Clinicopathological significance of RCAN2 production in gastric carcinoma

Aims Gastric cancer (GC) is one of the leading causes of cancer‐related death worldwide. Genes expressed only in cancer tissue may be useful biomarkers for cancer diagnosis and therapeutics. The aims of the present study were to analyse regulator of calcineurin 2 (RCAN2) in a large number of GCs, an...

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Veröffentlicht in:Histopathology 2019-02, Vol.74 (3), p.430-442
Hauptverfasser: Hattori, Yui, Sentani, Kazuhiro, Shinmei, Shunsuke, Oo, Htoo Zarni, Hattori, Takuya, Imai, Takeharu, Sekino, Yohei, Sakamoto, Naoya, Oue, Naohide, Niitsu, Hiroaki, Hinoi, Takao, Ohdan, Hideki, Yasui, Wataru
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Sprache:eng
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Zusammenfassung:Aims Gastric cancer (GC) is one of the leading causes of cancer‐related death worldwide. Genes expressed only in cancer tissue may be useful biomarkers for cancer diagnosis and therapeutics. The aims of the present study were to analyse regulator of calcineurin 2 (RCAN2) in a large number of GCs, and to investigate how these expression patterns correlate with clinicopathological parameters and various markers. Methods and results An immunohistochemical analysis of RCAN2 in 207 GC tissue samples showed that 110 (53%) GCs were positive for RCAN2. RCAN2‐positive GCs were more advanced in terms of TNM classification and tumour stage than RCAN2‐negative GCs. Furthermore, RCAN2 was an independent prognostic classifier for GC patients. The cell growth and invasiveness of RCAN2 small interfering RNA (siRNA)‐transfected GC cell lines were less than those of the negative control siRNA‐transfected cell lines, whereas those of RCAN2‐transfected cells were significantly increased as compared with those of empty vector‐transfected cells. RCAN2 siRNA inhibits the phosphorylation of AKT and p44/p42 (ERK1/2). RCAN2 was colocalised with EGFR, nuclear β‐catenin, MMP7, laminin‐γ2, VEGF‐A, and VEGF‐C. Conclusion These results suggest that RCAN2 is involved in tumour progression and is an independent prognostic classifier in patients with GC.
ISSN:0309-0167
1365-2559
DOI:10.1111/his.13764