his.sePublications
Change search
CiteExportLink to record
Permanent link

Direct link
Cite
Citation style
  • apa
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf
Deregulation of STAT-5 isoforms in the development of HPV-mediated cervical carcinogenesis
Department of Biotechnology, Panjab University, Chandigarh, India.
Department of Biotechnology, Panjab University, Chandigarh, India.ORCID iD: 0000-0003-2885-5708
Division of Molecular Genetics and Biochemistry, Institute of Cytology & Preventive Oncology (ICMR), Noida, India.
Department of Gynaecology and Obstetrics, PGIMER, Chandigarh, India.
Show others and affiliations
2010 (English)In: Journal of Receptor and Signal Transduction Research, ISSN 1079-9893, E-ISSN 1532-4281, Vol. 30, no 3, 178-188 p.Article in journal (Refereed) Published
Abstract [en]

BACKGROUND: Cervical cancer is the second most common cancer and is leading cause of cancer related deaths in women worldwide. High Risk-Human papillomavirus (HPV) types play an important role in cervical carcinogenesis. Considering the important role of signal transducer and activator of transcription-5 (STAT-5), an important member of JAK/STAT family which plays a crucial role in various cancers and HPV as a key mediator in the development of cervical carcinogenesis, the purpose of the current study was to examine the possible relationship between HPV infection and expression of STAT-5 gene isoforms in cervical cancer.

METHODS: A total of 120 fresh cervical tissue specimens comprising precancer (n = 12), cancer (n = 78) and normal controls (n = 30) were analyzed for HPV infection and expression pattern of STAT-5 mRNA (both isoforms STAT-5a and STAT-5b) and protein in different stages of cervical carcinoma biopsies by reverse-transcriptase-PCR, western blotting and immunohistochemistry.

RESULTS: A significantly increased expression of STAT-5 was detected in most of the cervical tumors (P < 0.001), whereas it was almost undetectable in normal controls. Also the study of relative contribution of STAT-5 isoforms revealed a higher expression pattern of STAT-5b and was associated with severity of the disease. On the contrary, STAT-5a was found to be significantly downregulated in cervical tumor tissues (P < 0.001). HPV infection was found in 90% of the cervical cancer cases and was significantly associated with STAT-5 overexpression (P = 0.001).

CONCLUSIONS: We observed for the first time the differential expression pattern of STAT-5 isoforms in cervical cancer and that STAT-5 may play an important role in the progression of HPV-mediated cervical cancer.

Place, publisher, year, edition, pages
Informa Healthcare, 2010. Vol. 30, no 3, 178-188 p.
Keyword [en]
Cervical cancer, HPV, STAT-5
National Category
Cancer and Oncology
Research subject
Medical sciences
Identifiers
URN: urn:nbn:se:his:diva-8996DOI: 10.3109/10799891003786218ISI: 000277004700006PubMedID: 20415542Scopus ID: 2-s2.0-77951632024OAI: oai:DiVA.org:his-8996DiVA: diva2:712812
Note

si

Available from: 2014-04-16 Created: 2014-04-16 Last updated: 2016-10-27Bibliographically approved

Open Access in DiVA

No full text

Other links

Publisher's full textPubMedScopus

Search in DiVA

By author/editor
Singh, Neha
In the same journal
Journal of Receptor and Signal Transduction Research
Cancer and Oncology

Search outside of DiVA

GoogleGoogle Scholar

Altmetric score

Total: 816 hits
CiteExportLink to record
Permanent link

Direct link
Cite
Citation style
  • apa
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf