RNA-binding proteins (RBPs) act as crucial regulators of gene expression within cells, exerting precise control over processes such as RNA splicing, transport, localization, stability, and translation through their specific binding to RNA molecules. The diversity and complexity of RBPs are particularly significant in cancer biology, as they directly impact a multitude of RNA metabolic events closely associated with tumor initiation and progression. The fragile X mental retardation protein (FMRP), as a member of the RBP family, is central to the neurodevelopmental disorder fragile X syndrome and increasingly recognized in the modulation of cancer biology through its influence on RNA metabolism. The protein’s versatility, stemming from its diverse RNA-binding domains, enables it to govern a wide array of transcript processing events. Modifications in FMRP’s expression or localization have been associated with the regulation of mRNAs linked to various processes pertinent to cancer, including tumor proliferation, metastasis, epithelial–mesenchymal transition, cellular senescence, chemotherapy/radiotherapy resistance, and immunotherapy evasion. In this review, we emphasize recent findings and analyses that suggest contrasting functions of this protein family in tumorigenesis. Our knowledge of the proteins that are regulated by FMRP is rapidly growing, and this has led to the identification of multiple targets for therapeutic intervention of cancer, some of which have already moved into clinical trials or clinical practice.

Autophagy is a conserved intracellular degradation system that plays a dual role in cell death; thus, therapies targeting autophagy in cancer are somewhat controversial. Ferroptosis is a new form of regulated cell death featured with the iron-dependent accumulation of lethal lipid ROS. This pathway is morphologically, biochemically and genetically distinct from other forms of cell death. Accumulating studies have revealed crosstalk between autophagy and ferroptosis at the molecular level. In this review, we summarize the mechanisms of ferroptosis and autophagy, and more importantly, their roles in the drug resistance of cancer. Numerous connections between ferroptosis and autophagy have been revealed, and a strong causal relationship exists wherein one process controls the other and can be utilized as potential therapeutic targets for cancer. The elucidation of when and how to modulate their crosstalk using therapeutic strategies depends on an understanding of the fine-tuned switch between ferroptosis and autophagy, and approaches designed to manipulate the intensity of autophagy might be the key.