Enolase 1 differentially contributes to cell transformation in lung cancer but not in esophageal cancer
Enolase transforms 2-phospho-D-glycerate into phosphoenolpyruvate during glycolysis. The human enolase (ENO) family comprises three members named ENO3, which is restricted to muscle tissues, ENO2, which is neuron- and neuroendocrine tissue-specific, and ENO1, which is expressed in almost all tissues...
Saved in:
| Published in | Oncology letters Vol. 19; no. 4; pp. 3189 - 3196 |
|---|---|
| Main Authors | , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Greece
Spandidos Publications
01.04.2020
Spandidos Publications UK Ltd D.A. Spandidos |
| Subjects | |
| Online Access | Get full text |
Cover
Loading…
| Abstract | Enolase transforms 2-phospho-D-glycerate into phosphoenolpyruvate during glycolysis. The human enolase (ENO) family comprises three members named ENO3, which is restricted to muscle tissues, ENO2, which is neuron- and neuroendocrine tissue-specific, and ENO1, which is expressed in almost all tissues. ENO1 is involved in various types of human cancer, including retinoblastoma, hepatocellular carcinoma, pancreatic cancer, renal cell carcinoma, cholangiocarcinoma and gastric cancer. Furthermore, ENO1 enhances cell transformation in numerous cancer cell lines. It has been reported that ENO1 is involved in various activities that are detrimental to cell transformation, including apoptosis and differentiation. However, a few studies demonstrated that ENO1 can be down- or upregulated in various types of lung cancer, which suggests that ENO1 has an ambiguous role in the development of lung cancer. The present study aimed to investigate the differential influences of ENO1 on various types of cancer, and to clarify the role of ENO1 in lung cancer in particular. Western blotting was performed to assess ENO1 protein expression levels in lung cancer and esophageal cancer tissues. Furthermore, exogenous ENO1 was overexpressed in cell lines derived from various tissues and single cell proliferation, flowcytometric analysis, and western blotting were performed to determine the cell proliferation rate, cell transformation status, cell cycle progression and the expression of cell cycle regulators, such as cyclins and cyclin-dependent kinases, and survival factors, such as MAPK and AKT. The results demonstrated that ENO1 was upregulated in collected panels of lung cancer tissues, but not in esophageal cancer tissues. In addition, overexpression of ectopic ENO1 promoted cell proliferation and survival in lung cancer cell lines, which was not the case in other cells, including an esophageal cell line. Furthermore, mechanistic analyses revealed that ENO1 enhanced cell proliferation by accelerating G
progression and upregulating G
phase cyclin-dependent kinase 6 (CDK6), and improved cell survival by upregulating p38 in the MAPK cascade and increasing p-AKT in the AKT cascade, in particular in lung cancer cell lines. Overall, the results from the present study demonstrated that ENO1 may contribute to the development of lung cancers, but not esophageal cancers. |
|---|---|
| AbstractList | Enolase transforms 2-phospho-D-glycerate into phosphoenolpyruvate during glycolysis. The human enolase (ENO) family comprises three members named ENO3, which is restricted to muscle tissues, ENO2, which is neuron- and neuroendocrine tissue-specific, and ENO1, which is expressed in almost all tissues. ENO1 is involved in various types of human cancer, including retinoblastoma, hepatocellular carcinoma, pancreatic cancer, renal cell carcinoma, cholangiocarcinoma and gastric cancer. Furthermore, ENO1 enhances cell transformation in numerous cancer cell lines. It has been reported that ENO1 is involved in various activities that are detrimental to cell transformation, including apoptosis