miR-140-5p is negatively correlated with proliferation, invasion, and tumorigenesis in malignant melanoma by targeting SOX4 via the Wnt/β-catenin and NF-κB cascades.
Our further investigation indicated miR-140-3p negatively affected the tumorigenesis of SqCLC by down-regulating the expression of BRD9, an oncogene in SqCLC.
Furthermore, knockdown of miR-140-5p obviously enhanced the proliferation and tumorigenesis and repressed the apoptosis of G401 cells, and these effects were all abolished when <i>TGFBR1</i> was down-regulated.
SNHG1, as a competing endogenous RNA (ceRNA) for miR-140, enhanced TLR4 expression and activated NF-κB signaling, thereby regulating growth and tumorigenesis in CCA.
Mouse xenograft models of OSCC were established to examine the influence of miR-140-5p on OSCC tumorigenesis in vivo during 35 days after OSCC cell injection.
MicroRNA-140-5p (miR-140-5p) was demonstrated to be involved in the tumorigenesis of various human cancers; however, its role in RB remains undetermined.
Given prevalent miR-140-5p downregulation in other cancers and major impact of Pin1 overexpression on activating numerous cancer-driving pathways including global miRNA downregulation, the miR-140-5p/Pin1 axis may play a major role in tumorigenesis and offer promising therapeutic targets for HCC and other cancers.
Our results suggest the existence of a novel miR-140-5p-PDGFRA pathway and indicate that miR-140-5p acts as a tumor suppressor during ovarian carcinogenesis.