miR-328 expression

This discrepancy might be attributed to different stages/grades of tumor tissues or other clinical characteristics. This review article focuses on the available literature to explore the functions of miR-328 in the development of human carcinogenesis.

18β-GRA promotes the synthesis of autophagosomes and inhibits GC cell proliferation by regulating the miR-328-3p/STAT3 signaling pathway.

Conversely, lnc-PKD2-2-3 knockdown exhibited the opposite effects (all P <0.05). Lnc-PKD2-2-3/miR-328/GPAM ceRNA network promotes CCA proliferation, invasion, and 5-FU chemoresistance.

Overexpression of FOXP3 partly reversed the effect of miR-328-3p mimics on the invasion and migration ability of IL-17-induced Caco-2 cells and the activities of MMP2 and MMP9 in the cells. Conclusion miR-328-3p inhibits the invasion and migration of IL-17-induced Caco-2 cells by down-regulating FOXP3.

Silencing of LINC00963 ameliorates PAH via modulating miR-328-3p/PFN1.

Transcriptome sequencing analysis revealed that LOXL4 was downregulated by miR-328-5p, which was confirmed by dual-luciferase reporter and western-blot assays. miR-328-5p showed targeted regulation of LOXL4 to promote cell proliferation and migration in NSCLC.

Circ-RPPH1 knockdown retarded cell malignant phenotypes and glycolysis via miR-328-3p/HMGA2 axis in BC, providing a potential therapeutic target for BC treatment.

Our study demonstrated that KDM4C may up-regulate MALAT1 expression, which decreases the expression of miR-328-3p. The downregulation of miR-328-3p increased the level of CCND2, which induced the Ara-C resistance in AML.

DHT regulates chemo-response via a mechanism independent of ABCG2 and miR-328-3p.

In summary, our study revealed that miR-328-3p targeting to PYCR1 suppressed the malignancy of LA cells by impeding cell proliferation and migration, while effectively promoting cell apoptosis.