• Human pathology · Sep 2014

    Reversed expression of GRIM-1 and GRP78 in human non-small cell lung cancer.

    • Hui-Mei Wu, Zi-Feng Jiang, Xiao-Yun Fan, Tong Wang, Ke-XuDepartment of Pulmonary Medicine, Anhui Geriatric Institute, the First Affiliated Hospital of Anhui Medical University, Hefei 230022, Anhui, PR China., Xue-Bo Yan, Yang Ma, Wei-Hua Xiao, and Rong-Yu Liu.
    • Department of Pulmonary Medicine, Anhui Geriatric Institute, the First Affiliated Hospital of Anhui Medical University, Hefei 230022, Anhui, PR China.
    • Hum. Pathol. 2014 Sep 1; 45 (9): 1936-43.

    AbstractGene associated with retinoid and interferon-induced mortality 1 (GRIM-1) acts as a tumor growth suppressor via apoptosis induction. However, GRIM-1 expression in human non-small cell lung cancer (NSCLC) and its potential interaction with another apoptosis-associated protein-glucose-regulated protein 78 (GRP78)-are as yet unknown. Using 40 surgical specimens, we showed significantly lower expression of GRIM-1 in NSCLC at both protein and messenger RNA (mRNA) levels compared with that in normal tissues (P < .01 and P < .001, respectively). Interestingly, these tumors tended to express higher basal amounts of GRP78 protein and mRNA (P < .05 and P < .001, respectively). Similarly, in the NSCLC tissues, weaker staining for GRIM-1 (main intensity + to ++) but stronger staining for GRP78 (main intensity +++ to ++++) was observed. Correlation analysis showed that protein and mRNA expression or the percentage of cells immunoreactive for GRIM-1 was negatively correlated with that of GRP78 (r = -0.279, r = -0.326, or r = -0.571, respectively). Coimmunoprecipitation and transient transfection revealed that GRIM-1 interacted with GRP78 and suppressed GRP78 protein expression. In addition, there was no correlation between GRIM-1 expression and clinical characteristics, whereas GRP78 expression was significantly correlated with tumor-nodes-metastasis (TNM) stage (stage 3 + 4 versus stage 1 + 2). In conclusion, the expression of GRIM-1 and GRP78 was negatively correlated in human NSCLC tissues, and the down-regulation of GRP78 by GRIM-1 provides a possible mechanism for their interaction. This study suggests a novel potential molecular pathway inactivated during the development of NSCLC. Copyright © 2014 Elsevier Inc. All rights reserved.

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