Research and Education Faculty, Multidisciplinary Science Cluster, Interdisciplinary Science Unit, Kochi University, Kohasu Oko-cho Nankoku-shi, Kochi 783-8505, Japan.
Graduate School of Medicine, Kochi University, Nankoku 783-8502, Japan.
Cells. 2019 Oct 30;8(11):1350. doi: 10.3390/cells8111350.
Cancer cells modulate their metabolism to proliferate and survive under the metabolic stress condition, which is known as endoplasmic reticulum (ER) stress. Therefore, cancer cells should suppress ER stress-mediated cell death and induce autophagy-which recycles metabolites to provide energy and new macromolecules. In this study, we demonstrate that the ER membrane protein BAP31 acts to suppress adaptation to ER stress conditions, induce cell death, and suppress autophagy by forming a BAP31-STX17 protein complex. The loss of BAP31 stimulates tumor growth in metabolic stress conditions in vivo and enhances invasion activity. Therefore, BAP31 stimulates cell death and inhibits autophagy, and it can be considered a novel tumor suppressor factor that acts by preventing ER stress adaptation.
癌细胞会调节其代谢以在代谢应激条件下增殖和存活，这被称为内质网（ER）应激。因此，癌细胞应该抑制 ER 应激介导的细胞死亡并诱导自噬——自噬可回收代谢物以提供能量和新的大分子。在这项研究中，我们证明 ER 膜蛋白 BAP31 通过形成 BAP31-STX17 蛋白复合物来抑制对 ER 应激条件的适应，诱导细胞死亡并抑制自噬。BAP31 的缺失会刺激体内代谢应激条件下的肿瘤生长并增强侵袭活性。因此，BAP31 可通过刺激细胞死亡和抑制自噬来发挥作用，它可以被认为是一种通过防止 ER 应激适应而起作用的新型肿瘤抑制因子。
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