Association of ATG4B and Phosphorylated ATG4B Proteins with Tumorigenesis and Prognosis in Oral Squamous Cell Carcinoma
Oral squamous cell carcinoma (OSCC) is one of the major leading causes of cancer death worldwide due to the limited availability of biomarkers and therapeutic targets. Autophagy related protease 4B (ATG4B) is an essential protease for the autophagy machinery, and ATG4B phosphorylation at Ser383/392...
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creator | Liu, Pei-Feng Chen, Hung-Chih Cheng, Jin-Shiung Tsai, Wei-Lun Lee, Huai-Pao Wang, Shu-Chi Peng, Wei-Hao Lee, Cheng-Hsin Ger, Luo-Ping Shu, Chih-Wen |
description | Oral squamous cell carcinoma (OSCC) is one of the major leading causes of cancer death worldwide due to the limited availability of biomarkers and therapeutic targets. Autophagy related protease 4B (ATG4B) is an essential protease for the autophagy machinery, and ATG4B phosphorylation at Ser383/392 increases its proteolytic activity. ATG4B expression and activation are crucial for cancer cell proliferation and invasion. However, the clinical relevance of ATG4B and phospho-Ser383/392-ATG4B for OSCC remains unknown, particularly in buccal mucosal SCC (BMSCC) and tongue SCC (TSCC). With a tissue microarray comprising specimens from 498 OSCC patients, including 179 BMSCC and 249 TSCC patients, we found that the protein levels of ATG4B and phospho-Ser383/392-ATG4B were elevated in the tumor tissues of BMSCC and TSCC compared with those in adjacent normal tissues. High protein levels of ATG4B were significantly associated with worse disease-specific survival (DSS) in OSCC patients, particularly in patients with tumors at advanced stages. In contrast, phospho-Ser383/392-ATG4B expression was correlated with poor disease-free survival (DFS) in TSCC patients. Moreover, ATG4B protein expression was positively correlated with phospho-Ser383/392-ATG4B expression in both BMSCC and TSCC. However, high coexpression levels of ATG4B and phospho-Ser383/392-ATG4B were associated with poor DFS only in TSCC patients, whereas they had no significant association with DSS in BMSCC and TSCC patients. In addition, silencing ATG4B with an antisense oligonucleotide (ASO) or small interfering RNA (siRNA) diminished cell proliferation of TW2.6 and SAS oral cancer cells. Further, knockdown of ATG4B reduced cell migration and invasion of oral cancer cells. Taken together, these findings suggest that ATG4B might be a biomarker for diagnosis/prognosis of OSCC and a potential therapeutic target for OSCC patients. |
doi_str_mv | 10.3390/cancers11121854 |
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Autophagy related protease 4B (ATG4B) is an essential protease for the autophagy machinery, and ATG4B phosphorylation at Ser383/392 increases its proteolytic activity. ATG4B expression and activation are crucial for cancer cell proliferation and invasion. However, the clinical relevance of ATG4B and phospho-Ser383/392-ATG4B for OSCC remains unknown, particularly in buccal mucosal SCC (BMSCC) and tongue SCC (TSCC). With a tissue microarray comprising specimens from 498 OSCC patients, including 179 BMSCC and 249 TSCC patients, we found that the protein levels of ATG4B and phospho-Ser383/392-ATG4B were elevated in the tumor tissues of BMSCC and TSCC compared with those in adjacent normal tissues. High protein levels of ATG4B were significantly associated with worse disease-specific survival (DSS) in OSCC patients, particularly in patients with tumors at advanced stages. In contrast, phospho-Ser383/392-ATG4B expression was correlated with poor disease-free survival (DFS) in TSCC patients. Moreover, ATG4B protein expression was positively correlated with phospho-Ser383/392-ATG4B expression in both BMSCC and TSCC. However, high coexpression levels of ATG4B and phospho-Ser383/392-ATG4B were associated with poor DFS only in TSCC patients, whereas they had no significant association with DSS in BMSCC and TSCC patients. In addition, silencing ATG4B with an antisense oligonucleotide (ASO) or small interfering RNA (siRNA) diminished cell proliferation of TW2.6 and SAS oral cancer cells. Further, knockdown of ATG4B reduced cell migration and invasion of oral cancer cells. Taken together, these findings suggest that ATG4B might be a biomarker for diagnosis/prognosis of OSCC and a potential therapeutic target for OSCC patients.