and differentiation. However, a few studies demonstrated that ENO1 can be down- or upregulated in various types of lung cancer, which suggests that ENO1 has an ambiguous role in the development of lung cancer. The present study aimed to investigate the differential influences of ENO1 on various types of cancer, and to clarify the role of ENO1 in lung cancer in particular. Western blotting was performed to assess ENO1 protein expression levels in lung cancer and esophageal cancer tissues. Furthermore, exogenous ENO1 was overexpressed in cell lines derived from various tissues and single cell proliferation, flowcytometric analysis, and western blotting were performed to determine the cell proliferation rate, cell transformation status, cell cycle progression and the expression of cell cycle regulators, such as cyclins and cyclin-dependent kinases, and survival factors, such as MAPK and AKT. The results demonstrated that ENO1 was upregulated in collected panels of lung cancer tissues, but not in esophageal cancer tissues. In addition, overexpression of ectopic ENO1 promoted cell proliferation and survival in lung cancer cell lines, which was not the case in other cells, including an esophageal cell line. Furthermore, mechanistic analyses revealed that ENO1 enhanced cell proliferation by accelerating G
progression and upregulating G
phase cyclin-dependent kinase 6 (CDK6), and improved cell survival by upregulating p38 in the MAPK cascade and increasing p-AKT in the AKT cascade, in particular in lung cancer cell lines. Overall, the results from the present study demonstrated that ENO1 may contribute to the development of lung cancers, but not esophageal cancers. Enolase transforms 2-phospho-D-glycerate into phosphoenolpyruvate during glycolysis. The human enolase (ENO) family comprises three members named ENO3, which is restricted to muscle tissues, ENO2, which is neuron- and neuroendocrine tissue-specific, and ENO1, which is expressed in almost all tissues. ENO1 is involved in various types of human cancer, including retinoblastoma, hepatocellular carcinoma, pancreatic cancer, renal cell carcinoma, cholangiocarcinoma and gastric cancer. Furthermore, ENO1 enhances cell transformation in numerous cancer cell lines. It has been reported that ENO1 is involved in various activities that are detrimental to cell transformation, including apoptosis and differentiation. However, a few studies demonstrated that ENO1 can be down-or upregulated in various types of lung cancer, which suggests that ENO1 has an ambiguous role in the development of lung cancer. The present study aimed to investigate the differential influences of ENO1 on various types of cancer, and to clarify the role of ENO1 in lung cancer in particular. Western blotting was performed to assess ENO1 protein expression levels in lung cancer and esophageal cancer tissues. Furthermore, exogenous ENO1 was overexpressed in cell lines derived from various tissues and single cell proliferation, flowcytometric analysis, and western blotting were performed to determine the cell proliferation rate, cell transformation status, cell cycle progression and the expression of cell cycle regulators, such as cyclins and cyclin-dependent kinases, and survival factors, such as MAPK and AKT The results demonstrated that ENO1 was upregulated in collected panels of lung cancer tissues, but not in esophageal cancer tissues. In addition, overexpression of ectopic ENO1 promoted cell proliferation and survival in lung cancer cell lines, which was not the case in other cells, including an esophageal cell line. Furthermore, mechanistic analyses revealed that ENO1 enhanced cell proliferation by accelerating [G.sub.1] progression and upregulating [G.sub.1] phase cyclin-dependent kinase 6 (CDK6), and improved cell survival by upregulating