The autophagy-independent role of BECN1 in colorectal cancer metastasis through regulating STAT3 signaling pathway activation
BECN1 is a critical regulator of autophagy, which plays important roles in tumor formation and metastasis. However, the autophagy-independent role of BECN1 and the clinical prediction value of BECN1 still need to be explored. Here, we observed significantly lower expression of BECN1 in colorectal ca...
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| creator | Hu, Fuqing Li, Geng Huang, Changsheng Hou, Zhenlin Yang, Xi Luo, Xuelai Feng, Yongdong Wang, Guihua Hu, Junbo Cao, Zhixin |
| description | BECN1 is a critical regulator of autophagy, which plays important roles in tumor formation and metastasis. However, the autophagy-independent role of BECN1 and the clinical prediction value of BECN1 still need to be explored. Here, we observed significantly lower expression of BECN1 in colorectal cancers (CRCs) compared with adjacent normal colon tissue, and downregulation of BECN1 was positively related to poor prognosis in CRC patients. In addition, we found that knockdown of BECN1 markedly promoted CRC cell motility and invasion. Bioinformatics gene set enrichment analysis (GSEA) revealed that low levels of BECN1 were significantly correlated with the STAT3 signaling pathway in CRC. Consistently, knockdown of BECN1 increased the phosphorylation of STAT3 and activated the STAT3 signaling pathway in CRC cells. Furthermore, we demonstrated that STAT3 was involved in the CRC metastasis mediated by knockdown of BECN1 in vitro and in vivo. Mechanistically, knockdown of BECN1 promoted the phosphorylation of STAT3 via regulation of the interaction between STAT and JAK2 but did not inhibit autophagy. Our study revealed that BECN1 served as a negative regulator of CRC metastasis by regulating STAT3 signaling pathway activation in an autophagy-independent manner. The BECN1/JAK2/STAT3 signaling pathway can be used as a potential therapeutic target for metastatic CRC. |
| doi_str_mv | 10.1038/s41419-020-2467-3 |
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However, the autophagy-independent role of BECN1 and the clinical prediction value of BECN1 still need to be explored. Here, we observed significantly lower expression of BECN1 in colorectal cancers (CRCs) compared with adjacent normal colon tissue, and downregulation of BECN1 was positively related to poor prognosis in CRC patients. In addition, we found that knockdown of BECN1 markedly promoted CRC cell motility and invasion. Bioinformatics gene set enrichment analysis (GSEA) revealed that low levels of BECN1 were significantly correlated with the STAT3 signaling pathway in CRC. Consistently, knockdown of BECN1 increased the phosphorylation of STAT3 and activated the STAT3 signaling pathway in CRC cells. Furthermore, we demonstrated that STAT3 was involved in the CRC metastasis mediated by knockdown of BECN1 in vitro and in vivo. Mechanistically, knockdown of BECN1 promoted the phosphorylation of STAT3 via regulation of the interaction between STAT and JAK2 but did not inhibit autophagy. Our study revealed that BECN1 served as a negative regulator of CRC metastasis by regulating STAT3 signaling pathway activation in an autophagy-independent manner. The BECN1/JAK2/STAT3 signaling pathway can be used as a potential therapeutic target for metastatic CRC.</description><identifier>ISSN: 2041-4889</identifier><identifier>EISSN: 2041-4889</identifier><identifier>DOI: 10.1038/s41419-020-2467-3</identifier><identifier>PMID: 32358527</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13/2 ; 14/1 ; 14/19 ; 38/109 ; 38/89 ; 631/67/1504/1885/1393 ; 631/80/84/2336 ; 96/31 ; Animals ; Antibodies ; Autophagy ; Autophagy - genetics ; Beclin-1 - genetics ; Biochemistry ; Bioinformatics ; Biomedical and Life Sciences ; Cell Biology ; Cell Culture ; Cell Line, Tumor ; Cell Movement ; Cell Proliferation - genetics ; Colonic Neoplasms - genetics ; Colorectal cancer ; Colorectal carcinoma ; Colorectal Neoplasms - genetics ; Colorectal Neoplasms - pathology ; Gene Expression Regulation, Neoplastic - genetics ; Gene set enrichment analysis ; Humans ; Immunology ; Janus kinase 2 ; Kinases ; Life Sciences ; Life Sciences & Biomedicine ; Metastases ; Metastasis ; Mice, Nude ; Neoplasm Metastasis - genetics ; Neoplasm Metastasis - pathology ; Phagocytosis ; Phosphorylation ; Science & Technology ; Signal transduction ; Signal Transduction - physiology ; Stat3 protein ; STAT3 Transcription Factor - genetics ; Therapeutic applications</subject><ispartof>Cell death & disease, 2020-05, Vol.11 (5), p.304-304, Article 304</ispartof><rights>The Author(s) 2020</rights><rights>The Author(s) 2020. This work is published under 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>true</woscitedreferencessubscribed><woscitedreferencescount>38</woscitedreferencescount><woscitedreferencesoriginalsourcerecordid>wos000531309100002</woscitedreferencesoriginalsourcerecordid><citedby>FETCH-LOGICAL-c470t-49ea02d411c8904276e3d232ce7cd9c7942279b50d30b0665aad662adc5ea3353</citedby><cites>FETCH-LOGICAL-c470t-49ea02d411c8904276e3d232ce7cd9c7942279b50d30b0665aad662adc5ea3353</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/PMC7195408/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7195408/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,315,729,782,786,866,887,2118,27933,27934,28257,41129,42198,51585,53800,53802</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32358527$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hu, Fuqing</creatorcontrib><creatorcontrib>Li, Geng</creatorcontrib><creatorcontrib>Huang, Changsheng</creatorcontrib><creatorcontrib>Hou, Zhenlin</creatorcontrib><creatorcontrib>Yang, Xi</creatorcontrib><creatorcontrib>Luo, Xuelai</creatorcontrib><creatorcontrib>Feng, Yongdong</creatorcontrib><creatorcontrib>Wang, Guihua</creatorcontrib><creatorcontrib>Hu, Junbo</creatorcontrib><creatorcontrib>Cao, Zhixin</creatorcontrib><title>The autophagy-independent role of BECN1 in colorectal cancer metastasis through regulating STAT3 signaling pathway activation</title><title>Cell death & disease</title><addtitle>Cell Death Dis</addtitle><addtitle>CELL DEATH DIS</addtitle><addtitle>Cell Death Dis</addtitle><description>BECN1 is a critical regulator of autophagy, which plays important roles in tumor formation and metastasis. However, the autophagy-independent role of BECN1 and the clinical prediction value of BECN1 still need to be explored. Here, we observed significantly lower expression of BECN1 in colorectal cancers (CRCs) compared with adjacent normal colon tissue, and downregulation of BECN1 was positively related to poor prognosis in CRC patients. In addition, we found that knockdown of BECN1 markedly promoted CRC cell motility and invasion. Bioinformatics gene set enrichment analysis (GSEA) revealed that low levels of BECN1 were significantly correlated with the STAT3 signaling pathway in CRC. Consistently, knockdown of BECN1 increased the phosphorylation of STAT3 and activated the STAT3 signaling pathway in CRC cells. Furthermore, we demonstrated that STAT3 was involved in the CRC metastasis mediated by knockdown of BECN1 in vitro and in vivo. Mechanistically, knockdown of BECN1 promoted the phosphorylation of STAT3 via regulation of the interaction between STAT and JAK2 but did not inhibit autophagy. Our study revealed that BECN1 served as a negative regulator of CRC metastasis by regulating STAT3 signaling pathway activation in an autophagy-independent manner. The BECN1/JAK2/STAT3 signaling pathway can be used as a potential therapeutic target for metastatic CRC.</description><subject>13/2</subject><subject>14/1</subject><subject>14/19</subject><subject>38/109</subject><subject>38/89</subject><subject>631/67/1504/1885/1393</subject><subject>631/80/84/2336</subject><subject>96/31</subject><subject>Animals</subject><subject>Antibodies</subject><subject>Autophagy</subject><subject>Autophagy - genetics</subject><subject>Beclin-1 - genetics</subject><subject>Biochemistry</subject><subject>Bioinformatics</subject><subject>Biomedical and Life Sciences</subject><subject>Cell Biology</subject><subject>Cell Culture</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement</subject><subject>Cell Proliferation - genetics</subject><subject>Colonic Neoplasms - genetics</subject><subject>Colorectal cancer</subject><subject>Colorectal carcinoma</subject><subject>Colorectal Neoplasms - genetics</subject><subject>Colorectal Neoplasms - pathology</subject><subject>Gene Expression Regulation, Neoplastic - 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physiology</topic><topic>Stat3 protein</topic><topic>STAT3 Transcription Factor - genetics</topic><topic>Therapeutic