Liu, Yingbin |
| description | Gallbladder cancer (GBC) is a major malignant carcinoma of the biliary tract with extremely poor prognosis. Currently, there is no useful therapy strategies for GBC treatment, indicating the unmet mechanism researches for GBC. In this study, our data showed that SNHG15 expression significantly up-regulated and its high expression associated with poor overall survival of patients suffer from GBC. Functional experiments showed that SNHG15 depletion delayed the proliferation and enhanced the apoptosis of GBC tumor cells under the nutrition stress condition, which further confirmed in the subcutaneous xenograft model and liver metastasis model. Mechanistically, SNHG15 could interact with AMPK and facilitate the phosphorylation of AMPK to Tuberous sclerosis complex TSC2, resulting in mTOR suppression and autophagy enhancement, and finally, conferring the GBC cell sustain proliferation under nutrition stress. Taken together, our findings revealed that SNHG15 promotes GBC tumor progression by enhancing the autophagy under poor nutrition tumor microenvironment, which could be a promising targets for GBC. |
| doi_str_mv | 10.1080/15384101.2023.2278339 |
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Currently, there is no useful therapy strategies for GBC treatment, indicating the unmet mechanism researches for GBC. In this study, our data showed that SNHG15 expression significantly up-regulated and its high expression associated with poor overall survival of patients suffer from GBC. Functional experiments showed that SNHG15 depletion delayed the proliferation and enhanced the apoptosis of GBC tumor cells under the nutrition stress condition, which further confirmed in the subcutaneous xenograft model and liver metastasis model. Mechanistically, SNHG15 could interact with AMPK and facilitate the phosphorylation of AMPK to Tuberous sclerosis complex TSC2, resulting in mTOR suppression and autophagy enhancement, and finally, conferring the GBC cell sustain proliferation under nutrition stress. Taken together, our findings revealed that SNHG15 promotes GBC tumor progression by enhancing the autophagy under poor nutrition tumor microenvironment, which could be a promising targets for GBC.</description><identifier>ISSN: 1538-4101</identifier><identifier>ISSN: 1551-4005</identifier><identifier>EISSN: 1551-4005</identifier><identifier>DOI: 10.1080/15384101.2023.2278339</identifier><identifier>PMID: 37937948</identifier><language>eng</language><publisher>United States: Taylor & Francis</publisher><subject>AMP-Activated Protein Kinases - metabolism ; Animals ; autophagy ; Carcinoma ; Cell Line, Tumor ; Cell Proliferation - genetics ; Gallbladder cancer ; Gallbladder Neoplasms - genetics ; Gallbladder Neoplasms - pathology ; Gene Expression Regulation, Neoplastic ; Humans ; Research Paper ; SNHG15 ; TSC2 ; Tumor Microenvironment</subject><ispartof>Cell cycle (Georgetown, Tex.), 2023-10, Vol.22 (19), p.2130-2141</ispartof><rights>2023 Informa UK Limited, trading as Taylor & Francis Group 2023</rights><rights>2023 Informa UK Limited, trading as Taylor & Francis Group 2023 Informa UK Limited, trading as Taylor & Francis Group</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c422t-a881c54509dd0a5f2f08a37479af6ee6ec651cf49ffcf8053e26f3a97805847e3</citedby><cites>FETCH-LOGICAL-c422t-a881c54509dd0a5f2f08a37479af6ee6ec651cf49ffcf8053e26f3a97805847e3</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/PMC10732635/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC10732635/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/37937948$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Min, He</creatorcontrib><creatorcontrib>Yang, Linhua</creatorcontrib><creatorcontrib>Xu, Xinsen</creatorcontrib><creatorcontrib>Geng, Yajun</creatorcontrib><creatorcontrib>Liu, Fatao</creatorcontrib><creatorcontrib>Liu, Yingbin</creatorcontrib><title>SNHG15 promotes gallbladder cancer progression by enhancing the autophagy of tumor cell under nutrition stress</title><title>Cell cycle (Georgetown, Tex.)</title><addtitle>Cell Cycle</addtitle><description>Gallbladder cancer (GBC) is a major malignant carcinoma of the biliary tract with extremely poor prognosis. Currently, there is no useful therapy strategies for GBC treatment, indicating the unmet mechanism researches for GBC. In this study, our data showed that SNHG15 expression significantly up-regulated and its high expression associated with poor overall survival of patients suffer from GBC. Functional experiments showed that SNHG15 depletion delayed the proliferation and enhanced the apoptosis of GBC tumor cells under the nutrition stress condition, which further confirmed in the subcutaneous xenograft model and liver metastasis model. Mechanistically, SNHG15 could interact with AMPK and facilitate the phosphorylation of AMPK to Tuberous sclerosis complex TSC2, resulting in mTOR suppression and autophagy enhancement, and finally, conferring the GBC cell sustain proliferation under nutrition stress. Taken together, our findings revealed that SNHG15 promotes GBC tumor progression by enhancing the autophagy under poor nutrition tumor microenvironment, which could be a promising targets for GBC.