p38 in the MAPK cascade and increasing p-AKT in the AKT cascade, in particular in lung cancer cell lines. Overall, the results from the present study demonstrated that ENO1 may contribute to the development of lung cancers, but not esophageal cancers. Enolase transforms 2-phospho-D-glycerate into phosphoenolpyruvate during glycolysis. The human enolase (ENO) family comprises three members named ENO3, which is restricted to muscle tissues, ENO2, which is neuron- and neuroendocrine tissue-specific, and ENO1, which is expressed in almost all tissues. ENO1 is involved in various types of human cancer, including retinoblastoma, hepatocellular carcinoma, pancreatic cancer, renal cell carcinoma, cholangiocarcinoma and gastric cancer. Furthermore, ENO1 enhances cell transformation in numerous cancer cell lines. It has been reported that ENO1 is involved in various activities that are detrimental to cell transformation, including apoptosis and differentiation. However, a few studies demonstrated that ENO1 can be down- or upregulated in various types of lung cancer, which suggests that ENO1 has an ambiguous role in the development of lung cancer. The present study aimed to investigate the differential influences of ENO1 on various types of cancer, and to clarify the role of ENO1 in lung cancer in particular. Western blotting was performed to assess ENO1 protein expression levels in lung cancer and esophageal cancer tissues. Furthermore, exogenous ENO1 was overexpressed in cell lines derived from various tissues and single cell proliferation, flowcytometric analysis, and western blotting were performed to determine the cell proliferation rate, cell transformation status, cell cycle progression and the expression of cell cycle regulators, such as cyclins and cyclin-dependent kinases, and survival factors, such as MAPK and AKT. The results demonstrated that ENO1 was upregulated in collected panels of lung cancer tissues, but not in esophageal cancer tissues. In addition, overexpression of ectopic ENO1 promoted cell proliferation and survival in lung cancer cell lines, which was not the case in other cells, including an esophageal cell line. Furthermore, mechanistic analyses revealed that ENO1 enhanced cell proliferation by accelerating G1 progression and upregulating G1 phase cyclin-dependent kinase 6 (CDK6), and improved cell survival by upregulating p38 in the MAPK cascade and increasing p-AKT in the AKT cascade, in particular in lung cancer cell lines. Overall, the results from the present study demonstrated that ENO1 may contribute to the development of lung cancers, but not esophageal cancers.Enolase transforms 2-phospho-D-glycerate into phosphoenolpyruvate during glycolysis. The human enolase (ENO) family comprises three members named ENO3, which is restricted to muscle tissues, ENO2, which is neuron- and neuroendocrine tissue-specific, and ENO1, which is expressed in almost all tissues. ENO1 is involved in various types of human cancer, including retinoblastoma, hepatocellular carcinoma, pancreatic cancer, renal cell carcinoma, cholangiocarcinoma and gastric cancer. Furthermore, ENO1 enhances cell transformation in numerous cancer cell lines. It has been reported that ENO1 is involved in various activities that are detrimental to cell transformation, including apoptosis and differentiation. However, a few studies demonstrated that ENO1 can be down- or upregulated in various types of lung cancer, which suggests that ENO1 has an ambiguous role in the development of lung cancer. The present study aimed to investigate the differential influences of ENO1 on various types of cancer, and to clarify the role of ENO1 in lung cancer in particular. Western blotting was performed to assess ENO1 protein expression levels in lung cancer and esophageal cancer tissues. Furthermore, exogenous