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From a 2DE-Gel Spot to Protein Function: Lesson Learned From HS1 in Chronic Lymphocytic Leukemia
Published on: October 19, 2014
The expression of heat shock protein A12B (HSPA12B) in non-Hodgkin's lymphomas
Yuejiao Huang1,2, Chunlei Peng1, Jie Tang2
1Department of Medical Oncology, Affiliated Tumor Hospital of Nantong University, Nantong, China.
Background:
Heat shock protein A12B (HSPA12B) plays a considerable protective role for cells, tissues, and organs against various noxious conditions. However, the expression of HSPA12B in cancer biology remains controversial. This study aimed to investigate the expression of HSPA12B and its role in cell adhesion mediated drug resistance (CAM-DR) of non-Hodgkin's lymphoma (NHL).
Methods:
In this study, the expression of HSPA12B in NHL was determined by immunohistochemical, and the effect of HSPA12B expression on the prognosis of NHL was analyzed by Kaplan-Meier curves. Then, the transfection technique was used to research the effect of HSPA12B in cell apoptosis. The most important was to study the expression changes of HSPA12B in the adhesion model and the effect of overexpression of HSPA12B on CAM-DR.
Results:
We analyzed the relationship between the expression levels of HSPA12B and clinical parameters in NHL. The expression of HSPA12B was directly related to the different NHL variants. We overexpressed HSPA12B in 2 NHL cell lines and found a subsequent reduction in apoptosis. More specifically, we used an adhesion assay to demonstrate that HSPA12B expression was induced in NHL cells when they adhered to fibronectin (FN) or bone marrow stroma cells (BMSCs). Finally, it was revealed that HSPA12B overexpression enhances CAM-DR.
Conclusions:
Our data suggest that HSPA12B may play a functional role in CAM-DR and is thus a potential novel target for NHL treatment.