</description><identifier>ISSN: 2072-6694</identifier><identifier>EISSN: 2072-6694</identifier><identifier>DOI: 10.3390/cancers11121854</identifier><identifier>PMID: 31771238</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Antibodies ; Antisense oligonucleotides ; Autophagy ; Biomarkers ; Cancer therapies ; Cell culture ; Cell growth ; Cell migration ; Cell proliferation ; Colorectal cancer ; Medical prognosis ; Mucosa ; Oral cancer ; Oral squamous cell carcinoma ; Patients ; Peptides ; Phagocytosis ; Phosphorylation ; Prognosis ; Protein expression ; Proteinase ; Proteins ; Proteolysis ; siRNA ; Squamous cell carcinoma ; Survival analysis ; Therapeutic applications ; Therapeutic targets ; Tumorigenesis</subject><ispartof>Cancers, 2019-11, Vol.11 (12), p.1854</ispartof><rights>2019 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2019 by the authors. 2019</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c421t-3eabf80b51148743e854219df619c4d079587f3fb3f4083d04ca74578dae96d33</citedby><cites>FETCH-LOGICAL-c421t-3eabf80b51148743e854219df619c4d079587f3fb3f4083d04ca74578dae96d33</cites><orcidid>0000-0002-7774-0002 ; 0000-0002-7849-8940</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6966594/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6966594/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27903,27904,53769,53771</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31771238$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Liu, Pei-Feng</creatorcontrib><creatorcontrib>Chen, Hung-Chih</creatorcontrib><creatorcontrib>Cheng, Jin-Shiung</creatorcontrib><creatorcontrib>Tsai, Wei-Lun</creatorcontrib><creatorcontrib>Lee, Huai-Pao</creatorcontrib><creatorcontrib>Wang, Shu-Chi</creatorcontrib><creatorcontrib>Peng, Wei-Hao</creatorcontrib><creatorcontrib>Lee, Cheng-Hsin</creatorcontrib><creatorcontrib>Ger, Luo-Ping</creatorcontrib><creatorcontrib>Shu, Chih-Wen</creatorcontrib><title>Association of ATG4B and Phosphorylated ATG4B Proteins with Tumorigenesis and Prognosis in Oral Squamous Cell Carcinoma</title><title>Cancers</title><addtitle>Cancers (Basel)</addtitle><description>Oral squamous cell carcinoma (OSCC) is one of the major leading causes of cancer death worldwide due to the limited availability of biomarkers and therapeutic targets. Autophagy related protease 4B (ATG4B) is an essential protease for the autophagy machinery, and ATG4B phosphorylation at Ser383/392 increases its proteolytic activity. ATG4B expression and activation are crucial for cancer cell proliferation and invasion. However, the clinical relevance of ATG4B and phospho-Ser383/392-ATG4B for OSCC remains unknown, particularly in buccal mucosal SCC (BMSCC) and tongue SCC (TSCC). With a tissue microarray comprising specimens from 498 OSCC patients, including 179 BMSCC and 249 TSCC patients, we found that the protein levels of ATG4B and phospho-Ser383/392-ATG4B were elevated in the tumor tissues of BMSCC and TSCC compared with those in adjacent normal tissues. High protein levels of ATG4B were significantly associated with worse disease-specific survival (DSS) in OSCC patients, particularly in patients with tumors at advanced stages. In contrast, phospho-Ser383/392-ATG4B expression was correlated with poor disease-free survival (DFS) in TSCC patients. Moreover, ATG4B protein expression was positively correlated with phospho-Ser383/392-ATG4B expression in both BMSCC and TSCC. However, high coexpression levels of ATG4B and phospho-Ser383/392-ATG4B were associated with poor DFS only in TSCC patients, whereas they had no significant association with DSS in BMSCC and TSCC patients. In addition, silencing ATG4B with an antisense oligonucleotide (ASO) or small interfering RNA (siRNA) diminished cell proliferation of TW2.6 and SAS oral cancer cells. Further, knockdown of ATG4B reduced cell migration and invasion of oral cancer cells. Taken together, these findings suggest that ATG4B might be a biomarker for diagnosis/prognosis of OSCC and a potential therapeutic target for OSCC patients.