ENO1 was overexpressed in cell lines derived from various tissues and single cell proliferation, flowcytometric analysis, and western blotting were performed to determine the cell proliferation rate, cell transformation status, cell cycle progression and the expression of cell cycle regulators, such as cyclins and cyclin-dependent kinases, and survival factors, such as MAPK and AKT. The results demonstrated that ENO1 was upregulated in collected panels of lung cancer tissues, but not in esophageal cancer tissues. In addition, overexpression of ectopic ENO1 promoted cell proliferation and survival in lung cancer cell lines, which was not the case in other cells, including an esophageal cell line. Furthermore, mechanistic analyses revealed that ENO1 enhanced cell proliferation by accelerating G1 progression and upregulating G1 phase cyclin-dependent kinase 6 (CDK6), and improved cell survival by upregulating p38 in the MAPK cascade and increasing p-AKT in the AKT cascade, in particular in lung cancer cell lines. Overall, the results from the present study demonstrated that ENO1 may contribute to the development of lung cancers, but not esophageal cancers. Enolase transforms 2-phospho-D-glycerate into phosphoenolpyruvate during glycolysis. The human enolase (ENO) family comprises three members named ENO3, which is restricted to muscle tissues, ENO2, which is neuron- and neuroendocrine tissue-specific, and ENO1, which is expressed in almost all tissues. ENO1 is involved in various types of human cancer, including retinoblastoma, hepatocellular carcinoma, pancreatic cancer, renal cell carcinoma, cholangiocarcinoma and gastric cancer. Furthermore, ENO1 enhances cell transformation in numerous cancer cell lines. It has been reported that ENO1 is involved in various activities that are detrimental to cell transformation, including apoptosis and differentiation. However, a few studies demonstrated that ENO1 can be down- or upregulated in various types of lung cancer, which suggests that ENO1 has an ambiguous role in the development of lung cancer. The present study aimed to investigate the differential influences of ENO1 on various types of cancer, and to clarify the role of ENO1 in lung cancer in particular. Western blotting was performed to assess ENO1 protein expression levels in lung cancer and esophageal cancer tissues. Furthermore, exogenous ENO1 was overexpressed in cell lines derived from various tissues and single cell proliferation, flowcytometric analysis, and western blotting were performed to determine the cell proliferation rate, cell transformation status, cell cycle progression and the expression of cell cycle regulators, such as cyclins and cyclin-dependent kinases, and survival factors, such as MAPK and AKT. The results demonstrated that ENO1 was upregulated in collected panels of lung cancer tissues, but not in esophageal cancer tissues. In addition, overexpression of ectopic ENO1 promoted cell proliferation and survival in lung cancer cell lines, which was not the case in other cells, including an esophageal cell line. Furthermore, mechanistic analyses revealed that ENO1 enhanced cell proliferation by accelerating G1 progression and upregulating G1 phase cyclin-dependent kinase 6 (CDK6), and improved cell survival by upregulating p38 in the MAPK cascade and increasing p-AKT in the AKT cascade, in particular in lung cancer cell lines. Overall, the results from the present study demonstrated that ENO1 may contribute to the development of lung cancers, but not esophageal cancers. Enolase transforms 2-phospho-D-glycerate into phosphoenolpyruvate during glycolysis. The human enolase (ENO) family comprises three members named ENO3, which is restricted to muscle tissues, ENO2, which is neuron- and neuroendocrine tissue-specific, and ENO1, which is