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The tumor suppressor DLC1 inhibits cancer progression and oncogenic autophagy in hepatocellular carcinoma
Downregulation of deleted in liver cancer 1 (DLC1) is associated with poor prognosis of various cancers, but its functional mechanisms in hepatocellular carcinoma (HCC) remains unclear. In the present study, we investigated the roles of DLC1 in tumor progression and autophagy of HCC. We found that D...
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| Published in: | Laboratory investigation 2018-08, Vol.98 (8), p.1014-1024 |
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| container_title | Laboratory investigation |
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| creator | Wu, Hui-Ta Xie, Cheng-Rong Lv, Jie Qi, He-Qiang Wang, Fei Zhang, Sheng Fang, Qin-Liang Wang, Fu-Qiang Lu, Yu-Yan Yin, Zhen-Yu |
| description | Downregulation of deleted in liver cancer 1 (DLC1) is associated with poor prognosis of various cancers, but its functional mechanisms in hepatocellular carcinoma (HCC) remains unclear. In the present study, we investigated the roles of DLC1 in tumor progression and autophagy of HCC. We found that DLC1 was frequently downregulated in HCC tissues. Underexpression of DLC1 correlated with AFP level, vascular invasion, poor differentiation, and poor prognosis. In vitro assays revealed that DLC1 not only suppressed the proliferation, migration, and invasion of HCC cells, but also inhibited autophagy of HCC cells. Mechanistic investigation revealed that DLC1 decreased TCF4 expression and the interaction between β-catenin and TCF4, then inactivated Wnt/β-catenin signaling. Additionally, DLC1 suppressed the ROCK1 activity and the dissociation of the Beclin1-Bcl2 complex, thereby inhibiting autophagy of HCC cells. In conclusion, our findings imply that loss of DLC1 contributes to the progression and oncogenic autophagy of HCC.
Deleted in liver cancer 1 (DLC1) is frequently down-regulated in hepatocellular carcinoma tissue and correlates with α-fetoprotein levels, vascular invasion, poor differentiation and poor prognosis. The authors show that DLC1 suppresses the proliferation, migration, invasion and autophagy of hepatocellular carcinoma cells through inactivating Wnt/β-catenin signaling and inhibition of the serine/threonine kinase ROCK1. |
| doi_str_mv | 10.1038/s41374-018-0062-3 |
| format | article |
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Deleted in liver cancer 1 (DLC1) is frequently down-regulated in hepatocellular carcinoma tissue and correlates with α-fetoprotein levels, vascular invasion, poor differentiation and poor prognosis. The authors show that DLC1 suppresses the proliferation, migration, invasion and autophagy of hepatocellular carcinoma cells through inactivating Wnt/β-catenin signaling and inhibition of the serine/threonine kinase ROCK1.</description><identifier>ISSN: 0023-6837</identifier><identifier>EISSN: 1530-0307</identifier><identifier>DOI: 10.1038/s41374-018-0062-3</identifier><identifier>PMID: 29785050</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Animals ; Autophagy ; Autophagy - genetics ; Cancer ; Carcinogenesis - genetics ; Carcinoma, Hepatocellular - genetics ; Carcinoma, Hepatocellular - metabolism ; Carcinoma, Hepatocellular - pathology ; Cell Line, Tumor ; Cell proliferation ; Cell Proliferation - genetics ; Gene Expression Regulation, Neoplastic ; GTPase-Activating Proteins - genetics ; GTPase-Activating Proteins - metabolism ; Hep G2 Cells ; Hepatocellular carcinoma ; Humans ; Liver ; Liver cancer ; Liver Neoplasms - genetics ; Liver Neoplasms - metabolism ; Liver Neoplasms - pathology ; Male ; Mice, Inbred BALB C ; Mice, Nude ; Phagocytosis ; Prognosis ; RNA Interference ; RNAi Therapeutics - methods ; Tumor Burden - genetics ; Tumor suppressor genes ; Tumor Suppressor Proteins - genetics ; Tumor Suppressor Proteins - metabolism ; Tumors ; Wnt protein ; Xenograft Model Antitumor Assays - methods ; β-Catenin</subject><ispartof>Laboratory investigation, 2018-08, Vol.98 (8), p.1014-1024</ispartof><rights>2018 United States & Canadian Academy of Pathology</rights><rights>Copyright Nature Publishing Group Aug 2018</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c424t-fb457e02ec925f976c5417160ecb153f4d9180d7d222ea9e865104ffe3567aa3</citedby><cites>FETCH-LOGICAL-c424t-fb457e02ec925f976c5417160ecb153f4d9180d7d222ea9e865104ffe3567aa3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,786,790,27957,27958</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29785050$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wu, Hui-Ta</creatorcontrib><creatorcontrib>Xie, Cheng-Rong</creatorcontrib><creatorcontrib>Lv, Jie</creatorcontrib><creatorcontrib>Qi, He-Qiang</creatorcontrib><creatorcontrib>Wang, Fei</creatorcontrib><creatorcontrib>Zhang, Sheng</creatorcontrib><creatorcontrib>Fang, Qin-Liang</creatorcontrib><creatorcontrib>Wang, Fu-Qiang</creatorcontrib><creatorcontrib>Lu, Yu-Yan</creatorcontrib><creatorcontrib>Yin, Zhen-Yu</creatorcontrib><title>The tumor suppressor DLC1 inhibits cancer progression and oncogenic autophagy in hepatocellular carcinoma</title><title>Laboratory investigation</title><addtitle>Lab Invest</addtitle><description>Downregulation of deleted in liver cancer 1 (DLC1) is associated with poor prognosis of various cancers, but its functional mechanisms in hepatocellular carcinoma (HCC) remains unclear. In the present study, we investigated the roles of DLC1 in tumor progression and autophagy of HCC. We found that DLC1 was frequently downregulated in HCC tissues. Underexpression of DLC1 correlated with AFP level, vascular invasion, poor differentiation, and poor prognosis. In vitro assays revealed that DLC1 not only suppressed the proliferation, migration, and invasion of HCC cells, but also inhibited autophagy of HCC cells. Mechanistic investigation revealed that DLC1 decreased TCF4 expression and the interaction between β-catenin and TCF4, then inactivated Wnt/β-catenin signaling. Additionally, DLC1 suppressed the ROCK1 activity and the dissociation of the Beclin1-Bcl2 complex, thereby inhibiting autophagy of HCC cells. In conclusion, our findings imply that loss of DLC1 contributes to the progression and oncogenic autophagy of HCC.