</description><subject>Antibodies</subject><subject>Antisense oligonucleotides</subject><subject>Autophagy</subject><subject>Biomarkers</subject><subject>Cancer therapies</subject><subject>Cell culture</subject><subject>Cell growth</subject><subject>Cell migration</subject><subject>Cell proliferation</subject><subject>Colorectal cancer</subject><subject>Medical prognosis</subject><subject>Mucosa</subject><subject>Oral cancer</subject><subject>Oral squamous cell carcinoma</subject><subject>Patients</subject><subject>Peptides</subject><subject>Phagocytosis</subject><subject>Phosphorylation</subject><subject>Prognosis</subject><subject>Protein expression</subject><subject>Proteinase</subject><subject>Proteins</subject><subject>Proteolysis</subject><subject>siRNA</subject><subject>Squamous cell carcinoma</subject><subject>Survival analysis</subject><subject>Therapeutic applications</subject><subject>Therapeutic targets</subject><subject>Tumorigenesis</subject><issn>2072-6694</issn><issn>2072-6694</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNpdkUtLAzEUhYMotqhrdxJw46aa1ySTjVCLLxAUrOuQZjJtykzSJjOK_96UVlGzuQn3u4d7cgA4xeiSUomujPbGxoQxJrgs2B4YEiTIiHPJ9n_dB-AkpSXKh1IsuDgEg1wFJrQcgo9xSsE43bngYajheHrPbqD2FXxZhLRahPjZ6M5Wu8ZLDJ11PsEP1y3gtG9DdHPrbXJpOxTD3IfNy3n4HHUDX9e9bkOf4MQ2DZzoaJwPrT4GB7Vukj3Z1SPwdnc7nTyMnp7vHyfjp5FhBHcjavWsLtGswJiVglGbfRIsq5pjaViFhCxKUdN6RmuGSlohZrRghSgrbSWvKD0C11vdVT9rbWWs7_JWahVdq-OnCtqpvx3vFmoe3hWXnBeSZYGLnUAM696mTrUumexFe5ttKUKxJPlrmcjo-T90Gfrosz1FCiYKXDC-oa62lIkhpWjrn2UwUptc1b9c88TZbw8__HeK9Aszyp_g</recordid><startdate>20191123</startdate><enddate>20191123</enddate><creator>Liu, Pei-Feng</creator><creator>Chen, Hung-Chih</creator><creator>Cheng, Jin-Shiung</creator><creator>Tsai, Wei-Lun</creator><creator>Lee, Huai-Pao</creator><creator>Wang, Shu-Chi</creator><creator>Peng, Wei-Hao</creator><creator>Lee, Cheng-Hsin</creator><creator>Ger, Luo-Ping</creator><creator>Shu, Chih-Wen</creator><general>MDPI AG</general><general>MDPI</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7T5</scope><scope>7TO</scope><scope>7XB</scope><scope>8FE</scope><scope>8FH</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>HCIFZ</scope><scope>LK8</scope><scope>M2O</scope><scope>M7P</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-7774-0002</orcidid><orcidid>https://orcid.org/0000-0002-7849-8940</orcidid></search><sort><creationdate>20191123</creationdate><title>Association of ATG4B and Phosphorylated ATG4B Proteins with Tumorigenesis and Prognosis in Oral Squamous Cell Carcinoma</title><author>Liu, Pei-Feng ; Chen, Hung-Chih ; Cheng, Jin-Shiung ; Tsai, Wei-Lun ; Lee, Huai-Pao ; Wang, Shu-Chi ; Peng, Wei-Hao ; Lee, Cheng-Hsin ; Ger, Luo-Ping ; Shu, Chih-Wen</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c421t-3eabf80b51148743e854219df619c4d079587f3fb3f4083d04ca74578dae96d33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Antibodies</topic><topic>Antisense oligonucleotides</topic><topic>Autophagy</topic><topic>Biomarkers</topic><topic>Cancer therapies</topic><topic>Cell culture</topic><topic>Cell growth</topic><topic>Cell migration</topic><topic>Cell proliferation</topic><topic>Colorectal cancer</topic><topic>Medical prognosis</topic><topic>Mucosa</topic><topic>Oral cancer</topic><topic>Oral squamous cell carcinoma</topic><topic>Patients</topic><topic>Peptides</topic><topic>Phagocytosis</topic><topic>Phosphorylation</topic><topic>Prognosis</topic><topic>Protein expression</topic><topic>Proteinase</topic><topic>Proteins</topic><topic>Proteolysis</topic><topic>siRNA</topic><topic>Squamous cell carcinoma</topic><topic>Survival analysis</topic><topic>Therapeutic applications</topic><topic>Therapeutic