CSC‐3436 inhibits TWIST‐induced epithelial–mesenchymal transition via the suppression of Twist/Bmi1/Akt pathway in head and neck squamous cell carcinoma
Head and neck squamous cell carcinoma (HNSCC) is one of the leading causes of cancer deaths worldwide, especially in male. With poor prognosis, significant portions of patients with HNSCC die due to cancer recurrence and tumor metastasis after chemotherapy and targeted therapies. The HNSCC FaDu cell...
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| Veröffentlicht in: | Journal of cellular physiology 2019-06, Vol.234 (6), p.9118-9129 |
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| creator | Lai, Ying‐Ju Yu, Wan‐Nien Kuo, Sheng‐Chu Ho, Chi‐Tang Hung, Chao‐Ming Way, Tzong‐Der Chen, Chiung‐Tong |
| description | Head and neck squamous cell carcinoma (HNSCC) is one of the leading causes of cancer deaths worldwide, especially in male. With poor prognosis, significant portions of patients with HNSCC die due to cancer recurrence and tumor metastasis after chemotherapy and targeted therapies. The HNSCC FaDu cell ectopic expression of Twist, a key transcriptional factor of epithelial–mesenchymal transition (EMT), which triggers EMT and results in the acquisition of a mesenchymal phenotype, was used as the cell model. Our results demonstrated that treatment with newly synthesized 2‐(3‐hydroxyphenyl)‐5‐methylnaphthyridin‐4‐one (CSC‐3436), a flavonoid derivative, elicited changes in its cell morphology, upregulated E‐cadherin messenger RNA and protein expression, downregulated N‐cadherin, vimentin, and CD133 (a marker associated with tumor‐initiating cells) in FaDu‐pCDH‐Twist cells. Moreover, CSC‐3436 exposure reduced B cell‐specific Moloney murine leukemia virus integration site 1 (Bmi1) expression regulated by Twist and further suppressed the direct co‐regulation of E‐cadherin by Twist and Bmi1. Interestingly, CSC‐3436 reduced EMT, cancer stemness, and migration/invasion abilities through the inhibition of the Twist/Bmi1‐Akt/β‐catenin pathway. Most importantly, our findings provided new evidence that CSC‐3436 played a crucial role in therapeutic targeting to Bmi1 and its molecular pathway in HNSCC, and it will be valuable in prognostic prediction and treatment.
2‐(3‐Hydroxyphenyl)‐5‐methylnaphthyridin‐4‐one (CSC‐3436) reduced Twist‐induced epithelial–mesenchymal transition, tumor‐initiating abilities and migration/invasion through the inhibition of the Twist/Bmi1‐Akt/β‐catenin pathway. Simultaneously, CSC‐3436 exposure reduced B cell‐specific Moloney murine leukemia virus integration site 1 (Bmi1) regulated by Twist and in further suppressed the direct co‐regulation of E‐cadherin by Twist and Bmi1. |
| doi_str_mv | 10.1002/jcp.27589 |
| format | Article |
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2‐(3‐Hydroxyphenyl)‐5‐methylnaphthyridin‐4‐one (CSC‐3436) reduced Twist‐induced epithelial–mesenchymal transition, tumor‐initiating abilities and migration/invasion through the inhibition of the Twist/Bmi1‐Akt/β‐catenin pathway. Simultaneously, CSC‐3436 exposure reduced B cell‐specific Moloney murine leukemia virus integration site 1 (Bmi1) regulated by Twist and in further suppressed the direct co‐regulation of E‐cadherin by Twist and Bmi1.</description><identifier>ISSN: 0021-9541</identifier><identifier>EISSN: 1097-4652</identifier><identifier>DOI: 10.1002/jcp.27589</identifier><identifier>PMID: 30341909</identifier><language>eng</language><publisher>United States: Wiley Subscription Services, Inc</publisher><subject>2‐(3‐hydroxyphenyl)‐5‐methylnaphthyridin‐4‐one (CSC‐3436) ; AKT protein ; Animals ; Antigens, CD - genetics ; Antigens, CD - metabolism ; Antineoplastic Agents - pharmacology ; B cell‐specific Moloney murine leukemia virus integration site 1 (Bmi1) ; Cadherins - genetics ; Cadherins - metabolism ; Cancer ; Cell Line, Tumor ; Cell morphology ; Cell Movement - drug effects ; Chemotherapy ; Cytology ; E-cadherin ; Ectopic expression ; Epithelial-Mesenchymal Transition - drug