Published online Nov 15, 2017. doi: 10.4251/wjgo.v9.i11.436
Peer-review started: June 6, 2017
First decision: July 26, 2017
Revised: July 31, 2017
Accepted: September 5, 2017
Article in press: September 6, 2017
Published online: November 15, 2017
To evaluate the immunohistochemical (IHC) expression of five biomarkers, commonly involved in epithelial mesenchymal/mesenchymal epithelial transition (EMT/MET), in gastrointestinal stromal tumors (GISTs).
In 80 consecutive GISTs the IHC examinations were performed using the EMT-related antibodies E-cadherin, N-cadherin, SLUG, V-set and immunoglobulin domain containing 1 (VSIG1) and CD44.
The positivity rate was 88.75% for SLUG, 83.75% for VSIG1, 36.25% for CD44 and 10% for N-cadherin. No correlation was noted between the examined markers and clinicopathological parameters. Nuclear positivity for SLUG and VSIG1 was observed in all cases with distant metastasis. The extra-gastrointestinal stromal tumors (e-GISTs) expressed nuclear positivity for VSIG1 and SLUG, with infrequent positivity for N-cadherin and CD44. The low overall survival was mainly dependent on VSIG1 negativity (P = 0.01) and nuclear positivity for SLUG and/or CD44.
GIST aggressivity may be induced by nuclear up-regulation of SLUG and loss or cytoplasm-to-nuclear translocation of VSIG1. SLUG and VSIG1 may act as activated nuclear transcription factors. The CD44, but not N-cadherin, might also have an independent prognostic value in these tumors. The role of the EMT/MET-related transcription factors in the evolution of GISTs, should be revisited with a larger dataset. This is the first study exploring the IHC pattern of VSIG1 in GISTs.
Core tip: In this paper we proved for the first time in the current literature the possible role of V-set and immunoglobulin domain containing 1 (VSIG1) in gastrointestinal stromal tumors (GISTs) in correlation with the expression of the other markers involved in the epithelial mesenchymal/mesenchymal epithelial transition. Based on the obtained results, we hypothesized that the GIST aggressivity may be induced by nuclear upregulation of SLUG and the loss or cytoplasm-to-nuclear translocation of VSIG1.