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Involvement of ER ‐α36 in the malignant growth of gastric carcinoma cells is associated with GRP 94 overexpression
Author(s) -
Fu Zhengqi,
Deng Hao,
Wang Xuming,
Yang Xiuping,
Wang Zhaoyi,
Liu Lijiang
Publication year - 2013
Publication title -
histopathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.626
H-Index - 124
eISSN - 1365-2559
pISSN - 0309-0167
DOI - 10.1111/his.12171
Subject(s) - immunohistochemistry , western blot , carcinogenesis , cancer , cancer research , biology , metastasis , receptor , medicine , endocrinology , pathology , gene , biochemistry
Aims This study aimed to examine the involvement of glucose‐regulated protein 94 ( GRP 94) in oestrogen receptor‐α36 ( ER ‐α36)‐mediated oestrogen signalling in gastric cancer development. Methods and results A total of 130 formalin‐fixed and paraffin‐embedded gastric tumour samples with corresponding normal gastric and tumour‐adjacent tissues were used. High levels of GRP 94 expression (2+ or 3+) were observed in 109 of 130 gastric carcinomas (83.85%) by immunohistochemistry, and in 13 of 18 tumour specimens (72.22%) with W estern blot analysis. GRP 94 expression was correlated positively with gender, tumour stage, lymph node metastasis and ER ‐α36 expression ( P < 0.05). Oestrogen treatment up‐regulated both GRP 94 and ER ‐α36 expression in gastric cancer SGC 7901 cells. In addition, steady state levels of GRP 94 protein were decreased in established gastric cancer SGC 7901 cells with knocked‐down levels of ER ‐α36 expression and in xenograft tumours formed by these cells. Forced expression of recombinant ER ‐α36 in SGC 7901 cells, however, up‐regulated the levels of GRP 94 expression. Conclusions Glucose‐regulated protein 94 is a downstream effector of ER ‐α36‐mediated oestrogen signalling, and may be involved in ER ‐α36 function during gastric carcinogenesis.