Insulin-like growth factor 2 messenger RNA (mRNA)-binding protein 2 (IGF2BP2) is a widely studied N⁶-methyladenosine (m⁶A) modification reader, primarily functioning to recognize and bind to m⁶A modification sites on the mRNA of downstream target genes, thereby enhancing their stability. Previous studies have suggested that the IGF2BP2-m⁶A modification plays an essential role in cellular functions and the progression of various diseases. In this review, we focus on summarizing the molecular mechanisms by which IGF2BP2 enhances the mRNA stability of downstream target genes through m⁶A modification, thereby regulating cell ferroptosis, epithelial–mesenchymal transition (EMT), stemness, angiogenesis, inflammatory responses, and lipid metabolism, ultimately affecting disease progression. Additionally, we update the related research progress on IGF2BP2. This article aims to elucidate the effects of IGF2BP2 on cell ferroptosis, EMT, stemness, angiogenesis, inflammatory responses, and lipid metabolism, providing a new perspective for a comprehensive understanding of the relationship between IGF2BP2 and cell functions such as ferroptosis and EMT, as well as the potential for targeted IGF2BP2 therapy for tumors and other diseases.

YBX1 is a member of the Y-box transcription factor family and is a multifunctional RNA/DNA-binding protein characterized by a highly conserved cold shock domain (CSD). YBX1 is localized in both the cytoplasm and nucleus, where it participates in various biological processes such as transcription, translation, and DNA damage repair. YBX1 is upregulated in numerous malignant tumors and is closely associated with tumor progression and poor prognosis, making it a recognized target for cancer therapy. This review introduces the role and mechanism of YBX1 in tumor progression, its function in embryonic development, bone differentiation, cartilage formation, and adipogenesis, the impact of upstream regulatory factors on its function, as well as the relationship between YBX1 and disease prognosis and treatment outcomes. This review aims to provide a comprehensive perspective on the function of YBX1.

Cancer cells are capable of surviving, proliferating, and invading or migrating within hypoxic environments by regulating various adaptive mechanisms. Due to the activation of oncogenes and the inactivation of tumor suppressor genes, and relative deficiencies in oxygen and nutrients, cancer cells demonstrate elevated production of reactive oxygen species (ROS), primarily sourced from NADPH oxidases (NOX family). A key aspect of the reorientation of tumor cell metabolism is the combating of cellular oxidative stress through the promotion of antioxidant molecule synthesis to counteract ROS production. Given that most cancers experience hypoxia and that NOX is closely linked to numerous redox‐dependent signaling pathways, the expression and function of NOX are altered in various malignancies. Therefore, this review summarizes the characteristics of NOX family members, their influence on tumor proliferation, invasion, and migration, the role of NOX in promoting tumor angiogenesis, the impact of NOX on the function of immune cells within the tumor microenvironment, and the potential of targeting NOX in tumor therapy. This aims to offer a fresh viewpoint on a comprehensive understanding of the functions of NOX family members.

Radiotherapy is the treatment of choice for nasopharyngeal cancer, but resistance to radiotherapy is the main obstacle. Previous studies have found that CD38 is involved in the occurrence and development of nasopharyngeal carcinoma and is closely related to the resistance of nasopharyngeal carcinoma cells to radiotherapy. In this study, targeted quantitative detection of energy metabolism and Co-IP combined with liquid chromatography-mass spectrometry suggested that CD38 may be closely related to ferroptosis. It was further found that CD38 inhibited the levels of ferroptosis-related indicators in nasopharyngeal carcinoma cells, and CD38 promoted radiotherapy resistance by inhibiting ferroptosis. Mechanistically, CD38, SLC7A11, and TRIM21 proteins interact with each other, and CD38 inhibits TRIM21-mediated ubiquitinated degradation of the SLC7A11 protein in its K48-linked form by competitively binding to the E3 ubiquitin ligase TRIM21. CD38 inhibits ferroptosis in nasopharyngeal carcinoma cells by stabilizing SLC7A11 proteins to activate the SLC7A11/GSH/GPX4 ferroptosis signaling axis, thereby promoting radiotherapy resistance. In summary, we demonstrated for the first time that CD38 stabilizes SLC7A11 proteins by competitively binding to TRIM21, and revealed a novel mechanism of the CD38/SLC7A11/GSH/GPX4 ferroptosis signaling axis in radiotherapy resistance in nasopharyngeal carcinoma cells, highlighting the potential of CD38 as a radiosensitizing target for nasopharyngeal carcinoma.

RNA-binding Fox-1 homolog 2 (RBFOX2) is a key RNA-binding protein that primarily functions by regulating alternative splicing. Furthermore, RBFOX2 regulates RNA metabolism across the transcriptional and multiple post-transcriptional stages, encompassing recognizing RNA epigenetic modifications, inhibiting transcription, regulating alternative polyadenylation, inhibiting miRNA processing, and stabilizing mRNA. Additionally, RBFOX2 is regulated by upstream factors such as RNA binding proteins, non-coding RNAs, and transcription factors. RBFOX2 is extensively involved in the regulation of development and the maintenance of physiological functions. The dysregulation of RBFOX2 is closely associated with tumors, cardiovascular diseases, developmental defects and metabolic diseases. In this review, we summarize the regulatory functions of RBFOX2 in terms of both alternative and non-alternative splicing, the upstream regulatory factors of RBFOX2, and its relationship with disease etiology and progression, with the aim of providing a comprehensive understanding of the role of RBFOX2 and offering new insights for the study of RBFOX2.