File Download
  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Impacts of Survivin and Caspase-3 on apoptosis and angiogenesis in oral cancer

TitleImpacts of Survivin and Caspase-3 on apoptosis and angiogenesis in oral cancer
Authors
KeywordsAngiogenesis
Apoptosis
Caspase-3
Oral cancer
Issue Date2017
PublisherSpandidos Publications. The Journal's web site is located at http://www.spandidos-publications.com/ol
Citation
Oncology Letters, 2017, v. 14 n. 3, p. 3774-3779 How to Cite?
AbstractThe present study aimed to investigate the impact of survivin and caspase-3 on apoptosis and angiogenesis in oral cancer. A total of 16 oral leukoplakia cases accompanied by low-moderate epithelial dysplasia, 12 cases of oral leukoplakia accompanied by severe epithelial dysplasia, 17 cases of high-moderate differentiated oral squamous cell carcinoma and 10 cases of normal oral mucosa were selected. Immunohistochemistry was used to detect the expression levels of survivin, caspase-3, and caspase inhibitor factor VIII in lesions from each group. Terminal deoxynucleo-tidyl transferase 2'-deoxyuridine, 5'-triphosphate nick end labeling was performed to detect the apoptotic index of oral leukoplakia and cancer tissue. Immunohistochemistry revealed increased expression levels of survivin in oral cancer tissues, as compared with the normal mucosa, whereas the expression of Caspase-3 was decreased during malignant transformation. Microvascular density (MVD) was increased from 28.49±11.87 strips/mm2 (mean ± standard deviation, normal control group) to 91.98±40.20 strips/mm2 (oral cancer group). Therefore, survivin may serve an important role in oral cancer, as its expression was increased in association with a downward trend in caspase-3 expression and apoptotic index, whereas MVD was significantly increased.
Persistent Identifierhttp://hdl.handle.net/10722/260315
ISSN
2023 Impact Factor: 2.5
2023 SCImago Journal Rankings: 0.644
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorLi, S-
dc.contributor.authorYang, Y-
dc.contributor.authorDing, Y-
dc.contributor.authorTang, X-
dc.contributor.authorSun, Z-
dc.date.accessioned2018-09-14T08:39:36Z-
dc.date.available2018-09-14T08:39:36Z-
dc.date.issued2017-
dc.identifier.citationOncology Letters, 2017, v. 14 n. 3, p. 3774-3779-
dc.identifier.issn1792-1074-
dc.identifier.urihttp://hdl.handle.net/10722/260315-
dc.description.abstractThe present study aimed to investigate the impact of survivin and caspase-3 on apoptosis and angiogenesis in oral cancer. A total of 16 oral leukoplakia cases accompanied by low-moderate epithelial dysplasia, 12 cases of oral leukoplakia accompanied by severe epithelial dysplasia, 17 cases of high-moderate differentiated oral squamous cell carcinoma and 10 cases of normal oral mucosa were selected. Immunohistochemistry was used to detect the expression levels of survivin, caspase-3, and caspase inhibitor factor VIII in lesions from each group. Terminal deoxynucleo-tidyl transferase 2'-deoxyuridine, 5'-triphosphate nick end labeling was performed to detect the apoptotic index of oral leukoplakia and cancer tissue. Immunohistochemistry revealed increased expression levels of survivin in oral cancer tissues, as compared with the normal mucosa, whereas the expression of Caspase-3 was decreased during malignant transformation. Microvascular density (MVD) was increased from 28.49±11.87 strips/mm2 (mean ± standard deviation, normal control group) to 91.98±40.20 strips/mm2 (oral cancer group). Therefore, survivin may serve an important role in oral cancer, as its expression was increased in association with a downward trend in caspase-3 expression and apoptotic index, whereas MVD was significantly increased.-
dc.languageeng-
dc.publisherSpandidos Publications. The Journal's web site is located at http://www.spandidos-publications.com/ol-
dc.relation.ispartofOncology Letters-
dc.subjectAngiogenesis-
dc.subjectApoptosis-
dc.subjectCaspase-3-
dc.subjectOral cancer-
dc.titleImpacts of Survivin and Caspase-3 on apoptosis and angiogenesis in oral cancer-
dc.typeArticle-
dc.identifier.emailYang, Y: yangyanq@hku.hk-
dc.identifier.authorityYang, Y=rp00045-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.3892/ol.2017.6626-
dc.identifier.scopuseid_2-s2.0-85026314777-
dc.identifier.hkuros291335-
dc.identifier.volume14-
dc.identifier.issue3-
dc.identifier.spage3774-
dc.identifier.epage3779-
dc.identifier.isiWOS:000408597700071-
dc.publisher.placeGreece-
dc.identifier.issnl1792-1074-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats