RBPs are involved in regulating several processes such as RNA alternative splicing, RNA decay, RNA translation, RNA translocation and so on. Over the last decades, researches have shown that dysregulation of RBPs contributes to cancer treatment resistance.
RBP inhibitors in combination with other treatments such as chemotherapy, radiotherapy, anti-HER2 therapy and immunotherapy might be a promising therapeutic option for patients who have developed treatment resistance. Therefore, in recent years, RBP-targeted therapies will be attractive to reverse therapeutic resistance.
In sum, RBPs play critical roles in the regulation of autoimmunity and autoinflammation at different steps and via different mechanisms. Proinflammatory RBPs promote innate inflammatory responses and GC responses via strengthening inflammatory mRNA expression and translation or constraining inhibitory immune signaling.
RBPs can regulate endocrine therapy resistance, chemotherapy resistance, targeted therapy resistance and immunotherapy resistance by conducting RNA alternative splicing, RNA decay, RNA translation, RNA translocation and other mechanisms [ 11 ].