Elevated lactate levels in solid tumors contribute to immunosuppression, metabolic reprogramming, and resistance to therapy. Although lactate oxidase (LOX) offers a viable strategy for in situ lactate depletion, its therapeutic efficacy is fundamentally limited by tumor hypoxia due to the oxygen dependence of LOX. Here, we report a hybrid nanomaterial-microbial system that enables hypoxia-resistant lactate catabolism through near-infrared (NIR)-IIb-triggered upconverson photosynthesis. This system integrates LOX-producing Escherichia coli (E. coli) with Chlorella (Chl) and lanthanide-doped upconversion nanoparticles (UCNPs), which convert deeply penetrating 1550 nm light into visible emission to drive oxygenic photosynthesis. Unlike conventional photosynthetic oxygenation approaches limited by shallow visible light penetration, this system enables spatiotemporally controlled oxygen generation deep within tumors, sustaining LOX activity under hypoxia. In murine tumor models, the hybrid symbionts significantly inhibited tumor growth, promoted T cell infiltration, and induced durable immune memory. This work establishes a versatile optogenetic-metabolic platform for overcoming oxygen-limited metabolism in cancer therapy via deep-tissue-activatable microbial photosynthesis.

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.