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Cell death discovery · 2023

CAMK2D: a novel molecular target for BAP1-deficient malignant mesothelioma.

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Karnan Sivasundaram, Ota Akinobu, Murakami Hideki, Rahman Md Lutfur, Wahiduzzaman Md, Hasan Muhammad Nazmul, Vu Lam Quang, Hanamura Ichiro, Inoko Akihito, Riku Miho, Ito Hideaki, Kaneko Yoshifumi, Hyodo Toshinori, Konishi Hiroyuki, Tsuzuki Shinobu, Hosokawa Yoshitaka

Аннотация

Malignant mesothelioma (MMe) is a rare but aggressive malignancy. Although the molecular genetics of MMe is known, including BRCA1-associated protein-1 (BAP1) gene alterations, the prognosis of MMe patients remains poor. Here, we generated BAP1 knockout (BAP1-KO) human mesothelial cell clones to develop molecular-targeted therapeutics based on genetic alterations in MMe. cDNA microarray and quantitative RT-PCR (qRT-PCR) analyses revealed high expression of a calcium/calmodulin-dependent protein kinase type II subunit delta (CAMK2D) gene in the BAP1-KO cells. CAMK2D was highly expressed in 70% of the human MMe tissues (56/80) and correlated with the loss of BAP1 expression, making it a potential diagnostic and therapeutic target for BAP1-deficient MMe. We screened an anticancer drugs library using BAP1-KO cells and successfully identified a CaMKII inhibitor, KN-93, which displayed a more potent and selective antiproliferative effect against BAP1-deficient cells than cisplatin or pemetrexed. KN-93 significantly suppressed the tumor growth in mice xenografted with BAP1-deficient MMe cells. This study is the first to provide a potential molecular-targeted therapeutic approach for BAP1-deficient MMe.