Establishment and characterization of a MALT lymphoma cell line carrying an API2‐MALT1 translocation

Abstract

MALT lymphomas with API2(BIRC3)‐MALT1 translocation usually have an indolent clinical course and rarely transform into aggressive lymphoma, and there have been no lymphoma cell lines carrying API2‐MALT1 translocation reported to date. We established a novel lymphoma cell line named BMA19, carrying the API2‐MALT1 translocation from a patient with histologic transformation of intestinal MALT lymphoma. The cells were suggested to carry API2‐MALT1 and MYC‐IGH translocations by chromosomal analysis, and these translocations were confirmed by polymerase chain reaction analysis. The expression of MYC was shown to be enhanced as a result of the MYC‐IGH translocation, and it is considered to have played a role in the histologic transformation of MALT lymphoma. Whole exome sequencing of BMA19 identified several nucleotide variations in genes reported to be mutated in previous studies of marginal zone lymphomas. The MALT1 inhibitor MI‐2 specifically decreased cell growth, and the BMA19 cell line was suggested to be still dependent on the API2‐MALT1 signal. Subtractive microarray analysis showed that one of the earliest events resulting from MALT1 inhibition is increased susceptibility to endoplasmic reticulum stress‐induced apoptosis. The BMA19 cell line is considered to conserve the biological properties of MALT lymphoma and is expected to be a valuable tool for research into the pathogenesis of MALT lymphoma with an API2‐MALT1 translocation.

Inhibition of MALT1 Alleviates Spinal Ischemia/Reperfusion Injury-Induced Neuroinflammation by Modulating Glial Endoplasmic Reticulum Stress in Rats

“…Recent studies illustrate that the change of MALT1 activity is associated with ERS, and NF-κB signal is also one of the triggers of ERS. 15 It was known that MALT1 plays a pivotal role in activating immune response by regulating and transducing NF-κB signaling. 13 We found that SCI/R injury activated NF-κB signaling and ERS, which suggested that NF-κB signaling might mediate the ERS.…”

“…Early studies suggested that MALT1 is an essential intermediate in antigen receptor activation of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) in response to stimulation of a subset of G protein-coupled receptors. [13][14][15] Recent studies have shown that changes in MALT1 activity are related to ERS induction. ERS activates the NLRP3 inflammasome via NF-κB to promote IL-1β secretion.…”

Characterization of LIMA1 and its emerging roles and potential therapeutic prospects in cancers

“…Its pathogenesis progresses in association with chronic inflammation (105). A gene fusion between apoptosisinhibitor-2 (API2) on chromosome 11 and the mucosa-associated lymphoid tissue translocation gene 1 (MALT1) on chromosome 18 formed the API2-MALT1 oncogenic chimera (106). This is the most common chromosomal translocation in MALT lymphomas and has disrupted the function of the MALT1 gene.…”