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. 2018 Oct 4;72(1):71-83.e7.
doi: 10.1016/j.molcel.2018.08.014. Epub 2018 Sep 13.

LncRNA CamK-A Regulates Ca 2+-Signaling-Mediated Tumor Microenvironment Remodeling

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LncRNA CamK-A Regulates Ca 2+-Signaling-Mediated Tumor Microenvironment Remodeling

Ling-Jie Sang et al. Mol Cell. .
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Abstract

Cancer cells entail metabolic adaptation and microenvironmental remodeling to survive and progress. Both calcium (Ca2+) flux and Ca2+-dependent signaling play a crucial role in this process, although the underlying mechanism has yet to be elucidated. Through RNA screening, we identified one long noncoding RNA (lncRNA) named CamK-A (lncRNA for calcium-dependent kinase activation) in tumorigenesis. CamK-A is highly expressed in multiple human cancers and involved in cancer microenvironment remodeling via activation of Ca2+-triggered signaling. Mechanistically, CamK-A activates Ca2+/calmodulin-dependent kinase PNCK, which in turn phosphorylates IκBα and triggers calcium-dependent nuclear factor κB (NF-κB) activation. This regulation results in the tumor microenvironment remodeling, including macrophage recruitment, angiogenesis, and tumor progression. Notably, our human-patient-derived xenograft (PDX) model studies demonstrate that targeting CamK-A robustly impaired cancer development. Clinically, CamK-A expression coordinates with the activation of CaMK-NF-κB axis, and its high expression indicates poor patient survival rate, suggesting its role as a potential biomarker and therapeutic target.

Keywords: Ca(2+); LncRNA; NF-κB; PDX; cancer; glycolysis; metabolism; signal transduction; tumor microenvironment.

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