UBE2C triggers HIF‐1α‐glycolytic flux in head and neck squamous cell carcinoma
Head and neck squamous cell carcinoma (HNSCC) is the most common malignancy in Taiwan. Therefore, refining the diagnostic sensitivity of biomarkers for early‐stage tumours and identifying therapeutic targets are critical for improving the survival rate of HNSCC patients. Metabolic reprogramming cont...
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| Veröffentlicht in: | Journal of cellular and molecular medicine 2022-07, Vol.26 (13), p.3716-3725 |
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| creator | Yang, Yi‐Fang Chang, Yu‐Chan Tsai, Kuo‐Wang Hung, Ming‐Hsin Kang, Bor‐Hwang |
| description | Head and neck squamous cell carcinoma (HNSCC) is the most common malignancy in Taiwan. Therefore, refining the diagnostic sensitivity of biomarkers for early‐stage tumours and identifying therapeutic targets are critical for improving the survival rate of HNSCC patients. Metabolic reprogramming contributes to cancer development and progression. Metabolic pathways, specifically, play a crucial role in these diverse biological and pathological processes, which include cell proliferation, differentiation, apoptosis and carcinogenesis. Here, we investigated the role and potential prognostic value of the ubiquitin‐conjugating enzyme E2 (UBE2) family in HNSCC. Gene expression database analysis followed by tumour comparison with non‐tumour tissue showed that UBE2C was upregulated in tumours and was associated with lymph node metastasis in HNSCC patients. Knockdown of UBE2C significantly reduced the invasion/migration abilities of SAS and CAL27 cells. UBE2C modulates glycolysis pathway activation and HIF‐1α expression in SAS and CAL27 cells. CoCl2 (HIF‐1α inducer) treatment restored the expression of glycolytic enzymes and the migration/invasion abilities of UBE2C knockdown cells. Based on our findings, UBE2C expression mediates HIF‐1α activation, increasing glycolysis pathway activation and the invasion/migration abilities of cancer cells. UBE2C may be an independent prognostic factor and a therapeutic target in HNSCC. |
| doi_str_mv | 10.1111/jcmm.17400 |
| format | Article |
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Therefore, refining the diagnostic sensitivity of biomarkers for early‐stage tumours and identifying therapeutic targets are critical for improving the survival rate of HNSCC patients. Metabolic reprogramming contributes to cancer development and progression. Metabolic pathways, specifically, play a crucial role in these diverse biological and pathological processes, which include cell proliferation, differentiation, apoptosis and carcinogenesis. Here, we investigated the role and potential prognostic value of the ubiquitin‐conjugating enzyme E2 (UBE2) family in HNSCC. Gene expression database analysis followed by tumour comparison with non‐tumour tissue showed that UBE2C was upregulated in tumours and was associated with lymph node metastasis in HNSCC patients. Knockdown of UBE2C significantly reduced the invasion/migration abilities of SAS and CAL27 cells. UBE2C modulates glycolysis pathway activation and HIF‐1α expression in SAS and CAL27 cells. CoCl2 (HIF‐1α inducer) treatment restored the expression of glycolytic enzymes and the migration/invasion abilities of UBE2C knockdown cells. Based on our findings, UBE2C expression mediates HIF‐1α activation, increasing glycolysis pathway activation and the invasion/migration abilities of cancer cells. UBE2C may be an independent prognostic factor and a therapeutic target in HNSCC.</description><identifier>ISSN: 1582-1838</identifier><identifier>EISSN: 1582-4934</identifier><identifier>DOI: 10.1111/jcmm.17400</identifier><identifier>PMID: 35615976</identifier><language>eng</language><publisher>England: John Wiley & Sons, Inc</publisher><subject>Apoptosis ; Cancer therapies ; Carcinogenesis ; Cell differentiation ; Cell migration ; Cell proliferation ; Datasets ; Gene expression ; Genomes ; Glycolysis ; Head & neck cancer ; Head and neck carcinoma ; HIF‐1α ; HNSCCUBE2C ; Lymph nodes ; Lymphatic system ; Malignancy ; Metabolic pathways ; Metastases ; Metastasis ; Oral cancer ; Original ; Patients ; Signal transduction ; Squamous cell carcinoma ; Survival analysis ; Therapeutic applications ; Therapeutic targets ; Tongue ; Tumors ; Ubiquitin</subject><ispartof>Journal of cellular and molecular medicine, 2022-07, Vol.26 (13), p.3716-3725</ispartof><rights>2022 The Authors. published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.</rights><rights>2022 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.</rights><rights>2022. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). 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Therefore, refining the diagnostic sensitivity of biomarkers for early‐stage tumours and identifying therapeutic targets are critical for improving the survival rate of HNSCC patients. Metabolic reprogramming contributes to cancer development and progression. Metabolic pathways, specifically, play a crucial role in these diverse biological and pathological processes, which include cell proliferation, differentiation, apoptosis and carcinogenesis. Here, we investigated the role and potential prognostic value of the ubiquitin‐conjugating enzyme E2 (UBE2) family in HNSCC. Gene expression database analysis followed by tumour comparison with non‐tumour tissue showed that UBE2C was upregulated in tumours and was associated with lymph node metastasis in HNSCC patients. Knockdown of UBE2C significantly reduced the invasion/migration abilities of SAS and CAL27 cells. UBE2C modulates glycolysis pathway activation and HIF‐1α expression in SAS and CAL27 cells. CoCl2 (HIF‐1α inducer) treatment restored the expression of glycolytic enzymes and the migration/invasion abilities of UBE2C knockdown cells. Based on our findings, UBE2C expression mediates HIF‐1α activation, increasing glycolysis pathway activation and the invasion/migration abilities of cancer cells. UBE2C may be an independent prognostic factor and a therapeutic target in HNSCC.