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Accumulation of BCL10 at the Perinuclear Region is Required for the BCL10-Mediated Nuclear Factor-Kappa B Activation

Objectives: The dysregulated overexpression of BCL10 that results from a specific chromosomal translocation t(1;14)(p22;q32) in mucosa-associated lymphoid tissue lymphoma has been shown to activate nuclear factor (NF)-ĸB, which may promote growth and survival in tumor cells. Accordingly, the molecular mechanisms underlying NF-ĸB activation may be responsible for lymphomagenesis. The aim of this study was to determine the molecular mechanisms underlying NF-ĸB activation by BCL10 overexpression. Methods: HeLa or COS-1 cells were transfected with BCL10, intracellular localization of BCL10 and the activation of NF-ĸB were analyzed. Results: BCL10 expressed at a high level exhibited a filamentous distribution at the perinuclear region, whereas BCL10 at a low level of expression displayed a diffuse cytoplasmic distribution. Furthermore, the BCL10-mediated NF-ĸB activation was efficiently inhibited by a Ca2+ chelating agent or a Ca2+ channel blocker. We also found that amino acids (107–119) of BCL10 are required for the formation of filamentous structures at the perinuclear region and NF-ĸB activation. Conclusion: These findings suggest that the filamentous pattern of overexpressed BCL10 at the perinuclear region adjacent to the endoplasmic reticulum is important for the BCL10-mediated NF-ĸB activation.