Glioma is the most common tumor of the central nervous system, and its poor prognosis can be linked to hypoxia and gene inactivation. Na⁺/Ca²⁺ exchanger 2 (NCX2) is expressed only in the normal brain and not in other tissues or glioma. We constructed a hypoxic microenvironment to more accurately understand the effect of NCX2 in glioma. Our previous experiments confirmed that NCX2 inhibited the growth of U87 cells in nude mice, indicating that NCX2 is a potential tumor suppressor gene. Malignant tumor cells are often exposed to an anoxic environment. To more accurately understand the effect of NCX2 in glioma, we constructed a hypoxic microenvironment. To detect the localization of NCX2 in transfected U87 cells, immunofluorescence was used. We tested the function of NCX2 in glioma, i.e., how it contributes to the cytosolic Ca²⁺ homeostasis by X-Rhod-1. We tested the cell proliferation of NCX2 in glioma in hypoxic using Cell counting kit-8 (CCK8). Cell migration and invasion were evaluated in 24-well transwell matrigel-coated or non-matrigel-coated in hypoxia. NCX2 promoted the proliferation of U87 cells in the hypoxic microenvironment. It inhibited the invasion and migration abilities of U87 cells. We demonstrated that NCX2 was located on the cell membrane and that it reduced intracellular Ca²⁺ levels and reactivated P53 and PTEN. We further demonstrated that NCX2 impaired cell invasion through the HIF-1α pathway in glioma. The results indicated that NCX2 plays a key role in glioma formation and tumor invasion functionality.

神经胶质瘤是中枢神经系统最常见的肿瘤，其预后不良可能与缺氧和基因失活有关。钠⁺ /钙²⁺交换器 2 (NCX2) 仅在正常大脑中表达，在其他组织或神经胶质瘤中不表达。我们构建了一个低氧微环境，以更准确地了解 NCX2 在神经胶质瘤中的作用。我们前期的实验证实NCX2能够抑制裸鼠U87细胞的生长，表明NCX2是一种潜在的抑癌基因。恶性肿瘤细胞经常暴露在缺氧环境中。为了更准确地了解NCX2在神经胶质瘤中的作用，我们构建了低氧微环境。为了检测NCX2在转染的U87细胞中的定位，使用了免疫荧光。我们测试了 NCX2 在神经胶质瘤中的功能，即它如何促进胞质 Ca ²⁺X-Rhod-1 的体内平衡。我们使用细胞计数试剂盒-8 (CCK8) 测试了缺氧条件下神经胶质瘤中 NCX2 的细胞增殖情况。在缺氧条件下，在 24 孔 Transwell 基质胶包被或非基质胶包被的 Transwell 中评估细胞迁移和侵袭。NCX2促进缺氧微环境中U87细胞的增殖。抑制U87细胞的侵袭和迁移能力。我们证明NCX2位于细胞膜上，并且它降低细胞内Ca ²⁺水平并重新激活P53和PTEN。我们进一步证明，NCX2 通过 HIF-1α 通路损害神经胶质瘤中的细胞侵袭。结果表明NCX2在神经胶质瘤形成和肿瘤侵袭功能中发挥关键作用。