Arylquin 1 (Potent Par-4 Secretagogue) Inhibits Tumor Progression and Induces Apoptosis in Colon Cancer Cells
Colorectal cancer (CRC) is one of the most common gastrointestinal cancers worldwide. Current therapeutic strategies mainly involve surgery and chemoradiotherapy; however, novel antitumor compounds are needed to avoid drug resistance in CRC, as well as the severe side effects of current treatments....
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| Veröffentlicht in: | International journal of molecular sciences 2022-05, Vol.23 (10), p.5645 |
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| description | Colorectal cancer (CRC) is one of the most common gastrointestinal cancers worldwide. Current therapeutic strategies mainly involve surgery and chemoradiotherapy; however, novel antitumor compounds are needed to avoid drug resistance in CRC, as well as the severe side effects of current treatments. In this study, we investigated the anticancer effects and underlying mechanisms of Arylquin 1 in CRC. The MTT assay was used to detect the viability of SW620 and HCT116 cancer cells treated with Arylquin 1 in a dose-dependent manner in vitro. Further, wound-healing and transwell migration assays were used to evaluate the migration and invasion abilities of cultured cells, and Annexin V was used to detect apoptotic cells. Additionally, Western blot was used to identify the expression levels of N-cadherin, caspase-3, cyclin D1, p-extracellular signal-regulated kinase (ERK), p-c-JUN N-terminal kinase (JNK), and phospho-p38, related to key signaling proteins, after administration of Arylquin 1. Xenograft experiments further confirmed the effects of Arylquin 1 on CRC cells in vivo. Arylquin 1 exhibited a dose-dependent reduction in cell viability in cultured CRC cells. It also inhibited cell proliferation, migration, and invasion, and induced apoptosis. Mechanistic analysis demonstrated that Arylquin 1 increased phosphorylation levels of ERK, JNK, and p38. In a mouse xenograft model, Arylquin 1 treatment diminished the growth of colon tumors after injection of cultured cancer cells. Arylquin 1 may have potential anticancer effects and translational significance in the treatment of CRC. |
| doi_str_mv | 10.3390/ijms23105645 |
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Current therapeutic strategies mainly involve surgery and chemoradiotherapy; however, novel antitumor compounds are needed to avoid drug resistance in CRC, as well as the severe side effects of current treatments. In this study, we investigated the anticancer effects and underlying mechanisms of Arylquin 1 in CRC. The MTT assay was used to detect the viability of SW620 and HCT116 cancer cells treated with Arylquin 1 in a dose-dependent manner in vitro. Further, wound-healing and transwell migration assays were used to evaluate the migration and invasion abilities of cultured cells, and Annexin V was used to detect apoptotic cells. Additionally, Western blot was used to identify the expression levels of N-cadherin, caspase-3, cyclin D1, p-extracellular signal-regulated kinase (ERK), p-c-JUN N-terminal kinase (JNK), and phospho-p38, related to key signaling proteins, after administration of Arylquin 1. Xenograft experiments further confirmed the effects of Arylquin 1 on CRC cells in vivo. Arylquin 1 exhibited a dose-dependent reduction in cell viability in cultured CRC cells. It also inhibited cell proliferation, migration, and invasion, and induced apoptosis. Mechanistic analysis demonstrated that Arylquin 1 increased phosphorylation levels of ERK, JNK, and p38. In a mouse xenograft model, Arylquin 1 treatment diminished the growth of colon tumors after injection of cultured cancer cells. Arylquin 1 may have potential anticancer effects and translational significance in the treatment of CRC.</description><identifier>ISSN: 1422-0067</identifier><identifier>ISSN: 1661-6596</identifier><identifier>EISSN: 1422-0067</identifier><identifier>DOI: 10.3390/ijms23105645</identifier><identifier>PMID: 35628455</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Annexin V ; Apoptosis ; c-Jun protein ; Cadherin ; Cancer therapies ; Caspase-3 ; Cell adhesion & migration ; Cell proliferation ; Cell viability ; Chemoradiotherapy ; Chemotherapy ; Colon ; Colon cancer ; Colorectal cancer ; Colorectal carcinoma ; Cyclin D1 ; Cytotoxicity ; Drug dosages ; Drug resistance ; Extracellular signal-regulated kinase ; JNK protein ; Kinases ; Medical prognosis ; Metastasis ; N-Cadherin ; Phosphorylation ; Prostate ; Proteins ; Transcription factors ; Tumors ; Wound healing ; Xenografts ; Xenotransplantation</subject><ispartof>International journal of molecular sciences, 2022-05, Vol.23 (10), p.5645</ispartof><rights>2022 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 (https://creativecommons.org/licenses/by/4.0/). 