effects ; epithelial–mesenchymal transition (EMT) ; Female ; Gene expression ; Gene Expression Regulation, Neoplastic ; Gene therapy ; Head & neck cancer ; Head and Neck Neoplasms - drug therapy ; Head and Neck Neoplasms - enzymology ; Head and Neck Neoplasms - genetics ; Head and Neck Neoplasms - pathology ; head and neck squamous cell carcinoma (HNSCC) ; Humans ; Leukemia ; Lymphocytes B ; Mesenchyme ; Metastases ; Mice, Inbred NOD ; Mice, SCID ; Morphology ; Naphthyridines - pharmacology ; Neoplasm Invasiveness ; Nuclear Proteins - genetics ; Nuclear Proteins - metabolism ; Phenotypes ; Polycomb Repressive Complex 1 - genetics ; Polycomb Repressive Complex 1 - metabolism ; Proteins ; Proto-Oncogene Proteins c-akt - metabolism ; Ribonucleic acid ; RNA ; Signal Transduction ; Squamous cell carcinoma ; Squamous Cell Carcinoma of Head and Neck - drug therapy ; Squamous Cell Carcinoma of Head and Neck - enzymology ; Squamous Cell Carcinoma of Head and Neck - genetics ; Squamous Cell Carcinoma of Head and Neck - secondary ; Therapeutic targets ; Tumors ; twist ; Twist-Related Protein 1 - genetics ; Twist-Related Protein 1 - metabolism ; Vimentin ; Viruses ; Xenograft Model Antitumor Assays</subject><ispartof>Journal of cellular physiology, 2019-06, Vol.234 (6), p.9118-9129</ispartof><rights>2018 Wiley Periodicals, Inc.</rights><rights>2019 Wiley Periodicals, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3539-e862412dac23457b56967c2ea9d2a1de18ed663365027fbdead9711c0c62da733</citedby><cites>FETCH-LOGICAL-c3539-e862412dac23457b56967c2ea9d2a1de18ed663365027fbdead9711c0c62da733</cites><orcidid>0000-0002-8423-8969</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fjcp.27589$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fjcp.27589$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>315,781,785,1418,27929,27930,45579,45580</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30341909$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lai, Ying‐Ju</creatorcontrib><creatorcontrib>Yu, Wan‐Nien</creatorcontrib><creatorcontrib>Kuo, Sheng‐Chu</creatorcontrib><creatorcontrib>Ho, Chi‐Tang</creatorcontrib><creatorcontrib>Hung, Chao‐Ming</creatorcontrib><creatorcontrib>Way, Tzong‐Der</creatorcontrib><creatorcontrib>Chen, Chiung‐Tong</creatorcontrib><title>CSC‐3436 inhibits TWIST‐induced epithelial–mesenchymal transition via the suppression of Twist/Bmi1/Akt pathway in head and neck squamous cell carcinoma</title><title>Journal of cellular physiology</title><addtitle>J Cell Physiol</addtitle><description>Head and neck squamous cell carcinoma (HNSCC) is one of the leading causes of cancer deaths worldwide, especially in male. With poor prognosis, significant portions of patients with HNSCC die due to cancer recurrence and tumor metastasis after chemotherapy and targeted therapies. The HNSCC FaDu cell ectopic expression of Twist, a key transcriptional factor of epithelial–mesenchymal transition (EMT), which triggers EMT and results in the acquisition of a mesenchymal phenotype, was used as the cell model. Our results demonstrated that treatment with newly synthesized 2‐(3‐hydroxyphenyl)‐5‐methylnaphthyridin‐4‐one (CSC‐3436), a flavonoid derivative, elicited changes in its cell morphology, upregulated E‐cadherin messenger RNA and protein expression, downregulated N‐cadherin, vimentin, and CD133 (a marker associated with tumor‐initiating cells) in FaDu‐pCDH‐Twist cells. Moreover, CSC‐3436 exposure reduced B cell‐specific Moloney murine leukemia virus integration site 1 (Bmi1) expression regulated by Twist and further suppressed the direct co‐regulation of E‐cadherin by Twist and Bmi1. Interestingly, CSC‐3436 reduced EMT, cancer stemness, and migration/invasion abilities through the inhibition of the Twist/Bmi1‐Akt/β‐catenin pathway. Most importantly, our findings provided new evidence that CSC‐3436 played a crucial role in therapeutic targeting to Bmi1 and its molecular pathway in HNSCC, and it will be valuable in prognostic prediction and treatment.