targets</topic><topic>Tumorigenesis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Liu, Pei-Feng</creatorcontrib><creatorcontrib>Chen, Hung-Chih</creatorcontrib><creatorcontrib>Cheng, Jin-Shiung</creatorcontrib><creatorcontrib>Tsai, Wei-Lun</creatorcontrib><creatorcontrib>Lee, Huai-Pao</creatorcontrib><creatorcontrib>Wang, Shu-Chi</creatorcontrib><creatorcontrib>Peng, Wei-Hao</creatorcontrib><creatorcontrib>Lee, Cheng-Hsin</creatorcontrib><creatorcontrib>Ger, Luo-Ping</creatorcontrib><creatorcontrib>Shu, Chih-Wen</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Research Library</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</collection><collection>Publicly Available Content Database</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 Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cancers</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Liu, Pei-Feng</au><au>Chen, Hung-Chih</au><au>Cheng, Jin-Shiung</au><au>Tsai, Wei-Lun</au><au>Lee, Huai-Pao</au><au>Wang, Shu-Chi</au><au>Peng, Wei-Hao</au><au>Lee, Cheng-Hsin</au><au>Ger, Luo-Ping</au><au>Shu, Chih-Wen</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Association of ATG4B and Phosphorylated ATG4B Proteins with Tumorigenesis and Prognosis in Oral Squamous Cell Carcinoma</atitle><jtitle>Cancers</jtitle><addtitle>Cancers (Basel)</addtitle><date>2019-11-23</date><risdate>2019</risdate><volume>11</volume><issue>12</issue><spage>1854</spage><pages>1854-</pages><issn>2072-6694</issn><eissn>2072-6694</eissn><abstract>Oral squamous cell carcinoma (OSCC) is one of the major leading causes of cancer death worldwide due to the limited availability of biomarkers and therapeutic targets. Autophagy related protease 4B (ATG4B) is an essential protease for the autophagy machinery, and ATG4B phosphorylation at Ser383/392 increases its proteolytic activity. ATG4B expression and activation are crucial for cancer cell proliferation and invasion. However, the clinical relevance of ATG4B and phospho-Ser383/392-ATG4B for OSCC remains unknown, particularly in buccal mucosal SCC (BMSCC) and tongue SCC (TSCC). With a tissue microarray comprising specimens from 498 OSCC patients, including 179 BMSCC and 249 TSCC patients, we found that the protein levels of ATG4B and phospho-Ser383/392-ATG4B were elevated in the tumor tissues of BMSCC and TSCC compared with those in adjacent normal tissues. High protein levels of ATG4B were significantly associated with worse disease-specific survival (DSS) in OSCC patients, particularly in patients with tumors at advanced stages. In contrast, phospho-Ser383/392-ATG4B expression was correlated with poor disease-free survival (DFS) in TSCC patients. Moreover, ATG4B protein expression was positively correlated with phospho-Ser383/392-ATG4B expression in both BMSCC and TSCC. However, high coexpression levels of ATG4B and phospho-Ser383/392-ATG4B were associated with poor DFS only in TSCC patients, whereas they had no significant association with DSS in BMSCC and TSCC patients. In addition, silencing ATG4B with an antisense oligonucleotide (ASO) or small interfering RNA (siRNA) diminished cell proliferation of TW2.6 and SAS oral cancer cells. Further, knockdown of ATG4B reduced cell migration and invasion of oral cancer cells. Taken together, these findings suggest that ATG4B might be a biomarker for diagnosis/prognosis of OSCC and a potential therapeutic target for OSCC patients.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>31771238</pmid><doi>10.3390/cancers11121854</doi><orcidid>https://orcid.org/0000-0002-7774-0002</orcidid><orcidid>https://orcid.org/0000-0002-7849-8940</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Antibodies Antisense oligonucleotides Autophagy Biomarkers Cancer therapies Cell culture Cell growth Cell migration Cell proliferation Colorectal cancer Medical prognosis Mucosa Oral cancer Oral squamous cell carcinoma Patients Peptides Phagocytosis Phosphorylation Prognosis Protein expression Proteinase Proteins Proteolysis siRNA Squamous cell carcinoma Survival analysis Therapeutic applications Therapeutic targets Tumorigenesis |
title | Association of ATG4B and Phosphorylated ATG4B Proteins with Tumorigenesis and Prognosis in Oral Squamous Cell Carcinoma |
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