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Current therapeutic strategies mainly involve surgery and chemoradiotherapy; however, novel antitumor compounds are needed to avoid drug resistance in CRC, as well as the severe side effects of current treatments. In this study, we investigated the anticancer effects and underlying mechanisms of Arylquin 1 in CRC. The MTT assay was used to detect the viability of SW620 and HCT116 cancer cells treated with Arylquin 1 in a dose-dependent manner in vitro. Further, wound-healing and transwell migration assays were used to evaluate the migration and invasion abilities of cultured cells, and Annexin V was used to detect apoptotic cells. Additionally, Western blot was used to identify the expression levels of N-cadherin, caspase-3, cyclin D1, p-extracellular signal-regulated kinase (ERK), p-c-JUN N-terminal kinase (JNK), and phospho-p38, related to key signaling proteins, after administration of Arylquin 1. Xenograft experiments further confirmed the effects of Arylquin 1 on CRC cells in vivo. Arylquin 1 exhibited a dose-dependent reduction in cell viability in cultured CRC cells. It also inhibited cell proliferation, migration, and invasion, and induced apoptosis. Mechanistic analysis demonstrated that Arylquin 1 increased phosphorylation levels of ERK, JNK, and p38. In a mouse xenograft model, Arylquin 1 treatment diminished the growth of colon tumors after injection of cultured cancer cells. Arylquin 1 may have potential anticancer effects and translational significance in the treatment of CRC.</description><subject>Annexin V</subject><subject>Apoptosis</subject><subject>c-Jun protein</subject><subject>Cadherin</subject><subject>Cancer therapies</subject><subject>Caspase-3</subject><subject>Cell adhesion & migration</subject><subject>Cell proliferation</subject><subject>Cell viability</subject><subject>Chemoradiotherapy</subject><subject>Chemotherapy</subject><subject>Colon</subject><subject>Colon cancer</subject><subject>Colorectal cancer</subject><subject>Colorectal carcinoma</subject><subject>Cyclin D1</subject><subject>Cytotoxicity</subject><subject>Drug dosages</subject><subject>Drug resistance</subject><subject>Extracellular signal-regulated kinase</subject><subject>JNK protein</subject><subject>Kinases</subject><subject>Medical prognosis</subject><subject>Metastasis</subject><subject>N-Cadherin</subject><subject>Phosphorylation</subject><subject>Prostate</subject><subject>Proteins</subject><subject>Transcription factors</subject><subject>Tumors</subject><subject>Wound healing</subject><subject>Xenografts</subject><subject>Xenotransplantation</subject><issn>1422-0067</issn><issn>1661-6596</issn><issn>1422-0067</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNpdkc1r3DAQxUVoySZpbz0XQS8pxKm-bV8Ci2k-IJCFbs9C1o53tdjSRrID-e-jkG3Y9DQD78dj3jyEvlFyyXlNfrntkBinRCohj9AJFYwVhKjy08E-Q6cpbQlhnMn6GM24VKwSUp6gYR6f-8fJeUzx-SKM4Ee8MLEQ-A_YCKNZh_UEP_Gd37jWjQkvpyFEvIhhHSElFzw2fpXl1WQh4fku7MaQXMLZsQl9lhvjLUTcQN-nL-hzZ_oEX_fzDP29_r1sbov7h5u7Zn5fWC7YWFRdV1NrK2oMUEUrRg1vBSOltExBKaGE2rK2JUpWCkxneN0STkrgVUnKleFn6OrNdze1A6xsThVNr3fRDSY-62Cc_qh4t9Hr8KRrKrigPBuc7w1ieJwgjXpwyeYIxkOYkmaqpEzV-b8Z_fEfug1T9DneK0VoLQhTmbp4o2wMKUXo3o-hRL_2qA97zPj3wwDv8L_i-AuaOZlE</recordid><startdate>20220518</startdate><enddate>20220518</enddate><creator>Chen, Yi-Ting</creator><creator>Tseng, Tzu-Ting</creator><creator>Tsai, Hung-Pei</creator><creator>Huang, Ming-Yii</creator><general>MDPI AG</general><general>MDPI</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PHGZM</scope><scope>PHGZT</scope><scope>PIMPY</scope><scope>PJZUB</scope><scope>PKEHL</scope><scope>PPXIY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-0817-1539</orcidid><orcidid>https://orcid.org/0000-0001-9432-5284</orcidid></search><sort><creationdate>20220518</creationdate><title>Arylquin 1 (Potent Par-4 Secretagogue) Inhibits Tumor Progression and Induces Apoptosis in Colon Cancer Cells</title><author>Chen, Yi-Ting ; Tseng, Tzu-Ting ; Tsai, Hung-Pei ; Huang, Ming-Yii</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c342t-8ff91cc81aae161821a3b42075c26e75e7e9c2bb06586eafa39b0307e38707da3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Annexin V</topic><topic>Apoptosis</topic><topic>c-Jun protein</topic><topic>Cadherin</topic><topic>Cancer therapies</topic><topic>Caspase-3</topic><topic>Cell adhesion & migration</topic><topic>Cell proliferation</topic><topic>Cell