</description><subject>Apoptosis</subject><subject>Cancer therapies</subject><subject>Carcinogenesis</subject><subject>Cell differentiation</subject><subject>Cell migration</subject><subject>Cell proliferation</subject><subject>Datasets</subject><subject>Gene expression</subject><subject>Genomes</subject><subject>Glycolysis</subject><subject>Head & neck cancer</subject><subject>Head and neck carcinoma</subject><subject>HIF‐1α</subject><subject>HNSCCUBE2C</subject><subject>Lymph nodes</subject><subject>Lymphatic system</subject><subject>Malignancy</subject><subject>Metabolic pathways</subject><subject>Metastases</subject><subject>Metastasis</subject><subject>Oral cancer</subject><subject>Original</subject><subject>Patients</subject><subject>Signal transduction</subject><subject>Squamous cell carcinoma</subject><subject>Survival analysis</subject><subject>Therapeutic applications</subject><subject>Therapeutic targets</subject><subject>Tongue</subject><subject>Tumors</subject><subject>Ubiquitin</subject><issn>1582-1838</issn><issn>1582-4934</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>BENPR</sourceid><recordid>eNp9kUtKZDEUhoMovicuoAk4kYbSvG_uRNDCJ4oDdRxSueeWKe9Dk7raNXMJvZXeiIvolXTKKqV1YAYngXx8nJ8foS1Kdmk6eyNX17s0E4QsoFUqNeuJnIvF-ZtqrlfQWowjQriiPF9GK1wqKvNMraLr28Mj1sfj4IdDCBGfnh3_fflNX_-kOawmrq0mY-9wWXW_sG_wHdgC26bADbh7HB87W7ddxA6qCjsbnG_a2m6gpdJWETbn9zq6PT666Z_2Lq5OzvoHFz0nhCY9ba0oCZOMFAMOpWYFB0EGKiskFEqBtVC4MpOU5UAKQXmppMiZY9SBEtLydbQ_8z50gzqx0IyDrcxD8LUNE9Nabz7_NP7ODNsnkzOpMyKTYGcuCO1jB3Fsah-nWWwDKZZhKiNE0TQSuv0FHbVdaFK8RGlJWC6YTtTPGeVCG2OA8mMZSsy0KzPtyrx1leAf_6__gb6XkwA6A559BZNvVOa8f3k5k_4DF8WhWA</recordid><startdate>202207</startdate><enddate>202207</enddate><creator>Yang, Yi‐Fang</creator><creator>Chang, Yu‐Chan</creator><creator>Tsai, Kuo‐Wang</creator><creator>Hung, Ming‐Hsin</creator><creator>Kang, Bor‐Hwang</creator><general>John Wiley & Sons, Inc</general><general>John Wiley and Sons Inc</general><scope>24P</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QP</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</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>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-9028-9834</orcidid><orcidid>https://orcid.org/0000-0003-0474-9935</orcidid><orcidid>https://orcid.org/0000-0003-3788-448X</orcidid><orcidid>https://orcid.org/0000-0001-7425-3156</orcidid></search><sort><creationdate>202207</creationdate><title>UBE2C triggers HIF‐1α‐glycolytic flux in head and neck squamous cell carcinoma</title><author>Yang, Yi‐Fang ; 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Therefore, refining the diagnostic sensitivity of biomarkers for early‐stage tumours and identifying therapeutic targets are critical for improving the survival rate of HNSCC patients. Metabolic reprogramming contributes to cancer development and progression. Metabolic pathways, specifically, play a crucial role in these diverse biological and pathological processes, which include cell proliferation, differentiation, apoptosis and carcinogenesis. Here, we investigated the role and potential prognostic value of the ubiquitin‐conjugating enzyme E2 (UBE2) family in HNSCC. Gene expression database analysis followed by tumour comparison with non‐tumour tissue showed that UBE2C was upregulated in tumours and was associated with lymph node metastasis in HNSCC patients. Knockdown of UBE2C significantly reduced the invasion/migration abilities of SAS and CAL27 cells. UBE2C modulates glycolysis pathway activation and HIF‐1α expression in SAS and CAL27 cells. CoCl2 (HIF‐1α inducer) treatment restored the expression of glycolytic enzymes and the migration/invasion abilities of UBE2C knockdown cells. Based on our findings, UBE2C expression mediates HIF‐1α activation, increasing glycolysis pathway activation and the invasion/migration abilities of cancer cells. UBE2C may be an independent prognostic factor and a therapeutic target in HNSCC.</abstract><cop>England</cop><pub>John Wiley & Sons, Inc</pub><pmid>35615976</pmid><doi>10.1111/jcmm.17400</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0002-9028-9834</orcidid><orcidid>https://orcid.org/0000-0003-0474-9935</orcidid><orcidid>https://orcid.org/0000-0003-3788-448X</orcidid><orcidid>https://orcid.org/0000-0001-7425-3156</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Apoptosis Cancer therapies Carcinogenesis Cell differentiation Cell migration Cell proliferation Datasets Gene expression Genomes Glycolysis Head & neck cancer Head and neck carcinoma HIF‐1α HNSCCUBE2C Lymph nodes Lymphatic system Malignancy Metabolic pathways Metastases Metastasis Oral cancer Original Patients Signal transduction Squamous cell carcinoma Survival analysis Therapeutic applications Therapeutic targets Tongue Tumors Ubiquitin |
| title | UBE2C triggers HIF‐1α‐glycolytic flux in head and neck squamous cell carcinoma |
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