2‐(3‐Hydroxyphenyl)‐5‐methylnaphthyridin‐4‐one (CSC‐3436) reduced Twist‐induced epithelial–mesenchymal transition, tumor‐initiating abilities and migration/invasion through the inhibition of the Twist/Bmi1‐Akt/β‐catenin pathway. Simultaneously, CSC‐3436 exposure reduced B cell‐specific Moloney murine leukemia virus integration site 1 (Bmi1) regulated by Twist and in further suppressed the direct co‐regulation of E‐cadherin by Twist and Bmi1.</description><subject>2‐(3‐hydroxyphenyl)‐5‐methylnaphthyridin‐4‐one (CSC‐3436)</subject><subject>AKT protein</subject><subject>Animals</subject><subject>Antigens, CD - genetics</subject><subject>Antigens, CD - metabolism</subject><subject>Antineoplastic Agents - pharmacology</subject><subject>B cell‐specific Moloney murine leukemia virus integration site 1 (Bmi1)</subject><subject>Cadherins - genetics</subject><subject>Cadherins - metabolism</subject><subject>Cancer</subject><subject>Cell Line, Tumor</subject><subject>Cell morphology</subject><subject>Cell Movement - drug effects</subject><subject>Chemotherapy</subject><subject>Cytology</subject><subject>E-cadherin</subject><subject>Ectopic expression</subject><subject>Epithelial-Mesenchymal Transition - drug effects</subject><subject>epithelial–mesenchymal transition (EMT)</subject><subject>Female</subject><subject>Gene expression</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Gene therapy</subject><subject>Head & neck cancer</subject><subject>Head and Neck Neoplasms - drug therapy</subject><subject>Head and Neck Neoplasms - enzymology</subject><subject>Head and Neck Neoplasms - genetics</subject><subject>Head and Neck Neoplasms - pathology</subject><subject>head and neck squamous cell carcinoma (HNSCC)</subject><subject>Humans</subject><subject>Leukemia</subject><subject>Lymphocytes B</subject><subject>Mesenchyme</subject><subject>Metastases</subject><subject>Mice, Inbred NOD</subject><subject>Mice, SCID</subject><subject>Morphology</subject><subject>Naphthyridines - pharmacology</subject><subject>Neoplasm Invasiveness</subject><subject>Nuclear Proteins - genetics</subject><subject>Nuclear Proteins - metabolism</subject><subject>Phenotypes</subject><subject>Polycomb Repressive Complex 1 - genetics</subject><subject>Polycomb Repressive Complex 1 - metabolism</subject><subject>Proteins</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Ribonucleic acid</subject><subject>RNA</subject><subject>Signal Transduction</subject><subject>Squamous cell carcinoma</subject><subject>Squamous Cell Carcinoma of Head and Neck - drug therapy</subject><subject>Squamous Cell Carcinoma of Head and Neck - enzymology</subject><subject>Squamous Cell Carcinoma of Head and Neck - genetics</subject><subject>Squamous Cell Carcinoma of Head and Neck - secondary</subject><subject>Therapeutic targets</subject><subject>Tumors</subject><subject>twist</subject><subject>Twist-Related Protein 1 - genetics</subject><subject>Twist-Related Protein 1 - metabolism</subject><subject>Vimentin</subject><subject>Viruses</subject><subject>Xenograft Model Antitumor Assays</subject><issn>0021-9541</issn><issn>1097-4652</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kc1u1DAURi0EosPAghdAltjQRTr-SZzxskQUiiqB1EEsozv2HcXTxEnthNHs-ghI7Hm4PgkeprBAYmXp-txzP-kj5CVnZ5wxsdia4UyUxVI_IjPOdJnlqhCPySz98UwXOT8hz2LcMsa0lvIpOZFM5lwzPSM_q-vq_u67zKWizjdu7cZIV18vr1dp6rydDFqKgxsbbB2093c_OozoTbPvoKVjAB_d6HpPvzmgCaJxGoaAMR5m_Yaudi6Oi7ed44vzm5EOMDY72KdTtEGwFLylHs0NjbcTdP0UqcG2pQaCcb7v4Dl5soE24ouHd06-XLxbVR-yq0_vL6vzq8zIQuoMl0rkXFgwQuZFuS6UVqURCNoK4Bb5Eq1SUqqCiXKztum0Ljk3zKi0VEo5J2-O3iH0txPGse5cPEQBjylVLbiQpZAqSebk9T_otp-CT-kStZQ6RWEH4emRMqGPMeCmHoLrIOxrzupDaXUqrf5dWmJfPRindYf2L_mnpQQsjsDOtbj_v6n-WH0-Kn8BaQWkcw</recordid><startdate>201906</startdate><enddate>201906</enddate><creator>Lai, Ying‐Ju</creator><creator>Yu, Wan‐Nien</creator><creator>Kuo, Sheng‐Chu</creator><creator>Ho, Chi‐Tang</creator><creator>Hung, Chao‐Ming</creator><creator>Way, Tzong‐Der</creator><creator>Chen, Chiung‐Tong</creator><general>Wiley Subscription Services, Inc</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>7TK</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>K9.