We show that NEAT1 is highly expressed in <b>P</b>apillary <b>T</b>hyroid <b>C</b>arcinoma cell line (PTC-1) and anaplastic thyroid cancer cell line (SW1736) as compared with the human thyroid follicular epithelial cell line (Nthy-ori 3-1). shRNA knockdown of NEAT1 led to the inhibition of cell growth, invasion, migration and <b>E</b>pithelial to <b>M</b>esenchymal <b>T</b>ransition (EMT) of thyroid cancer cells.
NEAT1 knockdown inhibited cervical cancer development through repressing cell proliferation, colony formation, capacity of migration, and invasion and also inducing the apoptosis.
NEAT1 promoted the progression of BC cells through inhibiting apoptosis‑associated genes and promoting cell cycle‑ and invasion‑associated gene expression, whereas miR‑107 served the opposite function.
In this study, we observed that the expression of NEAT1 was significantly upregulated in melanoma tissues, which remarkedly promoted the cells' proliferation, cell migration, and invasion in melanoma cell lines.
Comprehensive microarray-based analysis demonstrated that nuclear expression of LRP1B intracellular domain significantly increased long non-coding RNA nuclear paraspeckle assembly transcript 1 (NEAT1) expression, which facilitates breast cancer invasion with poor prognosis.
Overexpression of NEAT1 promoted proliferation and invasion while inhibited apoptosis in HCC cells, which was opposite to the effect of NEAT1 knockdown.
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.
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.