Graphene and graphene oxide (GO), as wonder materials, have penetrated nearly every field of research. One of their most attractive features is the functionality and assembly of graphene or GO, in which they can be considered to be chemically functionalized building blocks for creating unconventional porous graphene materials (PGMs) that not only combine the merits of both porous materials and graphene, but also have major advantages over other porous carbons for specific applications. The chemistry and approaches for functionalizing graphene and GO are first introduced, and typical procedures for pore creation (e.g., in-plane pores, 2D laminar pores, and 3D interconnected pore assemblies), self-assembly, and tailoring mechanisms for PGMs to highlight the significance of precise control over the pore morphology and pore size are summarized. Because of their unique pore structures, with different morphologies and intriguing properties, PGMs serve as key components in a variety of applications such as energy storage, electrocatalysis, and molecular separation. Finally, the challenges relating to PGMs from the understanding of chemical self-assembly to specific applications are discussed, and promising solutions on how to tackle them are presented. This provides an insightful outlook for the future development of the chemistry and applications of PGMs.

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Ferroptosis, implicated in several diseases, is a new form of programmed and nonapoptotic cell death triggered by iron-dependent lipid peroxidation after inactivation of the cystine/glutamate antiporter system xc–, which is composed of solute carrier family 7 membrane 11 (SLC7A11) and solute carrier family 3 membrane 2 (SLC3A2). Therefore, inducing ferroptosis through inhibiting the cystine/glutamate antiporter system xc– may be an effective way to treat cancer. In previous screening tests, we found that the benzopyran derivative 2-imino-6-methoxy-2H-chromene-3-carbothioamide (IMCA) significantly inhibited the viability of colorectal cancer cells. However, the impact of IMCA on ferroptosis remains unknown. Hence, this study investigated the effect of IMCA on ferroptosis and elucidated the underlying molecular mechanism. Results showed that IMCA significantly inhibited the cell viability of colorectal cancer cells in vitro and inhibited tumor growth with negligible organ toxicity in vivo. Further studies showed that IMCA significantly induced the ferroptosis of colorectal cancer cells. Mechanistically, IMCA downregulated the expression of SLC7A11 and decreased the contents of cysteine and glutathione, which resulted in reactive oxygen species accumulation and ferroptosis. Furthermore, overexpression of SLC7A11 significantly attenuated the ferroptosis caused by IMCA. In addition, IMCA regulated the activity of the AMPK/mTOR/p70S6k signaling pathway, which is related to the activity of SLC7A11 and ferroptosis. Collectively, our research provided experimental evidences on the activity and mechanism of ferroptosis induced by IMCA and revealed that IMCA might be a promising therapeutic drug for colorectal cancer.