MicroRNAs (miRNAs) are a class of non-coding RNAs that have crucial roles in gene expression patterns and molecular networks involved in a wide range of biological processes, including cell proliferation, apoptosis, differentiation, and migration [1], [2]. The miRNA processing involves several steps performed by the ribonuclease III enzymes Drosha and DICER [3]. Since more than 50% of miRNAs are located in cancer-associated genomic regions, miRNAs play a pivotal role in cancer pathogenesis [4], [5], so the biological functions of miRNAs have extensively been investigated in cancer. MiR-140 was first identified in the cartilage development of mouse embryos and zebrafish during bone development [6]. Afterward, the significant role of miR-140 in cancer was also unraveled, and its tumor suppressor functions were reported in human malignancies [7]. miR-140 gene is located on 16q22.1, and its pre-miRNA is processed to miR-140-3p and miR-140-5p, which regulate different targets and direct the proliferation and differentiation of different cell types [8]. It has been shown that miR-140 regulates several signaling cascades such as Wnt/β-catenin, PI3K/AKT, mTOR, and TGF-β1/Smad signaling. MiR-140-5p down-regulation can induce proliferation, migration, and invasion of several tumor types such as human tongue cancer, hepatocellular carcinoma, and colorectal cancer [9], [10]. Therefore, this miRNA can affect the pathogenesis of various cancers through the modulation of different pathways. These complicated interacting networks convey the importance of miR-140 in different aspects of carcinogenesis. Moreover, miR-140 plays an essential role in neoplastic cells' sensitivity to chemotherapeutic agents, such as temozolomide, cisplatin, doxorubicin, and radiotherapy, as well as many targeted therapies against cancer [11], [12]. This review aims to discuss different aspects of miR-140 function in human cancers and evaluate various pathways and involved hub genes.