Zhang Han, McCarty Nami
a Center for Stem Cell and Regenerative Disease , Brown Foundation Institute of Molecular Medicine for the Prevention of Human Diseases (IMM), the University of Texas-Health Science Center at Houston , Houston , TX USA.
Autophagy. 2017 Mar 4;13(3):627-628. doi: 10.1080/15548627.2016.1271516. Epub 2017 Jan 5.
Macroautophagy/autophagy is a well-established process involved in maintaining cellular homeostasis, but its role in cancer is complex and even controversial. Many studies have reported a correlative relationship between increased autophagy and evolving cancer cells under stress conditions such as nutrient or oxygen deprivation; however, there has been a lack of a plausible mechanistic link to properly target the autophagy process in the context of this microenvironment. We recently unveiled a positive regulatory loop involving TGM2 (transglutaminase 2)-NFKB/NF-κB signaling, IL6 and autophagy in cancer using mantle cell lymphoma (MCL) as a model system. These pathways are functionally connected to each other, thereby promoting malignant B cell survival and leading to enhanced lymphoma progression both in mice and in patients. Disruption of this network could provide an opportunity to increase the efficacies of current therapies and to reduce MCL drug resistance.
巨自噬/自噬是一个公认的参与维持细胞稳态的过程,但其在癌症中的作用复杂且颇具争议。许多研究报道,在营养或氧剥夺等应激条件下,自噬增加与癌细胞演变之间存在相关性;然而,在这种微环境下,缺乏一个合理的机制联系来恰当地靶向自噬过程。我们最近以套细胞淋巴瘤(MCL)为模型系统,揭示了癌症中一个涉及转谷氨酰胺酶2(TGM2)-NFKB/NF-κB信号传导、白细胞介素6(IL6)和自噬的正调控回路。这些通路在功能上相互连接,从而促进恶性B细胞存活,并导致小鼠和患者的淋巴瘤进展加剧。破坏这个网络可能为提高当前疗法的疗效和降低MCL耐药性提供机会。