Deleted in liver cancer 1 (DLC1) is frequently down-regulated in hepatocellular carcinoma tissue and correlates with α-fetoprotein levels, vascular invasion, poor differentiation and poor prognosis. The authors show that DLC1 suppresses the proliferation, migration, invasion and autophagy of hepatocellular carcinoma cells through inactivating Wnt/β-catenin signaling and inhibition of the serine/threonine kinase ROCK1.</description><subject>Animals</subject><subject>Autophagy</subject><subject>Autophagy - genetics</subject><subject>Cancer</subject><subject>Carcinogenesis - genetics</subject><subject>Carcinoma, Hepatocellular - genetics</subject><subject>Carcinoma, Hepatocellular - metabolism</subject><subject>Carcinoma, Hepatocellular - pathology</subject><subject>Cell Line, Tumor</subject><subject>Cell proliferation</subject><subject>Cell Proliferation - genetics</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>GTPase-Activating Proteins - genetics</subject><subject>GTPase-Activating Proteins - metabolism</subject><subject>Hep G2 Cells</subject><subject>Hepatocellular carcinoma</subject><subject>Humans</subject><subject>Liver</subject><subject>Liver cancer</subject><subject>Liver Neoplasms - 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In the present study, we investigated the roles of DLC1 in tumor progression and autophagy of HCC. We found that DLC1 was frequently downregulated in HCC tissues. Underexpression of DLC1 correlated with AFP level, vascular invasion, poor differentiation, and poor prognosis. In vitro assays revealed that DLC1 not only suppressed the proliferation, migration, and invasion of HCC cells, but also inhibited autophagy of HCC cells. Mechanistic investigation revealed that DLC1 decreased TCF4 expression and the interaction between β-catenin and TCF4, then inactivated Wnt/β-catenin signaling. Additionally, DLC1 suppressed the ROCK1 activity and the dissociation of the Beclin1-Bcl2 complex, thereby inhibiting autophagy of HCC cells. In conclusion, our findings imply that loss of DLC1 contributes to the progression and oncogenic autophagy of HCC.
Deleted in liver cancer 1 (DLC1) is frequently down-regulated in hepatocellular carcinoma tissue and correlates with α-fetoprotein levels, vascular invasion, poor differentiation and poor prognosis. The authors show that DLC1 suppresses the proliferation, migration, invasion and autophagy of hepatocellular carcinoma cells through inactivating Wnt/β-catenin signaling and inhibition of the serine/threonine kinase ROCK1.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>29785050</pmid><doi>10.1038/s41374-018-0062-3</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Autophagy Autophagy - genetics Cancer Carcinogenesis - genetics Carcinoma, Hepatocellular - genetics Carcinoma, Hepatocellular - metabolism Carcinoma, Hepatocellular - pathology Cell Line, Tumor Cell proliferation Cell Proliferation - genetics Gene Expression Regulation, Neoplastic GTPase-Activating Proteins - genetics GTPase-Activating Proteins - metabolism Hep G2 Cells Hepatocellular carcinoma Humans Liver Liver cancer Liver Neoplasms - genetics Liver Neoplasms - metabolism Liver Neoplasms - pathology Male Mice, Inbred BALB C Mice, Nude Phagocytosis Prognosis RNA Interference RNAi Therapeutics - methods Tumor Burden - genetics Tumor suppressor genes Tumor Suppressor Proteins - genetics Tumor Suppressor Proteins - metabolism Tumors Wnt protein Xenograft Model Antitumor Assays - methods β-Catenin |
| title | The tumor suppressor DLC1 inhibits cancer progression and oncogenic autophagy in hepatocellular carcinoma |
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