Non-coding RNAs (ncRNAs) are functional regulatory molecules that influence cellular processes, including chromatin remodeling, transcription, and signal transduction. They play key roles in cancer by acting as oncogenic drivers or tumor suppressors. Recent advances in sequencing technologies have revealed a vast diversity of ncRNAs, including microRNAs (miRNAs), long ncRNAs (lncRNAs), and circular RNAs (circRNAs), which regulate gene expression through complex interactions. These interactions form network motifs that are common in biological and social systems, and their disruption can lead to cancer progression. ncRNAs participate in various network motifs, such as feedback loops and feedforward loops, which regulate gene expression and cellular behavior. For example, feedback loops can maintain steady-state activity of signaling pathways, while feedforward loops can regulate gene expression in a sensitive manner. ncRNAs can also act as competitive endogenous RNAs (ceRNAs), competing for miRNA binding sites to influence gene expression. Some ncRNAs, like lncRNAs and circRNAs, can sequester miRNAs, thereby modulating their activity. The function of ncRNAs can be context-dependent, with the same ncRNA acting as an oncogene or tumor suppressor in different cancers or even within the same cancer type. Super genes, which produce multiple gene products from a single locus, can contribute to the complexity of ncRNA networks. These include type I supergenes, which produce either a protein or an lncRNA, and type II supergenes, which generate multiple functional products from a single transcript. Type III supergenes combine features of both. ncRNAs also regulate protein complexes, such as the SWI/SNF chromatin remodeling complex, and can influence the epigenetic state of genes. Additionally, ncRNAs can modulate mRNA stability and translation through interactions with proteins or miRNAs. For example, the lncRNA HOTAIR can recruit the Polycomb repressive complex 2 (PRC2) to modify chromatin, while the circRNA circ-ITCH can sequester miRNAs to regulate gene expression. Disruptions in ncRNA networks can lead to cancer, as seen in the formation of fusion circRNAs from chromosomal translocations. Altered adenosine-to-inosine editing can also affect miRNA targeting, influencing gene expression and cancer progression. Variations in 3'UTR sequences can alter miRNA binding sites, affecting gene regulation. Overall, ncRNAs are integral to gene regulatory networks and their dysregulation contributes to cancer development and progression. Understanding these networks is crucial for developing new therapeutic strategies targeting ncRNAs in cancer.Non-coding RNAs (ncRNAs) are functional regulatory molecules that influence cellular processes, including chromatin remodeling, transcription, and signal transduction. They play key roles in cancer by acting as oncogenic drivers or tumor suppressors. Recent advances in sequencing technologies have revealed a vast diversity of ncRNAs, including microRNAs (miRNAs), long ncRNAs (lncRNAs), and circular RNAs (circRNAs), which regulate gene expression through complex interactions. These interactions form network motifs that are common in biological and social systems, and their disruption can lead to cancer progression. ncRNAs participate in various network motifs, such as feedback loops and feedforward loops, which regulate gene expression and cellular behavior. For example, feedback loops can maintain steady-state activity of signaling pathways, while feedforward loops can regulate gene expression in a sensitive manner. ncRNAs can also act as competitive endogenous RNAs (ceRNAs), competing for miRNA binding sites to influence gene expression. Some ncRNAs, like lncRNAs and circRNAs, can sequester miRNAs, thereby modulating their activity. The function of ncRNAs can be context-dependent, with the same ncRNA acting as an oncogene or tumor suppressor in different cancers or even within the same cancer type. Super genes, which produce multiple gene products from a single locus, can contribute to the complexity of ncRNA networks. These include type I supergenes, which produce either a protein or an lncRNA, and type II supergenes, which generate multiple functional products from a single transcript. Type III supergenes combine features of both. ncRNAs also regulate protein complexes, such as the SWI/SNF chromatin remodeling complex, and can influence the epigenetic state of genes. Additionally, ncRNAs can modulate mRNA stability and translation through interactions with proteins or miRNAs. For example, the lncRNA HOTAIR can recruit the Polycomb repressive complex 2 (PRC2) to modify chromatin, while the circRNA circ-ITCH can sequester miRNAs to regulate gene expression. Disruptions in ncRNA networks can lead to cancer, as seen in the formation of fusion circRNAs from chromosomal translocations. Altered adenosine-to-inosine editing can also affect miRNA targeting, influencing gene expression and cancer progression. Variations in 3'UTR sequences can alter miRNA binding sites, affecting gene regulation. Overall, ncRNAs are integral to gene regulatory networks and their dysregulation contributes to cancer development and progression. Understanding these networks is crucial for developing new therapeutic strategies targeting ncRNAs in cancer.