In summary, this study is the first to report that SH inhibits human glioblastoma cell proliferation by inducing cell cycle arrest and attenuates the metastasis of U87 and SF767 cells through the following mechanisms (Figure 7): (1) suppressing the expression of MMP-2/-9 via NFκB inactivation; (2) reversing the endogenous EMT through ER stress-mediated autophagy; and (3) reversing the exogenous EMT stimulated by the tumor inflammatory microenvironment. Here, NFKB1 is linked to glioblastoma.