Department of Neurosurgery, The Second People's Hospital of Huai'an, The Affiliated Huai'an Hospital of Xuzhou Medical University, Huai'an, China.
Department of Gastroenterology, Lianshui County People's Hospital Affiliated to Kangda College of Nanjing Medical University, Huai'an, China.
J Biochem Mol Toxicol. 2021 Aug;35(8):e22824. doi: 10.1002/jbt.22824. Epub 2021 May 28.
The pseudogene annexin A2 pseudogene 2 (ANXA2P2) is highly expressed in glioblastoma (GBM). However, its role and mechanism involved in the progression of GBM remain poorly understood. ANXA2P2 messenger RNA expression was measured by quantitative reverse transcription-polymerase chain reaction. The protein levels were detected by Western blot. Cell viability was evaluated by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and lactate dehydrogenase (LDH) release assays. Cell invasive ability was investigated by the transwell assay and by epithelial-mesenchymal transition (EMT). Cell apoptosis was examined by flow cytometry. The results showed that ANXA2P2 expression was increased in GBM tissues and cells. Silencing of ANXA2P2 inhibited the activation of the phosphoinositide 3-kinase (PI3K)/protein kinase B (PKB) pathway in GBM cells. Knockdown of ANXA2P2 decreased cell viability, promoted LDH release, suppressed cell invasive ability, and EMT, and induced cell apoptosis in GBM cells. The addition of the PI3K/PKB activator 740Y-P abrogated the effects of ANXA2P2 knockdown on cell viability, LDH release, invasive ability, and apoptosis. In conclusion, knockdown of ANXA2P2 inhibited cell viability and invasion but promoted the apoptotic rate by suppressing the PI3K/PKB pathway in GBM cells. ANXA2P2 may represent a new target for the treatment of GBM.
假基因膜联蛋白 A2 假基因 2（ANXA2P2）在胶质母细胞瘤（GBM）中高度表达。然而，其在 GBM 进展中所涉及的作用和机制仍知之甚少。通过定量逆转录-聚合酶链反应测量 ANXA2P2 信使 RNA 的表达。通过 Western blot 检测蛋白水平。通过 3-(4,5-二甲基噻唑-2-基)-2,5-二苯基四氮唑溴盐和乳酸脱氢酶（LDH）释放测定评估细胞活力。通过 Transwell 测定和上皮-间充质转化（EMT）研究细胞侵袭能力。通过流式细胞术检查细胞凋亡。结果表明，ANXA2P2 在 GBM 组织和细胞中表达增加。沉默 ANXA2P2 抑制了 GBM 细胞中磷酸肌醇 3-激酶（PI3K）/蛋白激酶 B（PKB）途径的激活。ANXA2P2 的敲低降低了 GBM 细胞的活力，促进了 LDH 的释放，抑制了细胞侵袭能力和 EMT，并诱导了细胞凋亡。PI3K/PKB 激活剂 740Y-P 的添加消除了 ANXA2P2 敲低对细胞活力、LDH 释放、侵袭能力和凋亡的影响。总之，沉默 ANXA2P2 通过抑制 GBM 细胞中的 PI3K/PKB 通路抑制细胞活力和侵袭，但促进了细胞凋亡率。ANXA2P2 可能代表治疗 GBM 的一个新靶点。