viability</topic><topic>Chemoradiotherapy</topic><topic>Chemotherapy</topic><topic>Colon</topic><topic>Colon cancer</topic><topic>Colorectal cancer</topic><topic>Colorectal carcinoma</topic><topic>Cyclin D1</topic><topic>Cytotoxicity</topic><topic>Drug dosages</topic><topic>Drug resistance</topic><topic>Extracellular signal-regulated kinase</topic><topic>JNK protein</topic><topic>Kinases</topic><topic>Medical prognosis</topic><topic>Metastasis</topic><topic>N-Cadherin</topic><topic>Phosphorylation</topic><topic>Prostate</topic><topic>Proteins</topic><topic>Transcription factors</topic><topic>Tumors</topic><topic>Wound healing</topic><topic>Xenografts</topic><topic>Xenotransplantation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chen, Yi-Ting</creatorcontrib><creatorcontrib>Tseng, Tzu-Ting</creatorcontrib><creatorcontrib>Tsai, Hung-Pei</creatorcontrib><creatorcontrib>Huang, Ming-Yii</creatorcontrib><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>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</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>Research Library Prep</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</collection><collection>ProQuest Central (New)</collection><collection>ProQuest One Academic (New)</collection><collection>Publicly Available Content Database</collection><collection>ProQuest Health & Medical Research Collection</collection><collection>ProQuest One Academic Middle East (New)</collection><collection>ProQuest One Health & Nursing</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>International journal of molecular sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chen, Yi-Ting</au><au>Tseng, Tzu-Ting</au><au>Tsai, Hung-Pei</au><au>Huang, Ming-Yii</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Arylquin 1 (Potent Par-4 Secretagogue) Inhibits Tumor Progression and Induces Apoptosis in Colon Cancer Cells</atitle><jtitle>International journal of molecular sciences</jtitle><addtitle>Int J Mol Sci</addtitle><date>2022-05-18</date><risdate>2022</risdate><volume>23</volume><issue>10</issue><spage>5645</spage><pages>5645-</pages><issn>1422-0067</issn><issn>1661-6596</issn><eissn>1422-0067</eissn><abstract>Colorectal cancer (CRC) is one of the most common gastrointestinal cancers worldwide. Current therapeutic strategies mainly involve surgery and chemoradiotherapy; however, novel antitumor compounds are needed to avoid drug resistance in CRC, as well as the severe side effects of current treatments. In this study, we investigated the anticancer effects and underlying mechanisms of Arylquin 1 in CRC. The MTT assay was used to detect the viability of SW620 and HCT116 cancer cells treated with Arylquin 1 in a dose-dependent manner in vitro. Further, wound-healing and transwell migration assays were used to evaluate the migration and invasion abilities of cultured cells, and Annexin V was used to detect apoptotic cells. Additionally, Western blot was used to identify the expression levels of N-cadherin, caspase-3, cyclin D1, p-extracellular signal-regulated kinase (ERK), p-c-JUN N-terminal kinase (JNK), and phospho-p38, related to key signaling proteins, after administration of Arylquin 1. Xenograft experiments further confirmed the effects of Arylquin 1 on CRC cells in vivo. Arylquin 1 exhibited a dose-dependent reduction in cell viability in cultured CRC cells. It also inhibited cell proliferation, migration, and invasion, and induced apoptosis. Mechanistic analysis demonstrated that Arylquin 1 increased phosphorylation levels of ERK, JNK, and p38. In a mouse xenograft model, Arylquin 1 treatment diminished the growth of colon tumors after injection of cultured cancer cells. Arylquin 1 may have potential anticancer effects and translational significance in the treatment of CRC.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>35628455</pmid><doi>10.3390/ijms23105645</doi><orcidid>https://orcid.org/0000-0002-0817-1539</orcidid><orcidid>https://orcid.org/0000-0001-9432-5284</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Annexin V Apoptosis c-Jun protein Cadherin Cancer therapies Caspase-3 Cell adhesion & migration Cell proliferation Cell viability Chemoradiotherapy Chemotherapy Colon Colon cancer Colorectal cancer Colorectal carcinoma Cyclin D1 Cytotoxicity Drug dosages Drug resistance Extracellular signal-regulated kinase JNK protein Kinases Medical prognosis Metastasis N-Cadherin Phosphorylation Prostate Proteins Transcription factors Tumors Wound healing Xenografts Xenotransplantation |
| title | Arylquin 1 (Potent Par-4 Secretagogue) Inhibits Tumor Progression and Induces Apoptosis in Colon Cancer Cells |
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