Department of Neurosurgery, Affiliated Hospital of Xuzhou Medical College, Xuzhou, Jiangsu, PR China.
Oncol Rep. 2012 Jul;28(1):269-75. doi: 10.3892/or.2012.1796. Epub 2012 May 4.
Glioblastoma multiforme is the most aggressive type of brain tumor with a strong ability to invade and migrate into surrounding normal brain tissues, leading to high tumor recurrence and mortality. Most of class-3 semaphorins, especially SEMA3A, SEMA3B and SEMA3F, have been reported to have strong tumor inhibition ability, but the role of SEMA3G in tumor biology is largely unknown. We report here that SEMA3G possesses anti-migration and anti-invasion ability. To determine the potential effects of SEMA3G on migratory and invasive ability, we generated stable SEMA3G expression U251MG cells. We found that stably overexpressed SEMA3G inhibited the migratory and invasive behavior of U251MG cells. In addition, treatment with SEMA3G conditioned media also decreased the migratory and invasive ability of parental U251MG cells. Furthermore, SEMA3G also inhibited the activity of MMP2, an index of tumor invasion ability. Thus, our results suggest that SEMA3G inhibited tumor cell migration and invasion, which may be obtained through cell autonomous or paracrine mechanisms, and SEMA3G is a potential target for antitumor migration and invasion.
多形性胶质母细胞瘤是最具侵袭性的脑肿瘤之一，具有很强的侵袭和迁移到周围正常脑组织的能力，导致高肿瘤复发和死亡率。大多数 3 类神经丝氨酸蛋白酶，特别是 SEMA3A、SEMA3B 和 SEMA3F，已被报道具有很强的肿瘤抑制能力，但 SEMA3G 在肿瘤生物学中的作用在很大程度上是未知的。我们在这里报告 SEMA3G 具有抗迁移和抗侵袭能力。为了确定 SEMA3G 对迁移和侵袭能力的潜在影响，我们生成了稳定表达 SEMA3G 的 U251MG 细胞。我们发现，稳定过表达的 SEMA3G 抑制了 U251MG 细胞的迁移和侵袭行为。此外，SEMA3G 条件培养基的处理也降低了亲本 U251MG 细胞的迁移和侵袭能力。此外，SEMA3G 还抑制了 MMP2 的活性，MMP2 是肿瘤侵袭能力的一个指标。因此，我们的结果表明，SEMA3G 抑制肿瘤细胞的迁移和侵袭，这可能是通过细胞自主或旁分泌机制获得的，SEMA3G 是抗肿瘤迁移和侵袭的潜在靶点。
