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Sökning: WFRF:(Zhang Xu) > (2005-2009) > X-Radiation Induces...

  • Han, Y.First Affiliated Hospital, Shenyang (författare)

X-Radiation Induces Non-Small-Cell Lung Cancer Apoptosis by Upregulation of Axin Expression

  • Artikel/kapitelEngelska2009

Förlag, utgivningsår, omfång ...

  • Elsevier BV,2009
  • printrdacarrier

Nummerbeteckningar

  • LIBRIS-ID:oai:DiVA.org:liu-21205
  • https://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-21205URI
  • https://doi.org/10.1016/j.ijrobp.2009.05.040DOI

Kompletterande språkuppgifter

  • Språk:engelska
  • Sammanfattning på:engelska

Ingår i deldatabas

Klassifikation

  • Ämneskategori:ref swepub-contenttype
  • Ämneskategori:art swepub-publicationtype

Anmärkningar

  • Purpose: Axis inhibition (Axin) is an important negative regulator of the Wnt pathway. This study investigated the relationship between Axin expression and sensitivity to X-rays in non-small-cell lung cancer (NSCLC) to find a useful indicator of radiosensitivity. Methods and Materials: Tissue from NSCLC patients, A549 cells, and BE1 cells expressing Axin were exposed to 1-Gy of X-radiation. Axin and p53 expression levels were detected by immunohistochemistry and reverse transcription-PCR. Apoptosis was determined by TUNEL (terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling) assay and FACS (fluorescence-activate cell sorter) analysis. Caspase-3 activity was determined by Western blotting. Phospho-JNK expression was determined by immunofluorescence. Results: The expression of Axin was significantly lower in NSCLC tissues than in normal lung tissues (p less than 0.05). Axin expression correlates with differentiation, TNM staging, and lymph node metastasis of NSCLC (p less than 0.05). Its expression negatively correlates with the expression of p53(mt) (p=0.000) and positively correlates with apoptosis (p=0.002). The prognosis of patients with high expression of Axin was better than those with low expression. X-radiation increases Axin expression in NSCLC tissue, and caspase-3 is significantly higher in samples in which Axin is increased (p less than 0.05). Both X-radiation and Axin induce apoptosis of A549 and BE1 cells; however, the combination of the two enhances the apoptotic effect (p less than 0.05). In A549 cells, inhibition of p53 blocks Axin-induced apoptosis, whereas in BE1 cells, the JNK pathway is required. Conclusions: Axin induces the p53 apoptotic pathway in cells where this pathway is intact; however, in cells expressing p53(mt), Axin induces apoptosis via the JNK pathway. Elevated Axin expression following X-ray exposure is a reliable indicator for determining the radiosensitivity of NSCLC.

Ämnesord och genrebeteckningar

  • Apoptosis; Axin; Lung neoplasm; Radiosensitization; X-ray
  • MEDICINE
  • MEDICIN

Biuppslag (personer, institutioner, konferenser, titlar ...)

  • Wang, Y.First Affiliated Hospital, Shenyang (författare)
  • Xu, H.-T.First Affiliated Hospital, Shenyang (författare)
  • Yang, L.-H.First Affiliated Hospital, Shenyang (författare)
  • Wei, Q.First Affiliated Hospital, Shenyang (författare)
  • Liu, Y.First Affiliated Hospital, Shenyang (författare)
  • Zhang, Y.First Affiliated Hospital, Shenyang (författare)
  • Zhao, Y.First Affiliated Hospital, Shenyang (författare)
  • Dai, S.-D.First Affiliated Hospital, Shenyang (författare)
  • Miao, Y.First Affiliated Hospital, Shenyang (författare)
  • Yu, J.-H.First Affiliated Hospital, Shenyang (författare)
  • Zhang, J.-Y.First Affiliated Hospital, Shenyang (författare)
  • Li, G.First Affiliated Hospital, Shenyang (författare)
  • Yuan, XimingÖstergötlands Läns Landsting,Linköpings universitet,Institutionen för klinisk och experimentell medicin,Hälsouniversitetet,Arbets- och miljömedicin(Swepub:liu)ximyu81 (författare)
  • Wang, E.-H.First Affiliated Hospital, Shenyang (författare)
  • First Affiliated Hospital, ShenyangInstitutionen för klinisk och experimentell medicin (creator_code:org_t)

Sammanhörande titlar

  • Ingår i:International Journal of Radiation Oncology Biology Physics: Elsevier BV75:2, s. 518-5260360-3016

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