Division of Translational Science, National Cancer Center, 323 Ilsan-ro, Ilsandong-gu, Goyang-si, Gyeonggi-do 10408, Korea.
Department of Cancer Biomedical Science, National Cancer Center, 323 Ilsan-ro, Ilsandong-gu, Goyang-si, Gyeonggi-do 10408, Korea.
Int J Mol Sci. 2020 Nov 26;21(23):8982. doi: 10.3390/ijms21238982.
Glioblastoma is a type of aggressive brain tumor that grows very fast and evades surrounding normal brain, lead to treatment failure. Glioblastomas are associated with Akt activation due to somatic alterations in PI3 kinase/Akt pathway and/or PTEN tumor suppressor. Sodium meta-arsenite, KML001 is an orally bioavailable, water-soluble, and trivalent arsenical and it shows antitumoral effects in several solid tumor cells via inhibiting oncogenic signaling, including Akt and MAPK. Here, we evaluated the effect of sodium meta-arsenite, KML001, on the growth of human glioblastoma cell lines with different PTEN expression status and Akt activation, including PTEN-deficient cells (U87-MG and U251) and PTEN-positive cells (LN229). The growth-inhibitory effect of KML001 was stronger in U87-MG and U251 cells, which exhibited higher Akt activity than LN229 cells. KML001 deactivated Akt and decreased its protein levels via proteasomal degradation in U87-MG cells. KML001 upregulated mutant PTEN levels via inhibition of its proteasomal degradation. KML001 inhibited cell growth more effectively in active Akt-overexpressing LN229 cells than in mock-expressing LN229 cells. Consistent with these results, KML001 sensitized PTEN-deficient cells more strongly to growth inhibition than it did PTEN-positive cells in prostate and breast cancer cell lines. Finally, we illustrated in vivo anti-tumor effects of KML001 using an intracranial xenograft mouse model. These results suggest that KML001 could be an effective chemotherapeutic drug for the treatment of glioblastoma cancer patients with higher Akt activity and PTEN loss.
胶质母细胞瘤是一种侵袭性脑肿瘤,生长非常迅速,能够逃避周围正常的大脑组织,导致治疗失败。由于 PI3 激酶/Akt 通路和/或 PTEN 肿瘤抑制因子的体细胞改变,胶质母细胞瘤与 Akt 激活有关。亚砷酸钠(KML001)是一种口服生物利用度高、水溶性好的三价砷剂,通过抑制致癌信号,包括 Akt 和 MAPK,在几种实体肿瘤细胞中表现出抗肿瘤作用。在这里,我们评估了亚砷酸钠(KML001)对不同 PTEN 表达状态和 Akt 激活的人胶质母细胞瘤细胞系生长的影响,包括 PTEN 缺失细胞(U87-MG 和 U251)和 PTEN 阳性细胞(LN229)。KML001 在 Akt 活性高于 LN229 细胞的 U87-MG 和 U251 细胞中抑制生长的作用更强。KML001 通过蛋白酶体降解使 Akt 失活并降低其蛋白水平。在 Akt 过表达的 LN229 细胞中,KML001 通过抑制其蛋白酶体降解而上调突变型 PTEN 水平。KML001 在 Akt 过表达的 LN229 细胞中比在模拟表达的 LN229 细胞中更有效地抑制细胞生长。与这些结果一致,KML001 在前列腺癌和乳腺癌细胞系中使 PTEN 缺失细胞比 PTEN 阳性细胞对生长抑制更为敏感。最后,我们使用颅内异种移植小鼠模型说明了 KML001 的体内抗肿瘤作用。这些结果表明,KML001 可能是一种有效的化学治疗药物,用于治疗 Akt 活性较高和 PTEN 缺失的胶质母细胞瘤癌症患者。