expressed in almost all tissues. ENO1 is involved in various types of human cancer, including retinoblastoma, hepatocellular carcinoma, pancreatic cancer, renal cell carcinoma, cholangiocarcinoma and gastric cancer. Furthermore, ENO1 enhances cell transformation in numerous cancer cell lines. It has been reported that ENO1 is involved in various activities that are detrimental to cell transformation, including apoptosis and differentiation. However, a few studies demonstrated that ENO1 can be down- or upregulated in various types of lung cancer, which suggests that ENO1 has an ambiguous role in the development of lung cancer. The present study aimed to investigate the differential influences of ENO1 on various types of cancer, and to clarify the role of ENO1 in lung cancer in particular. Western blotting was performed to assess ENO1 protein expression levels in lung cancer and esophageal cancer tissues. Furthermore, exogenous ENO1 was overexpressed in cell lines derived from various tissues and single cell proliferation, flowcytometric analysis, and western blotting were performed to determine the cell proliferation rate, cell transformation status, cell cycle progression and the expression of cell cycle regulators, such as cyclins and cyclin-dependent kinases, and survival factors, such as MAPK and AKT. The results demonstrated that ENO1 was upregulated in collected panels of lung cancer tissues, but not in esophageal cancer tissues. In addition, overexpression of ectopic ENO1 promoted cell proliferation and survival in lung cancer cell lines, which was not the case in other cells, including an esophageal cell line. Furthermore, mechanistic analyses revealed that ENO1 enhanced cell proliferation by accelerating G 1 progression and upregulating G 1 phase cyclin-dependent kinase 6 (CDK6), and improved cell survival by upregulating p38 in the MAPK cascade and increasing p-AKT in the AKT cascade, in particular in lung cancer cell lines. Overall, the results from the present study demonstrated that ENO1 may contribute to the development of lung cancers, but not esophageal cancers. |
| Audience | Academic |
| Author | Liao, Yu‑Ting Chen, Kun‑Chieh Yu, Chang‑Tze Chen, Jo‑Mei Huang, Yun‑Ru Chiu, Shao‑Chih |
| AuthorAffiliation | 3 Graduate Institute of Immunology, China Medical University, Taichung 40402, Taiwan, R.O.C 5 Department of Life Sciences, National Chung Hsing University, Taichung 402, Taiwan, R.O.C 4 Division of Chest Medicine, Department of Internal Medicine, Taichung Veterans General Hospital, Taichung 40705, Taiwan, R.O.C 1 Department of Applied Chemistry, National Chi Nan University, Puli, Nantou 54561, Taiwan, R.O.C 2 Center for Neuropsychiatry, China Medical University Hospital, Taichung 40447, Taiwan, R.O.C |
| AuthorAffiliation_xml | – name: 3 Graduate Institute of Immunology, China Medical University, Taichung 40402, Taiwan, R.O.C – name: 2 Center for Neuropsychiatry, China Medical University Hospital, Taichung 40447, Taiwan, R.O.C – name: 5 Department of Life Sciences, National Chung Hsing University, Taichung 402, Taiwan, R.O.C – name: 1 Department of Applied Chemistry, National Chi Nan University, Puli, Nantou 54561, Taiwan, R.O.C – name: 4 Division of Chest Medicine, Department of Internal Medicine, Taichung Veterans General Hospital, Taichung 40705, Taiwan, R.O.C |
