NEAT1 knockdown suppressed RCC cell proliferation by inhibiting cell cycle progression, and inhibited RCC cell migration and invasion by reversing the epithelial-to-mesenchymal transition phenotype.
By contrast, inhibition of miR-365 eliminated suppressive effects of NEAT1 knockdown on OSCC cell migration and invasion. miR-365 was significantly downregulated in OSCC tissue and cell lines and an inverse correlation between miR-365 and NEAT1 expression in OSCC tissue was observed.
Our findings indicate that upregulation of NEAT1 may promote proliferation, migration and invasion of gastric cancer cells via targeting miR-335-5p/ROCK1 axis.
In addition, the colony formation assay, wound healing assay and matrigel invasion assay results indicated that downregulation of NEAT1 inhibited colony formation, cell migration and invasion.
In addition, NEAT1 knock-down suppressed cell invasion and migration and inhibited the mRNA and protein expression levels of epithelial-mesenchymal transition-related markers in ccRCC cell lines.
Functionally, knockdown of NEAT1 significantly inhibited cell proliferation and invasion and induced cell cycle arrest at the G0/G1 phase and apoptosis, whereas inhibition of miR‑365 abolished the suppressive effect of NEAT1 knockdown on cellular processes.
NEAT1 knockdown inhibited cervical cancer development through repressing cell proliferation, colony formation, capacity of migration, and invasion and also inducing the apoptosis.
We showed that lung cancer cells overexpressing NEAT1 or MALAT1 and the Oct4-silenced cells reconstituted with NEAT1 or MALAT1 promoted cell proliferation, migration and invasion.
High levels of NEAT1 promoted the clinical features of HCC, including the number of tumor nodes, metastasis, clinical TNM stage, the status of portal vein tumor embolus, vaso-invasion and the infiltration of tumor cells.
NEAT1 upregulated protein expression in the Wnt/β-catenin signaling pathway, while resveratrol reversed the negative effect of NEAT1 overexpression on MM cells through the Wnt/β-catenin signaling pathway, and hence suppressed MM cell reproduction, migration and invasion.