miRNA已经成为其靶基因表达的关键调节因子，由于其在癌症发生和发展等各种细胞过程中的参与引起了重要关注。在涉及癌症的miRNA广泛复杂的库中，miR-136-5p作为一种新兴miRNA而出现，并具有多种作用。已经证明miR-136-5p在人类癌症中的失调。越来越多的证据表明，miR-136-5p主要起到肿瘤抑制剂的作用。这些数据表明，miR-136-5p参与了细胞增殖、迁移、侵袭、EMT和凋亡等各种细胞过程的调节。此外，miR-136-5p在人类癌症中展示了显著的潜在作为预后和诊断标志物，以及在癌症化疗中的有效介体。此外，miR-136-5p与患者的临床病理特征相关，提出其可用于癌症分期和患者生存。因此，全面理解不同癌症中miR-136-5p失调的精确分子基础对揭示其治疗的重要性至关重要。在这里，我们就miR-136-5p作为潜在肿瘤抑制剂的分子基础以及其在癌症诊断、预后和化疗中的重要性进行了讨论。最后，我们还讨论了将miRNA作为治疗靶点的挑战以及miR-136-5p在人类癌症中的重要性前景。版权所有 © 2023 Elsevier GmbH. 保留所有权利。

MiRNAs have emerged as crucial modulators of the expression of their target genes, attracting significant attention due to their engagement in various cellular processes, like cancer onset and development. Amidst the extensive repertoire of miRNAs implicated in cancer, miR-136-5p has emerged as an emerging miRNA with diverse roles. Dysregulation of miR-136-5p has been proved in human cancers. Accumulating evidence suggests that miR-136-5p mainly functions as a tumor suppressor. These data proposed that miR-136-5p is engaged in the regulation of various cellular processes, like cell proliferation, migration, invasion, EMT, and apoptosis. In addition, miR-136-5p has demonstrated substantial potential as a prognostic and diagnostic marker in human cancers as well as an effective mediator in cancer chemotherapy. Furthermore, miR-136-5p was shown to be correlated with clinicopathological features of affected patients, proposing that it could be used for cancer staging and patient survival. Therefore, a comprehensive comprehension of the precise molecular basis governing miR-136-5p dysregulation in different cancers is vital for unraveling its therapeutic importance. Here, we have discussed the molecular basis of miR-136-5p as a potential tumor suppressor as well as its importance in cancer diagnosis, prognosis, and chemotherapy. Finally, we have discussed the challenge of using miRNAs as a therapeutic target as well as the prospect regarding the importance of miR-136-5p in human cancers.Copyright © 2023 Elsevier GmbH. All rights reserved.