| Author_xml | – sequence: 1 givenname: Jo‑Mei surname: Chen fullname: Chen, Jo‑Mei organization: Department of Applied Chemistry, National Chi Nan University, Puli, Nantou 54561, Taiwan, R.O.C – sequence: 2 givenname: Shao‑Chih surname: Chiu fullname: Chiu, Shao‑Chih organization: Center for Neuropsychiatry, China Medical University Hospital, Taichung 40447, Taiwan, R.O.C – sequence: 3 givenname: Kun‑Chieh surname: Chen fullname: Chen, Kun‑Chieh organization: Division of Chest Medicine, Department of Internal Medicine, Taichung Veterans General Hospital, Taichung 40705, Taiwan, R.O.C – sequence: 4 givenname: Yun‑Ru surname: Huang fullname: Huang, Yun‑Ru organization: Department of Applied Chemistry, National Chi Nan University, Puli, Nantou 54561, Taiwan, R.O.C – sequence: 5 givenname: Yu‑Ting surname: Liao fullname: Liao, Yu‑Ting organization: Department of Applied Chemistry, National Chi Nan University, Puli, Nantou 54561, Taiwan, R.O.C – sequence: 6 givenname: Chang‑Tze surname: Yu fullname: Yu, Chang‑Tze organization: Department of Applied Chemistry, National Chi Nan University, Puli, Nantou 54561, Taiwan, R.O.C |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/32256815$$D View this record in MEDLINE/PubMed |
| BookMark | eNptkstrHSEUh6WkNGmaZbdFKJRu5nZ0HHU2hRDSBwS6adfiOM5cg6O36gTy3_dMcpPmhujCx_nOT8_jLToKMViE3pN608iOfol-Q2tabwhhVLxCJ0R0tCK1pEePe8GO0VnO1zWMlhMp-Rt03FDacknaEzRdhuh1tpjgwY2jTTYUp72_xSaGkly_FJtxidhY73FJOuQxplkXFwN2AfslTNjoYGzCwOIQy3ptc9xt9WS13xvfodej9tme7ddT9Ofb5e-LH9XVr-8_L86vKtOSplQNkUQLSijvzTjIpu9kK8dGso7CgfUDo9oaLuXQU8E5a40FgnDGOjAS05yir_e6u6Wf7WAgnKS92iU363Sronbq0BLcVk3xRgnIFG1rEPi8F0jx72JzUbPLa_A62LhkRRspeMe4oIB-fIZexyUFCA8oIQVrpej-U5P2VrkwRnjXrKLqnFMu4PtEArV5gYI52NlBKezo4P7A4dMThy1kumxz9MtamHwIfniakcdUPPQAAM09YFLMOdlRGVfuCgxfcF6RWq3NpqJXa7Opu2YDr-qZ14Pwy_w_HATTdQ |
| CitedBy_id | crossref_primary_10_1155_2021_9910962 crossref_primary_10_3389_fcell_2021_670019 crossref_primary_10_3389_fgene_2020_614726 crossref_primary_10_3389_fonc_2020_593706 crossref_primary_10_1021_acs_est_0c03824 crossref_primary_10_1038_s41598_023_32308_x crossref_primary_10_1155_2023_4965223 crossref_primary_10_1080_15384047_2022_2054244 |
| ContentType | Journal Article |
| Copyright | Copyright: © Chen et al. COPYRIGHT 2020 Spandidos Publications Copyright Spandidos Publications UK Ltd. 2020 Copyright: © Chen et al. 2020 |
| Copyright_xml | – notice: Copyright: © Chen et al. – notice: COPYRIGHT 2020 Spandidos Publications – notice: Copyright Spandidos Publications UK Ltd. 2020 – notice: Copyright: © Chen et al. 2020 |
| DBID | AAYXX CITATION NPM 3V. 7X7 7XB 8FI 8FJ 8FK ABUWG AFKRA AN0 BENPR CCPQU FYUFA GHDGH K9. M0S PHGZM PHGZT PKEHL PPXIY PQEST PQQKQ PQUKI 7X8 5PM |
| DOI | 10.3892/ol.2020.11427 |
| DatabaseName | CrossRef PubMed ProQuest Central (Corporate) Health & Medical Collection ProQuest Central (purchase pre-March 2016) Hospital Premium Collection Hospital Premium Collection (Alumni Edition) ProQuest Central (Alumni) (purchase pre-March 2016) ProQuest Central (Alumni Edition) ProQuest Central UK/Ireland British Nursing Database ProQuest Central ProQuest One Community College Health Research Premium Collection Health Research Premium Collection (Alumni) ProQuest Health & Medical Complete (Alumni) Health & Medical Collection (Alumni Edition) ProQuest Central Premium ProQuest One Academic (New) ProQuest One Academic Middle East (New) ProQuest One Health & Nursing ProQuest One Academic Eastern Edition (DO NOT USE) ProQuest One Academic ProQuest One Academic UKI Edition MEDLINE - Academic PubMed Central (Full Participant titles) |
| DatabaseTitle | CrossRef PubMed ProQuest One Academic Middle East (New) ProQuest One Academic Eastern Edition ProQuest Health & Medical Complete (Alumni) British Nursing Index with Full Text ProQuest Central (Alumni Edition) ProQuest One Community College ProQuest Hospital Collection ProQuest One Health & Nursing Health Research Premium Collection (Alumni) ProQuest Hospital Collection (Alumni) ProQuest Central ProQuest Health & Medical Complete Health Research Premium Collection ProQuest One Academic UKI Edition Health and Medicine Complete (Alumni Edition) ProQuest Central (New) ProQuest One Academic ProQuest Central (Alumni) ProQuest One Academic (New) MEDLINE - Academic |