</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-8423-8969</orcidid></search><sort><creationdate>201906</creationdate><title>CSC‐3436 inhibits TWIST‐induced epithelial–mesenchymal transition via the suppression of Twist/Bmi1/Akt pathway in head and neck squamous cell carcinoma</title><author>Lai, Ying‐Ju ; Yu, Wan‐Nien ; Kuo, Sheng‐Chu ; Ho, Chi‐Tang ; Hung, Chao‐Ming ; Way, Tzong‐Der ; Chen, Chiung‐Tong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3539-e862412dac23457b56967c2ea9d2a1de18ed663365027fbdead9711c0c62da733</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>2‐(3‐hydroxyphenyl)‐5‐methylnaphthyridin‐4‐one (CSC‐3436)</topic><topic>AKT protein</topic><topic>Animals</topic><topic>Antigens, CD - genetics</topic><topic>Antigens, CD - metabolism</topic><topic>Antineoplastic Agents - pharmacology</topic><topic>B cell‐specific Moloney murine leukemia virus integration site 1 (Bmi1)</topic><topic>Cadherins - genetics</topic><topic>Cadherins - metabolism</topic><topic>Cancer</topic><topic>Cell Line, Tumor</topic><topic>Cell morphology</topic><topic>Cell Movement - drug effects</topic><topic>Chemotherapy</topic><topic>Cytology</topic><topic>E-cadherin</topic><topic>Ectopic expression</topic><topic>Epithelial-Mesenchymal Transition - drug effects</topic><topic>epithelial–mesenchymal transition (EMT)</topic><topic>Female</topic><topic>Gene expression</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Gene therapy</topic><topic>Head & neck cancer</topic><topic>Head and Neck Neoplasms - drug therapy</topic><topic>Head and Neck Neoplasms - enzymology</topic><topic>Head and Neck Neoplasms - genetics</topic><topic>Head and Neck Neoplasms - pathology</topic><topic>head and neck squamous cell carcinoma (HNSCC)</topic><topic>Humans</topic><topic>Leukemia</topic><topic>Lymphocytes B</topic><topic>Mesenchyme</topic><topic>Metastases</topic><topic>Mice, Inbred NOD</topic><topic>Mice, SCID</topic><topic>Morphology</topic><topic>Naphthyridines - pharmacology</topic><topic>Neoplasm Invasiveness</topic><topic>Nuclear Proteins - genetics</topic><topic>Nuclear Proteins - metabolism</topic><topic>Phenotypes</topic><topic>Polycomb Repressive Complex 1 - genetics</topic><topic>Polycomb Repressive Complex 1 - metabolism</topic><topic>Proteins</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>Ribonucleic acid</topic><topic>RNA</topic><topic>Signal Transduction</topic><topic>Squamous cell carcinoma</topic><topic>Squamous Cell Carcinoma of Head and Neck - drug therapy</topic><topic>Squamous Cell Carcinoma of Head and Neck - enzymology</topic><topic>Squamous Cell Carcinoma of Head and Neck - genetics</topic><topic>Squamous Cell Carcinoma of Head and Neck - secondary</topic><topic>Therapeutic targets</topic><topic>Tumors</topic><topic>twist</topic><topic>Twist-Related Protein 1 - genetics</topic><topic>Twist-Related Protein 1 - metabolism</topic><topic>Vimentin</topic><topic>Viruses</topic><topic>Xenograft Model Antitumor Assays</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lai, Ying‐Ju</creatorcontrib><creatorcontrib>Yu, Wan‐Nien</creatorcontrib><creatorcontrib>Kuo, Sheng‐Chu</creatorcontrib><creatorcontrib>Ho, Chi‐Tang</creatorcontrib><creatorcontrib>Hung, Chao‐Ming</creatorcontrib><creatorcontrib>Way, Tzong‐Der</creatorcontrib><creatorcontrib>Chen, Chiung‐Tong</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of cellular physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lai, Ying‐Ju</au><au>Yu, Wan‐Nien</au><au>Kuo, Sheng‐Chu</au><au>Ho, Chi‐Tang</au><au>Hung, Chao‐Ming</au><au>Way, Tzong‐Der</au><au>Chen, Chiung‐Tong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>CSC‐3436 inhibits TWIST‐induced epithelial–mesenchymal transition via the suppression of Twist/Bmi1/Akt pathway in head and neck squamous cell carcinoma</atitle><jtitle>Journal of cellular physiology</jtitle><addtitle>J Cell Physiol</addtitle><date>2019-06</date><risdate>2019</risdate><volume>234</volume><issue>6</issue><spage>9118</spage><epage>9129</epage><pages>9118-9129</pages><issn>0021-9541</issn><eissn>1097-4652</eissn><abstract>Head