</description><subject>AMP-Activated Protein Kinases - metabolism</subject><subject>Animals</subject><subject>autophagy</subject><subject>Carcinoma</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation - genetics</subject><subject>Gallbladder cancer</subject><subject>Gallbladder Neoplasms - genetics</subject><subject>Gallbladder Neoplasms - pathology</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Humans</subject><subject>Research Paper</subject><subject>SNHG15</subject><subject>TSC2</subject><subject>Tumor Microenvironment</subject><issn>1538-4101</issn><issn>1551-4005</issn><issn>1551-4005</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kUuPFCEUhYnROA_9CRqWbqrlUVRRKzUTnZlkogt1TWjqUl2GghaoMf3vBbtnohsTkku455x7yYfQK0o2lEjylgouW0rohhHGN4z1kvPhCTqnQtCmJUQ8rXcumyo6Qxcp_SCEyX6gz9EZ74dyWnmO_NfPN9dU4H0MS8iQ8KSd2zo9jhCx0d6UUnpThJTm4PH2gMHvyvvsJ5x3gPWaw36npwMOFud1CcUGzuHV1wS_5jjnaky5RrxAz6x2CV6e6iX6_unjt6ub5u7L9e3Vh7vGtIzlRktJjWgFGcaRaGGZJVLzvu0HbTuADkwnqLHtYK2xkggOrLNcD325y7YHfoneHXP363aB0YDPUTu1j_Oi40EFPat_O37eqSncK0p6zjouSsKbU0IMP1dIWS1zqj_THsKaFJOy7CPkH6k4Sk0MKUWwj3MoURWWeoClKix1glV8r_9e8tH1QKcI3h8Fs7chLvpXiG5UWR9ciDZWCEnx_8_4DS9Lpn8</recordid><startdate>20231002</startdate><enddate>20231002</enddate><creator>Min, He</creator><creator>Yang, Linhua</creator><creator>Xu, Xinsen</creator><creator>Geng, Yajun</creator><creator>Liu, Fatao</creator><creator>Liu, Yingbin</creator><general>Taylor & Francis</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>7X8</scope><scope>5PM</scope></search><sort><creationdate>20231002</creationdate><title>SNHG15 promotes gallbladder cancer progression by enhancing the autophagy of tumor cell under nutrition stress</title><author>Min, He ; Yang, Linhua ; Xu, Xinsen ; Geng, Yajun ; Liu, Fatao ; Liu, Yingbin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c422t-a881c54509dd0a5f2f08a37479af6ee6ec651cf49ffcf8053e26f3a97805847e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>AMP-Activated Protein Kinases - metabolism</topic><topic>Animals</topic><topic>autophagy</topic><topic>Carcinoma</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation - genetics</topic><topic>Gallbladder cancer</topic><topic>Gallbladder Neoplasms - genetics</topic><topic>Gallbladder Neoplasms - pathology</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Humans</topic><topic>Research Paper</topic><topic>SNHG15</topic><topic>TSC2</topic><topic>Tumor Microenvironment</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Min, He</creatorcontrib><creatorcontrib>Yang, Linhua</creatorcontrib><creatorcontrib>Xu, Xinsen</creatorcontrib><creatorcontrib>Geng, Yajun</creatorcontrib><creatorcontrib>Liu, Fatao</creatorcontrib><creatorcontrib>Liu, Yingbin</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cell cycle (Georgetown, Tex.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Min, He</au><au>Yang, Linhua</au><au>Xu, Xinsen</au><au>Geng, Yajun</au><au>Liu, Fatao</au><au>Liu, Yingbin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>SNHG15 promotes gallbladder cancer progression by enhancing the autophagy of tumor cell under nutrition stress</atitle><jtitle>Cell cycle (Georgetown, Tex.)</jtitle><addtitle>Cell Cycle</addtitle><date>2023-10-02</date><risdate>2023</risdate><volume>22</volume><issue>19</issue><spage>2130</spage><epage>2141</epage><pages>2130-2141</pages><issn>1538-4101</issn><issn>1551-4005</issn><eissn>1551-4005</eissn><abstract>Gallbladder cancer (GBC) is a major malignant carcinoma of the biliary tract with extremely poor prognosis. Currently, there is no useful therapy strategies for GBC treatment, indicating the unmet mechanism researches for GBC. In this study, our data showed that SNHG15 expression significantly up-regulated and its high expression associated with poor overall survival of patients suffer from GBC. Functional experiments showed that SNHG15 depletion delayed the proliferation and enhanced the apoptosis of GBC tumor cells under the nutrition stress condition, which further confirmed in the subcutaneous xenograft model and liver metastasis model. Mechanistically, SNHG15 could interact with AMPK and facilitate the phosphorylation of AMPK to Tuberous sclerosis complex TSC2, resulting in mTOR suppression and autophagy enhancement, and finally, conferring the GBC cell sustain proliferation under nutrition stress. Taken together, our findings revealed that SNHG15 promotes GBC tumor progression by enhancing the autophagy under poor nutrition tumor microenvironment, which could be a promising targets for GBC.</abstract><cop>United States</cop><pub>Taylor & Francis</pub><pmid>37937948</pmid><doi>10.1080/15384101.2023.2278339</doi><tpages>12</tpages></addata></record> |
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| subjects | AMP-Activated Protein Kinases - metabolism Animals autophagy Carcinoma Cell Line, Tumor Cell Proliferation - genetics Gallbladder cancer Gallbladder Neoplasms - genetics Gallbladder Neoplasms - pathology Gene Expression Regulation, Neoplastic Humans Research Paper SNHG15 TSC2 Tumor Microenvironment |
| title | SNHG15 promotes gallbladder cancer progression by enhancing the autophagy of tumor cell under nutrition stress |
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