| DatabaseTitleList | PubMed MEDLINE - Academic ProQuest One Academic Middle East (New) |
| Database_xml | – sequence: 1 dbid: NPM name: PubMed url: https://proxy.k.utb.cz/login?url=http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed sourceTypes: Index Database – sequence: 2 dbid: 7X7 name: Health & Medical Collection url: https://search.proquest.com/healthcomplete sourceTypes: Aggregation Database |
| DeliveryMethod | fulltext_linktorsrc |
| Discipline | Medicine |
| EISSN | 1792-1082 |
| EndPage | 3196 |
| ExternalDocumentID | PMC7074250 A626785118 32256815 10_3892_ol_2020_11427 |
| Genre | Journal Article |
| GeographicLocations | United States Taiwan |
| GeographicLocations_xml | – name: Taiwan – name: United States |
| GroupedDBID | --- 0R~ 53G 7X7 8FI 8FJ AAKDD AAYXX ABDBF ABJNI ABUWG ACGFS ACUHS ADBBV AENEX AFKRA AHMBA ALIPV ALMA_UNASSIGNED_HOLDINGS AN0 BENPR BNQBC BPHCQ BVXVI C45 CCPQU CITATION EBD EBS EJD ESX F5P FYUFA H13 HMCUK HUR HZ~ IAO IHR IHW IPNFZ ITC O9- OK1 OVD PHGZM PHGZT PQQKQ PROAC RIG RPM TEORI UKHRP W2D 3V. NPM PMFND 7XB 8FK K9. PKEHL PPXIY PQEST PQUKI 7X8 5PM |
| ID | FETCH-LOGICAL-c513t-3181a72126bcfd83b9858f3849283b4bd42aec688db276645ce985164494bd1c3 |
| IEDL.DBID | 7X7 |
| ISSN | 1792-1074 |
| IngestDate | Thu Aug 21 18:25:48 EDT 2025 Thu Jul 10 22:47:50 EDT 2025 Mon Jul 14 08:38:55 EDT 2025 Tue Jun 17 20:58:59 EDT 2025 Tue Jun 10 20:48:37 EDT 2025 Thu May 22 21:17:27 EDT 2025 Thu Jan 02 22:58:53 EST 2025 Tue Jul 01 01:58:52 EDT 2025 Thu Apr 24 22:51:48 EDT 2025 |
| IsDoiOpenAccess | true |
| IsOpenAccess | true |
| IsPeerReviewed | false |
| IsScholarly | true |
| Issue | 4 |
| Keywords | lung cancer enolase 1 cyclin-dependent kinase 6 esophageal cancer p38 protein kinase B |
| Language | English |
| License | Copyright: © Chen et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. |
| LinkModel | DirectLink |
| MergedId | FETCHMERGED-LOGICAL-c513t-3181a72126bcfd83b9858f3849283b4bd42aec688db276645ce985164494bd1c3 |
| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 Contributed equally |
| OpenAccessLink | https://pubmed.ncbi.nlm.nih.gov/PMC7074250 |
| PMID | 32256815 |
| PQID | 2378745879 |
| PQPubID | 2044954 |
| PageCount | 8 |
| ParticipantIDs | pubmedcentral_primary_oai_pubmedcentral_nih_gov_7074250 proquest_miscellaneous_2387694672 proquest_journals_2378745879 gale_infotracmisc_A626785118 gale_infotracacademiconefile_A626785118 gale_healthsolutions_A626785118 pubmed_primary_32256815 crossref_citationtrail_10_3892_ol_2020_11427 crossref_primary_10_3892_ol_2020_11427 |
| ProviderPackageCode | CITATION AAYXX |
| PublicationCentury | 2000 |
| PublicationDate | 2020-04-01 |
| PublicationDateYYYYMMDD | 2020-04-01 |
| PublicationDate_xml | – month: 04 year: 2020 text: 2020-04-01 day: 01 |
| PublicationDecade | 2020 |
| PublicationPlace | Greece |
| PublicationPlace_xml | – name: Greece – name: Athens |
| PublicationTitle | Oncology letters |
| PublicationTitleAlternate | Oncol Lett |
| PublicationYear | 2020 |
| Publisher | Spandidos Publications Spandidos Publications UK Ltd D.A. Spandidos |
| Publisher_xml | – name: Spandidos Publications – name: Spandidos Publications UK Ltd – name: D.A. Spandidos |
| SSID | ssj0000561886 |
| Score | 2.2717693 |
| Snippet | Enolase transforms 2-phospho-D-glycerate into phosphoenolpyruvate during glycolysis. The human enolase (ENO) family comprises three members named ENO3, which... |
| SourceID | pubmedcentral proquest gale pubmed crossref |
| SourceType | Open Access Repository Aggregation Database Index Database Enrichment Source |
| StartPage | 3189 |
| SubjectTerms | Age Analysis Aprotinin Biotechnology Cancer Cell cycle Cell growth Cyclin-dependent kinases EDTA Esophageal cancer Gastric cancer Immunoglobulins Kidney cancer Kinases Liver cancer Lung cancer Medical prognosis Membranes Oncology Pancreatic cancer Patients Penicillin Plasmids Proteins Retina Retinoblastoma Scientific equipment industry Statistical analysis Stomach cancer |