and neck squamous cell carcinoma (HNSCC) is one of the leading causes of cancer deaths worldwide, especially in male. With poor prognosis, significant portions of patients with HNSCC die due to cancer recurrence and tumor metastasis after chemotherapy and targeted therapies. The HNSCC FaDu cell ectopic expression of Twist, a key transcriptional factor of epithelial–mesenchymal transition (EMT), which triggers EMT and results in the acquisition of a mesenchymal phenotype, was used as the cell model. Our results demonstrated that treatment with newly synthesized 2‐(3‐hydroxyphenyl)‐5‐methylnaphthyridin‐4‐one (CSC‐3436), a flavonoid derivative, elicited changes in its cell morphology, upregulated E‐cadherin messenger RNA and protein expression, downregulated N‐cadherin, vimentin, and CD133 (a marker associated with tumor‐initiating cells) in FaDu‐pCDH‐Twist cells. Moreover, CSC‐3436 exposure reduced B cell‐specific Moloney murine leukemia virus integration site 1 (Bmi1) expression regulated by Twist and further suppressed the direct co‐regulation of E‐cadherin by Twist and Bmi1. Interestingly, CSC‐3436 reduced EMT, cancer stemness, and migration/invasion abilities through the inhibition of the Twist/Bmi1‐Akt/β‐catenin pathway. Most importantly, our findings provided new evidence that CSC‐3436 played a crucial role in therapeutic targeting to Bmi1 and its molecular pathway in HNSCC, and it will be valuable in prognostic prediction and treatment.
2‐(3‐Hydroxyphenyl)‐5‐methylnaphthyridin‐4‐one (CSC‐3436) reduced Twist‐induced epithelial–mesenchymal transition, tumor‐initiating abilities and migration/invasion through the inhibition of the Twist/Bmi1‐Akt/β‐catenin pathway. Simultaneously, CSC‐3436 exposure reduced B cell‐specific Moloney murine leukemia virus integration site 1 (Bmi1) regulated by Twist and in further suppressed the direct co‐regulation of E‐cadherin by Twist and Bmi1.</abstract><cop>United States</cop><pub>Wiley Subscription Services, Inc</pub><pmid>30341909</pmid><doi>10.1002/jcp.27589</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0002-8423-8969</orcidid></addata></record> |
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| subjects | 2‐(3‐hydroxyphenyl)‐5‐methylnaphthyridin‐4‐one (CSC‐3436) AKT protein Animals Antigens, CD - genetics Antigens, CD - metabolism Antineoplastic Agents - pharmacology B cell‐specific Moloney murine leukemia virus integration site 1 (Bmi1) Cadherins - genetics Cadherins - metabolism Cancer Cell Line, Tumor Cell morphology Cell Movement - drug effects Chemotherapy Cytology E-cadherin Ectopic expression Epithelial-Mesenchymal Transition - drug effects epithelial–mesenchymal transition (EMT) Female Gene expression Gene Expression Regulation, Neoplastic Gene therapy Head & neck cancer Head and Neck Neoplasms - drug therapy Head and Neck Neoplasms - enzymology Head and Neck Neoplasms - genetics Head and Neck Neoplasms - pathology head and neck squamous cell carcinoma (HNSCC) Humans Leukemia Lymphocytes B Mesenchyme Metastases Mice, Inbred NOD Mice, SCID Morphology Naphthyridines - pharmacology Neoplasm Invasiveness Nuclear Proteins - genetics Nuclear Proteins - metabolism Phenotypes Polycomb Repressive Complex 1 - genetics Polycomb Repressive Complex 1 - metabolism Proteins Proto-Oncogene Proteins c-akt - metabolism Ribonucleic acid RNA Signal Transduction Squamous cell carcinoma Squamous Cell Carcinoma of Head and Neck - drug therapy Squamous Cell Carcinoma of Head and Neck - enzymology Squamous Cell Carcinoma of Head and Neck - genetics Squamous Cell Carcinoma of Head and Neck - secondary Therapeutic targets Tumors twist Twist-Related Protein 1 - genetics Twist-Related Protein 1 - metabolism Vimentin Viruses Xenograft Model Antitumor Assays |
| title | CSC‐3436 inhibits TWIST‐induced epithelial–mesenchymal transition via the suppression of Twist/Bmi1/Akt pathway in head and neck squamous cell carcinoma |
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