Skip to main content
Fig. 2 | Biomarker Research

Fig. 2

From: Sestrin2 in cancer: a foe or a friend?

Fig. 2

The involvement of Sestrin2 in oxidative stress, inflammation, ER stress, autophagy, and apoptosis of cancer cells. Sestrin2 can attenuate oxidative stress and inflammation and directly or indirectly inhibit ER stress. In return, inflammation, oxidative stress and ER stress upregulate Sestrin2 to ameliorate the damage. Severe activation of ER stress and oxidative stress leads to excessive activation of autophagy and apoptosis. This can shorten cancer cells survival. However, mild to moderate activation of ER stress may enhance cancer cells survival by activating autophagy. Autophagy allows cancer cells to recover in stress conditions, while excessive activation of autophagy leads to cancer cells death. Although Sestrin2 inhibits ER stress, it can promote autophagy via downregulation of mTORC1. Furthermore, it has been observed that Sestrin2 can induce apoptosis in cancer cells, independent of its effects on autophagy, ER stress, and oxidative stress

Back to article page