Gliomas are the most common and fatal brain tumors worldwide. Abnormal DNA promoter methylation is an important mechanism for gene loss of tumor suppressors. A long non-coding RNA colorectal adenocarcinoma hypermethylated (CAHM) has been reported to be nearly deleted in glioblastomas (GBMs). Nevertheless, the roles of CAHM in gliomas remain unknown up to now. In the present study, 969 glioma samples downloaded from the CGGA and Gravendeel databases were included. We found that CAHM expression was correlated with glioma grades, molecular subtype, IDH mutation status, and 1q/19p codel status. In glioma cells, CAHM is hypermethylated by DNA methyltransferase1 (DNMT1) and the loss of CAHM expression could be reversed by 5-Aza-2′-deoxycytidine (5-Aza), a specific inhibitor of DNA methyltransferases. Besides, the expression of CAHM was negatively associated with overall survival in both primary and recurrent gliomas. Moreover, the result of Gene Ontology (GO) analysis suggested that CAHM participated in negatively regulating cell development, nervous system development, neurogenesis, and integrin-mediated signaling pathway. Overexpression of CAHM inhibited glioma cell proliferation, clone formation, and invasion. Further exploring results showed that CAHM overexpression suppressed glioma migration and invasion through SPAK/MAPK pathway. Collectively, this study disclosed that CAHM might be a suppressor in gliomas.

神经胶质瘤是全世界最常见和致命的脑肿瘤。异常的DNA启动子甲基化是肿瘤抑制基因缺失的重要机制。据报道，在胶质母细胞瘤 (GBMs) 中，一个长链非编码 RNA 高甲基化 (CAHM) 结直肠腺癌几乎被删除。然而，到目前为止，CAHM 在胶质瘤中的作用仍然未知。在本研究中，包括从 CGGA 和 Gravendeel 数据库下载的 969 个胶质瘤样本。我们发现 CAHM 表达与胶质瘤分级、分子亚型、IDH 突变状态和 1q/19p 编码状态相关。在神经胶质瘤细胞中，CAHM 被 DNA 甲基转移酶 1 (DNMT1) 高甲基化，并且 CAHM 表达的丧失可以被 DNA 甲基转移酶的特异性抑制剂 5-Aza-2'-脱氧胞苷 (5-Aza) 逆转。除了，CAHM 的表达与原发性和复发性胶质瘤的总生存率呈负相关。此外，基因本体论（GO）分析结果表明，CAHM参与负调控细胞发育、神经系统发育、神经发生和整合素介导的信号通路。CAHM 的过表达抑制胶质瘤细胞增殖、克隆形成和侵袭。进一步探索结果表明，CAHM 过表达通过 SPAK/MAPK 通路抑制胶质瘤迁移和侵袭。总的来说，这项研究揭示了 CAHM 可能是胶质瘤的抑制因子。和整合素介导的信号通路。CAHM 的过表达抑制胶质瘤细胞增殖、克隆形成和侵袭。进一步探索结果表明，CAHM 过表达通过 SPAK/MAPK 通路抑制胶质瘤迁移和侵袭。总的来说，这项研究揭示了 CAHM 可能是胶质瘤的抑制因子。和整合素介导的信号通路。CAHM 的过表达抑制胶质瘤细胞增殖、克隆形成和侵袭。进一步探索结果表明，CAHM 过表达通过 SPAK/MAPK 通路抑制胶质瘤迁移和侵袭。总的来说，这项研究揭示了 CAHM 可能是胶质瘤的抑制因子。