Abstract:
BACKGROUND:Epithelial protein lost in neoplasm-α (EPLIN-α) is a cytoskeletal protein whose expression is often lost or is aberrant in cancerous cells and tissues and whose loss is believed to be involved in aggressive phenotype. Our current study examined this molecule in human oesophageal tissues and investigated the cellular impact of EPLIN-α on oesophageal cancer cells. MATERIALS AND METHODS:Expression of the EPLIN-α transcript in human oesophageal tissues (tumour, paratumour and normal) was determined using the Quantitative Polymerase Chain Reaction (Q-PCR) method. In vitro models, including invasion, cellular migration (Electrical Cell substrate Impedance Sensing based method), cell growth and matrix adhesion assays were employed in order to assess the biological influence of EPLIN-α expression on KYSE150 oesophageal cancer cells. RESULTS:EPLIN-α expression was lower in tumour tissues compared to normal tissue. Grade 3-5 tumours had slightly lower levels of EPLIN-α compared with those of grade 2. Patients who died of oesophageal cancer had significantly lower levels of EPLIN-α compared to those who remained disease-free (p=0.022). Lower levels of EPLIN-α transcript were seen in advanced oesophageal cancer, including TNM stages 2 to 4. Reduced EPLIN-α expression was associated with lymphatic metastasis and local advanced T-stage cancer, including T2-T4. Forced expression of EPLIN-α in oesophageal cancer cells rendered cells less invasive and reduced their cell growth rate in vitro. CONCLUSION:Our study suggests that EPLIN-α is expressed at lower levels in oesophageal cancer tissues. This down-regulation has a prognostic value. Together with the findings that EPLIN-α inhibits cellular growth and invasion, we conclude that EPLIN-α is a tumour suppressor of oesophageal cancer.
journal_name
Anticancer Resjournal_title
Anticancer researchauthors
Liu Y,Sanders AJ,Zhang L,Jiang WGsubject
Has Abstractpub_date
2012-04-01 00:00:00pages
1283-9issue
4eissn
0250-7005issn
1791-7530pii
32/4/1283journal_volume
32pub_type
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