Kirsten RAS viral oncogene homolog (KRAS) is one of the most frequently mutated oncogenes in human cancers. Its mutations result in constitutive activation of the protein, which drives the mitogen-activated protein kinase (MAPK) and phosphoinositide 3-kinase (PI3K) signaling pathways and promotes tumor progression. Meanwhile, microRNAs (miRNAs), as key post-transcriptional regulators, can directly or indirectly modulate the activity of the KRAS signaling network, forming a bidirectional regulatory axis. This review summarizes the complex interplay between KRAS and miRNAs: on one hand, specific miRNAs suppress oncogenic signaling by targeting KRAS or its upstream/downstream effectors; on the other hand, mutant KRAS actively hijacks miRNA biogenesis, processing, and function, leading to a global reprogramming of miRNA expression that drives tumor progression, immune evasion, and drug resistance. In-depth dissection of this dynamic regulatory mechanism not only offers novel insights into the biology of KRAS-driven tumors, but also establishes a theoretical foundation for developing miRNA-based therapeutic interventions.