play important functions in the pathogenesis of several cancer types, including pros­tate cancer (PCa). Within the framework of prostate cancer, non-coding RNAs have the capacity to function as either oncogenic or tumor-suppressive agents. ncRNAs have the potential to participate in the prostate cancer progression by inuencing the signaling of the androgen receptor (AR), the degradation process of AR via

The early indication of the involvement of miRNAs in tumorigenesis was pre­sented by Croce and his collaborators, who discovered a tumor-suppressive sequence located at chromosome 13q14 [14]. The research conducted has shown a high fre­quency of deletions in the area indicated above among individuals diagnosed with chronic lymphocytic leukemia. Additionally, it has been observed that this sequence encodes two distinct miRNA genes, namely miR-16a and miR-15a. The miRNA genes in question exhibit deletions or experience transcriptional downregulation in blood-related tumors, such as chronic lymphocytic leukemia [14]. Subsequent investigations have provided additional evidence indicating that both miR-15a and miR-16a serve as tumor-suppressive miRNAs by promoting cell death via the repression of an anti-apoptotic protein known as B-cell lymphoma 2 (Bcl-2). Notably, Bcl-2 is found to be excessively expressed in blood-related tumors [15,

In addition, it is noteworthy that a tumor-suppressive family of miRNAs, known as miR-200, plays a pivotal role in EMT regulation. The family comprises miR-200a/ b/c, -141, and -429. Research was conducted to examine the impact of miR-200c-3p on the invasiveness of prostate cancer cells. The ndings revealed a considerable downregulation of miR-200c-3p in human prostate cancer cell lines, such as PC3 and DU145, in comparison to the normal prostatic epithelial cell line (RWPE1). The inhibitory effects of miR-200c-3p on cell motility, cell migration, and cell invasion have been suggested to occur via its targeting of zinc nger E-box binding homeobox 2 (ZEB2), which acts as a repressor of E-cadherin and a promoter of EMT [50]. The inhibition of miR-200b in prostate cancer has been shown to downregulate epithelial­mesenchymal transition, hinder growth, and impede metastasis via a route mediated by ZEB1, which is comparable to previous ndings [51]. In a study, it was observed that the downregulation of miR-141-3p plays a role in the metastasis and invasiveness of prostate cancer by activating the nuclear factor kappa b (NF- κB) signaling pathway [52]. Moreover, miR-141-3p enrichment enhances the stemness features in prostate cancer stem cells (PCSCs) by inhibiting a group of genes associated with promoting metastasis, such as Ras homologous (Rho) GTPases, EZH2, and CD44 [53]. Furthermore, the reduced expression of miR-204 5p was linked with disease progres­sion and metastasis, in addition to its established function in regulating cell prolifera­tion and cell death through the apoptosis pathway. Wa and colleagues demonstrated that miR-204-5p exerts inhibitory effects on invasion, migration, and bone metastasis. These effects are achieved through the suppression of NF-κB signaling, which is accomplished by targeting three key proteins at the same time: tumor necrosis factor receptor-associated factor 1 (TRAF1), TGF-β activated kinase 1 (MAP3K7) binding protein 3 (TAB3), and mitogen- activated protein kinase kinase kinase 3 (MAP3K3) [54]. Furthermore, many studies have provided insights into the signicant incorpora- tion of the miR-34a tumor suppressor in the invasiveness of prostate cancer, with a noticeable decrease in its expression reported in prostate tumors [55]. The study con­ducted by Liang and coworkers demonstrated the inhibitory impact of miR-34a on the Wnt signaling pathway, leading to the suppression of migration and invasion associ­ated with EMT in prostate tumors [56]. Liu’s team showed that miR-34a has a role in the development of resistance to paclitaxel-based chemotherapy in prostate cancer cells. This resistance is achieved by the direct inhibition of the JAG1/Notch1 axis [57]. Furthermore, Yan and coworkers (2015) provided evidence for the engagement of miR-34a in the regulation of PCSCs and the process of metastasis by its direct repres­sion of CD44 expression. In addition, a comprehensive analysis was conducted in a recent study to thoroughly examine the participation of many microRNAs, such as miR-185, miR-148, and miR-145in the regulation of the phenotype of PCSCs and their contribution to the invasive and metastatic properties of prostate cancer [58, 59].