XAF1 expression levels in a non-small cell lung cancer cohort and its potential association with carcinogenesis
XAF1 expression levels in a non-small cell lung cancer cohort and its potential association with carcinogenesis
Data
2017
Autores
Schluckebier, Luciene
Aran, Veronica
Moraes, Joyce de
Paiva, Heitor
Sternberg, Cinthya
Ferreira, Carlos Gil
Journal Title
Journal ISSN
Volume Title
Publisher
Oncology Reports
Resumo
Abstract. The process of lung carcinogenesis is still not
well understood and involves different levels of regulation of
several genes. The search for molecular biomarkers, which
can be applicable to clinical practice, has been the focus of
various studies. XIAP-associated factor 1 (XAF1) was previ-
ously shown to be downregulated in many types of tumors,
including squamous cell lung cancer. XAF1 is a pro-apoptotic
protein and its restoration was found to sensitize cancer cells
to apoptotic stimuli; however, the precise mechanism involved
in the downregulation of XAF1 in tumors is unknown and
promoter hypermethylation or heat-shock transcription
factor 1 (HSF1) may be involved. Therefore, the aim of the
present study was to evaluate the expression of XAF1 in tumors
and adjacent non-tumor specimens from non-small cell lung
cancer (NSCLC) patients, and its potential association with
various factors including clinicopathological characteristics
and other genes involved in NSCLC. Our results indicated
that XAF1 expression was markedly altered in NSCLC tumor
samples when compared to that found in normal lung tissues.
Predominantly, XAF1 was downregulated in the tumors,
except in never-smoker patients. In addition, XAF1 may also
be important in the whole cell stress mechanism where the p53
status is crucial.
Description
Palavras-chave
lung cancer, XIAP-associated factor 1, human, genes, p53, p53, heat shock transcription factor 1, carcinogenesis
Citação
Schluckebier L, Aran V, De Moraes J, Paiva H, Sternberg C, Ferreira CG. XAF1 expression levels in a non-small cell lung cancer cohort and its potential association with carcinogenesis. Oncol Rep. 2017 Jul;38(1):402-410. doi: 10.3892/or.2017.5680.