| Title | Enolase 1 differentially contributes to cell transformation in lung cancer but not in esophageal cancer |
| URI | https://www.ncbi.nlm.nih.gov/pubmed/32256815 https://www.proquest.com/docview/2378745879 https://www.proquest.com/docview/2387694672 https://pubmed.ncbi.nlm.nih.gov/PMC7074250 |
| Volume | 19 |
| hasFullText | 1 |
| inHoldings | 1 |
| isFullTextHit | |
| isPrint | |
| link | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwfV3da9RAEB-0BfFF6nfshyuIvhja3Wz246lUuVKEFhEL97Ykm40Wwqb20of-951JcvEi6Ovt3GVvMt87Oz-A98pLZbLAU1VzmUp0sGkRBCYrwZTaeHQaPRjM-YU6u5Rfl_lyLLitxrbKtU3sDXXVeqqRH4pM02R2o-3x9e-UUKPodHWE0HgI2zS6jFq69FJPNRaKjk0P9ohiJ1LqPRzGbKKXFoctnTyIflouYcpsuKW_jfOGd5p3Tm64otMdeDLGkOxkeOlP4UGIz-DR-XhK_hx-LiImrKvAOFvjn6AeN80d6xvTCeEqrFjXMqras24jdG0ju4qsQQPAPInDDUNaFtuOPg6EeIDmBx89LL6Ay9PFjy9n6QiokPqcZx3dlOYFpnxClb6uTFZak5s6M9JikFHKspKiCF4ZU5VCKyVzH5ACEyppcZH77CVsxTaG18BKXQRbcSu9sJIf-cJbWdQ2L2pd4C_bBD6t-en8OG2cQC8ah1kHsd-1jSP2u579CXyYyK-HMRv_InxLL8cNt0Qn9XQnmJhpih5NAh97ClJQfCLubLhngPumUVczyr0ZJSqWny-vBcCNir1yf8QwgXfTMn2TmtViaG-JBl2MRQ8kEng1yMv0p8h-KsPzBPRMkiYCGvc9X4lXv_qx35rKGPnRm_9vaxceE7eG5qI92OpubsM-xk1dedArxwFsf15cfPt-D-u5Fv4 |
| linkProvider | ProQuest |
| linkToHtml | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwtV1Lb9QwEB6VrQRcEG8ChRqJx4WojeMk9gGhAlttaXeFUCv1ZhLHaStFTummQv1T_EZm8mKDBLdeM5PEmYznYY_nA3gVGxHL0AZ-XATCF-hg_dRyTFaszBJp0Gk0YDDzRTw7El-Oo-M1-NWfhaGyyt4mNoY6rwytkW_xMKHO7DJRH85_-IQaRburPYRGqxb79uonpmzL93uf8f--5nx3evhp5neoAr6JgrCm48JBinkPjzNT5DLMlIxkEUqh0NNmIssFT62JpcwznsSxiIxFDswqhEJiYEJ87g1YFyGmMhNY_zhdfP02rOpQPC4beElUdO5TtWPb2BPjAr5V0V4Hb_rzEorNiiP82x2s-MNxreaK89u9C3e6qJXttGp2D9asuw83592-_AM4mTpMkZeWBaxHXEHLUZZXrCmFJ0wtu2R1xWifgNUrwXLl2JljJZocZkgBLxjyMlfVdNkSxgIaPHx1S3wIR9ci7EcwcZWzT4BlSWpVHihhuBLBtkmNEmmhorRIUnyy8uBdL09tuv7mBLNRasxzSPy6KjWJXzfi9-DNwH7eNvb4F-Mm_RzdnksdDILewVQwoXhVevC24SCTgG_EkbUnG3Dc1FxrxLkx4sSpbMbkXgF0Z0qW-o_ie_ByINOdVB7nbHVJPOjUFPo87sHjVl-GjyKLHcsg8iAZadLAQA3GxxR3dto0Gk9o4STafvr_YW3Crdnh_EAf7C32n8Ftklxb2rQBk_ri0j7HqK3OXnRThcH3656dvwFP6lIV |
| linkToPdf | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwtV1Lb9QwEB6VIlVcEG9SCjUSjwvRNo7jxwGhinbVUlpxoNLeTOI4UClK2m4q1L_Gr2MmLzZIcOt1Pes4k3na4_kAXkknpI59FMoiEqFABxumnmOy4nWmtEOn0YLBHJ_Ig1PxaZEs1uDXcBeGyioHm9ga6rx2tEc-47GizuxamVnRl0V82Zt_OL8ICUGKTloHOI1ORI789U9M35bvD_fwW7_mfL7_9eNB2CMMhC6J4oauDkcp5kBcZq7IdZwZnegi1sKg181Elgueeie1zjOupBSJ80iBGYYwOBi5GOe9BbdVjLOhLqmFGvd3KDLXLdAkijwPqe6xa_GJEQKf1XTqwdtOvYRns-IS_3YMK55xWrW54gbn9-BuH7-y3U7g7sOarx7AxnF_Qv8Qvu9XmCwvPYvYgL2CNqQsr1lbFE_oWn7JmprRiQFrVsLmumJnFSvR-DBHonjJkJZVdUM_e0JbQNOHj-4GH8HpjbD6MaxXdeWfAstU6k0eGeG4EdGOS50RaWGStFApzmwCeDfw07q-0zkBbpQWMx5iv61LS-y3LfsDeDOSn3ctPv5FuE0fx3Y3VEfTYHcxKVQUueoA3rYUZBzwibiy7o4DrpvabE0otyaUqNRuOjwIgO2NytL-UYEAXo7D9E8qlKt8fUU06N4Mej8ewJNOXsaXItstdZQEoCaSNBJQq_HpSHX2o205rmgLJdnZ_P-ytmEDddJ-Pjw5egZ3iHFdjdMWrDeXV_45hm9N9qLVEwbfbloxfwNhtlTl |
| openUrl | ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Enolase+1+differentially+contributes+to+cell+transformation+in+lung+cancer+but+not+in+esophageal+cancer&rft.jtitle=Oncology+letters&rft.au=Chen%2C+Jo-Mei+Maureen&rft.au=Chiu%2C+Shao-Chih&rft.au=Chen%2C+Kun-Chieh&rft.au=Huang%2C+Yun-Ru+Jaoying&rft.date=2020-04-01&rft.pub=D.A.+Spandidos&rft.issn=1792-1074&rft.eissn=1792-1082&rft.volume=19&rft.issue=4&rft.spage=3189&rft.epage=3196&rft_id=info:doi/10.3892%2Fol.2020.11427&rft_id=info%3Apmid%2F32256815&rft.externalDocID=PMC7074250 |
| thumbnail_l | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=1792-1074&client=summon |
| thumbnail_m | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=1792-1074&client=summon |
| thumbnail_s | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=1792-1074&client=summon |