Zhu Zhengyang, Fang Chaoyou, Xu Houshi, Yuan Ling, Du Yichao, Ni Yunjia, Xu Yuanzhi, Shao Anwen, Zhang Anke, Lou Meiqing
Department of Neurosurgery, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Department of Neurosurgery, Huashan Hospital, Shanghai Medical College, Fudan University, Shanghai, China.
Front Oncol. 2022 Aug 15;12:976557. doi: 10.3389/fonc.2022.976557. eCollection 2022.
Glioma is the most common malignant intracranial tumor and exhibits diffuse metastasis and a high recurrence rate. The invasive property of glioma results from cell detachment. Anoikis is a special form of apoptosis that is activated upon cell detachment. Resistance to anoikis has proven to be a protumor factor. Therefore, it is suggested that anoikis resistance commonly occurs in glioma and promotes diffuse invasion. Several factors, such as integrin, E-cadherin, EGFR, IGFR, Trk, TGF-β, the Hippo pathway, NF-κB, eEF-2 kinase, MOB2, hypoxia, acidosis, ROS, Hsp and protective autophagy, have been shown to induce anoikis resistance in glioma. In our present review, we aim to summarize the underlying mechanism of resistance and the therapeutic potential of these molecules.
神经胶质瘤是最常见的颅内恶性肿瘤,具有弥漫性转移和高复发率。神经胶质瘤的侵袭特性源于细胞脱离。失巢凋亡是细胞脱离时激活的一种特殊形式的细胞凋亡。对失巢凋亡的抗性已被证明是一种促肿瘤因子。因此,有人提出失巢凋亡抗性在神经胶质瘤中普遍存在并促进弥漫性侵袭。几种因素,如整合素、E-钙黏蛋白、表皮生长因子受体(EGFR)、胰岛素样生长因子受体(IGFR)、酪氨酸激酶受体(Trk)、转化生长因子-β(TGF-β)、河马通路、核因子-κB(NF-κB)、真核生物延伸因子2激酶(eEF-2激酶)、MOB2、缺氧、酸中毒、活性氧(ROS)、热休克蛋白(Hsp)和保护性自噬,已被证明可诱导神经胶质瘤中的失巢凋亡抗性。在本综述中,我们旨在总结抗性的潜在机制以及这些分子的治疗潜力。