<p>miR-665 Suppresses the Epithelial–Mesenchymal Transition and Progression of Gastric Cancer by Targeting <em>CRIM1</em></p>

Abstract

Background: Gastric cancer (GC) is one of the most common aggressive cancers and is characterized by high mortality. Increasing evidence has shown that microRNA-665 (miRNA-665) serves as inhibiting-miRNA in cancers. However, the role of miR-665 in GC is yet unclear. Methods: miR-665 was first analyzed using bioinformatics. Subsequent quantitative realtime PCR was used to detect miR-665 expression levels in different GC cell lines and tissues. The function of miR-665 in GC cells was determined via Cell Counting Kit 8, colony formation, wound healing, and transwell assays. Furthermore, Western blotting was utilized to measure the expression level of epithelial-mesenchymal transition (EMT)-related proteins. The target prediction and luciferase reporter assays were performed to confirm the binding between miR-665 and 3ʹ-UTR of the CRIM1 gene. In addition, rescue assays were used to determine whether CRIM1 upregulation abolished the inhibitory effect of miR-665. Results: The expression of miR-665 was significantly decreased in GC patients and GC cell lines. Clinical and pathological analyses showed that the low expression of miR-665 was significantly associated with high TNM stage (P = 0.007), distant metastasis (P = 0.031), and poor differentiation (P = 0.029). Endogenic mimics of miR-665 remarkably suppressed GC cell proliferation, migration, invasion, and EMT in in vitro experiments. Inhibition of miR-665 expression induced the opposite effects. The results of the bioinformatics analysis and dual-luciferase assay showed that miR-665 targeted the 3ʹ-UTR of the CRIM1 gene. Rescue assays revealed that overexpression of CRIM1 attenuated the inhibitory effects of miR-665 in GC progression and EMT. Conclusion: The overall study results demonstrated that miR-665 inhibits tumor progression and EMT in GC by targeting CRIM1, indicating that miR-665 might be a potential therapeutic target in the treatment of GC patients.

MicroRNA-1269b inhibits gastric cancer development through regulating methyltransferase-like 3 (METTL3)

“…MiRNA expression profile is related to the characteristics of diverse cancers and can be used for screening differentially expressed miRNAs [22,23]. Through microarray analysis, we found that the expression of miR-4636, miR-1298, miR-4268, miR-4290, miR-1275, miR-148a-3p, miR-375, miR-943 and miR-665 were downregulated in GC tissues, which is consistent with the previous research findings [9,[24][25][26][27][28][29][30][31]. Herein, we mainly focused on miR-1269b.…”

LncRNA DCST1-AS1 Promotes Endometrial Cancer Progression by Modulating the MiR-665/HOXB5 and MiR-873-5p/CADM1 Pathways

“…In osteosarcoma, miR-665 regulates Rab23 expression to inhibit tumor invasion and metastasis ( 35 ). Additionally, miR-665 suppresses epithelial–mesenchymal transition (EMT) and gastric cancer progression by targeting cysteine-rich motor neuron protein 1 (CRIM1) ( 36 ). However, little is known about the function of miR-665 in EC as well as the association between lncRNA DCST1-AS1 with miR-665.…”

Downregulation of MIAT reduces the proliferation and migratory and invasive abilities of retinoblastoma cells by sponging miR‑665 and regulating LASP1

“…Increasing research efforts have been engaged to elucidate the anti-tumour roles of miR-665 in human cancer (38)(39)(40). For example, miR-665 downregulation was reported to reverse the suppressive effects of the lncRNA RHPN1-AS1 on the proliferation and migratory and invasive abilities of OC cells (38).…”