RNA-binding proteins (RBPs) play fundamental roles in most aspects of cell regulation, specifically in post-transcriptional modifications, thanks to their versatile RNA-binding domains and structural adaptability. This versatility permits RBPs to regulate the fate of numerous RNA transcripts within a cell to maintain cellular balance. They establish dynamic interactions with coding RNAs and non-coding RNAs, as well as with other proteins, establishing functional units known as ribonucleoprotein complexes (RNPs). These RNPs are responsible for regulating processes such as RNA splicing, stability, or polyadenylation of mRNA and localization, post-translation modifications, and RNA degradation. Disruptions in RBP-RNA networks lead to cancer advancement, though our understanding of their contributions remains fragmented. Cancer is a complicated and diverse disease primarily driven by genetic mutations impacting oncogenic or tumor-suppressive pathways and has seen a shift in perspective over the last two decades. It has become increasingly evident that cancer cells exploit post-transcriptional mechanisms to modulate protein expression levels rapidly and effectively. This enables the cells to adapt swiftly to both internal and external signals, facilitating their survival and growth in the local microenvironment. Furthermore, RBPs are mostly dysregulated in numerous classes of cancer. This dysregulation has significant consequences and effects on the expression and function of both oncogenic and tumor-suppressive proteins. Consequently, unraveling the intricate network of interactions between RBPs and their RNA targets associated with cancer provides valuable insights into tumor biology. Additionally, it may reveal novel therapeutic targets for cancer treatment. In this chapter, we review a comprehensive perspective on how RBPs contribute to cancer initiation, progression, and metastasis and discuss their potential role in the diagnosis and treatment of cancers.