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.
Furthermore, the ectopic expression of NEAT1_1 in OVCAR-3 cell lines promoted cell proliferation and invasion, whereas knockdown of NEAT1_1 did the opposite.
The present study aimed to explore the role of long non-coding RNA NEAT1 (NEAT1) in mediating non-small cell lung cancer (NSCLC) cell migration and invasion, as well as the underlying regulatory mechanisms.
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.
In summary, lncRNA NEAT1 is high-expressed in GC and functions as an oncogene to modulate apoptosis, invasion, proliferation and chemotherapy resistance of GC cells, which might be a novel potential therapeutic target for GC.
Overexpression of NEAT1 promoted proliferation and invasion while inhibited apoptosis in HCC cells, which was opposite to the effect of NEAT1 knockdown.
NEAT1 knockout inhibited thyroid cancer cell survival, migration and invasion, along with reduced β‑catenin (a direct target of miRNA‑214) protein expression.
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.
Furthermore, inhibition of miR-194 reversed the suppression of proliferation and invasion and the promotion of apoptosis induced by NEAT1 depletion in osteosarcoma cells.
Results showed that NEAT1 expression in colorectal cancer was up-regulated in 72.0% (172/239) cases compared with corresponding normal counterparts, and related to tumor differentiation, invasion, metastasis and TNM stage.