applications</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hu, Fuqing</creatorcontrib><creatorcontrib>Li, Geng</creatorcontrib><creatorcontrib>Huang, Changsheng</creatorcontrib><creatorcontrib>Hou, Zhenlin</creatorcontrib><creatorcontrib>Yang, Xi</creatorcontrib><creatorcontrib>Luo, Xuelai</creatorcontrib><creatorcontrib>Feng, Yongdong</creatorcontrib><creatorcontrib>Wang, Guihua</creatorcontrib><creatorcontrib>Hu, Junbo</creatorcontrib><creatorcontrib>Cao, Zhixin</creatorcontrib><collection>Springer Nature OA/Free Journals</collection><collection>Web of Science - Science Citation Index Expanded - 2020</collection><collection>Web of Science Core Collection</collection><collection>Science Citation Index Expanded</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 Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</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>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</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 Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Access via ProQuest (Open Access)</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cell death & disease</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hu, Fuqing</au><au>Li, Geng</au><au>Huang, Changsheng</au><au>Hou, Zhenlin</au><au>Yang, Xi</au><au>Luo, Xuelai</au><au>Feng, Yongdong</au><au>Wang, Guihua</au><au>Hu, Junbo</au><au>Cao, Zhixin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The autophagy-independent role of BECN1 in colorectal cancer metastasis through regulating STAT3 signaling pathway activation</atitle><jtitle>Cell death & disease</jtitle><stitle>Cell Death Dis</stitle><stitle>CELL DEATH DIS</stitle><addtitle>Cell Death Dis</addtitle><date>2020-05-01</date><risdate>2020</risdate><volume>11</volume><issue>5</issue><spage>304</spage><epage>304</epage><pages>304-304</pages><artnum>304</artnum><issn>2041-4889</issn><eissn>2041-4889</eissn><abstract>BECN1 is a critical regulator of autophagy, which plays important roles in tumor formation and metastasis. However, the autophagy-independent role of BECN1 and the clinical prediction value of BECN1 still need to be explored. Here, we observed significantly lower expression of BECN1 in colorectal cancers (CRCs) compared with adjacent normal colon tissue, and downregulation of BECN1 was positively related to poor prognosis in CRC patients. In addition, we found that knockdown of BECN1 markedly promoted CRC cell motility and invasion. Bioinformatics gene set enrichment analysis (GSEA) revealed that low levels of BECN1 were significantly correlated with the STAT3 signaling pathway in CRC. Consistently, knockdown of BECN1 increased the phosphorylation of STAT3 and activated the STAT3 signaling pathway in CRC cells. Furthermore, we demonstrated that STAT3 was involved in the CRC metastasis mediated by knockdown of BECN1 in vitro and in vivo. Mechanistically, knockdown of BECN1 promoted the phosphorylation of STAT3 via regulation of the interaction between STAT and JAK2 but did not inhibit autophagy. Our study revealed that BECN1 served as a negative regulator of CRC metastasis by regulating STAT3 signaling pathway activation in an autophagy-independent manner. The BECN1/JAK2/STAT3 signaling pathway can be used as a potential therapeutic target for metastatic CRC.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>32358527</pmid><doi>10.1038/s41419-020-2467-3</doi><tpages>13</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 13/2 14/1 14/19 38/109 38/89 631/67/1504/1885/1393 631/80/84/2336 96/31 Animals Antibodies Autophagy Autophagy - genetics Beclin-1 - genetics Biochemistry Bioinformatics Biomedical and Life Sciences Cell Biology Cell Culture Cell Line, Tumor Cell Movement Cell Proliferation - genetics Colonic Neoplasms - genetics Colorectal cancer Colorectal carcinoma Colorectal Neoplasms - genetics Colorectal Neoplasms - pathology Gene Expression Regulation, Neoplastic - genetics Gene set enrichment analysis Humans Immunology Janus kinase 2 Kinases Life Sciences Life Sciences & Biomedicine Metastases Metastasis Mice, Nude Neoplasm Metastasis - genetics Neoplasm Metastasis - pathology Phagocytosis Phosphorylation Science & Technology Signal transduction Signal Transduction - physiology Stat3 protein STAT3 Transcription Factor - genetics Therapeutic applications |
| title | The autophagy-independent role of BECN1 in colorectal cancer metastasis through regulating STAT3 signaling pathway activation |
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