Scratch wound healing assay and transwell invasion assay were conducted to test the effects of MALAT1 and miR-206 on migration and invasion of trophoblast cells.
Previous studies in our lab found that long non-coding RNA (lncRNAs) Metastasis-Associated Lung Adenocarcinoma Transcript 1 (MALAT1) was up regulated in HCC cells, which could affect the metastasis and invasion of HCC.
Transfection of MALAT1 siRNA suppressed its expression in endometrial cells, inhibited cell proliferation or invasion, enhanced caspase 3 activity, decreased NF-κB/iNOS or MMP-9 expression (p<0.05 comparing to control group).
The expression of metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is increased in numerous types of tumors and is involved in tumor cell proliferation, migration, invasion and apoptosis.
CONCLUSIONS High MALAT1 expression promotes the proliferation, migration, and invasion of non-small cell lung cancer via the ERK/MAPK signaling pathway.
Knockdown of MALAT1 or overexpression of miR-200a-3p inhibited cell proliferation, migration and invasion but increased apoptosis and autophagy formation in ATC cells.
The present study indicated that resveratrol inhibited migration and invasion in human gastric cancer cells via suppressing MALAT1-mediated epithelial-to-mesenchymal transition, providing novel evidence for understanding the anticancer mechanism of resveratrol.
Rescue experiments further demonstrated that MALAT1 knockdown partially reversed anti‑miR‑34a‑mediated promotion on OS cell viability, migration and invasion; overexpression of CCND1 partially reversed the effects of MALAT1 silencing on OS progression.
CCK-8 assay, transwell migration and invasion assay were performed to investigate the effects of MALAT1 knockdown on the proliferation, migration and invasion of tongue cancer cells, respectively.
MiR-145-5p overexpression in PC3-DTX led to inhibited cell proliferation, migration and invasion as well as reduced chemoresistance to DTX, which was attenuated by MALAT1.
We also showed that MALAT1 promoted epithelial-mesenchymal transition, cell migration, and invasion by activating Akt/mTOR signaling in A549 and H1299 cells. miR-206 was a direct downstream target of MALAT1 in NSCLC.
The levels of MALAT1 are reported to be overexpressed in most tumor tissues or sera, and the expression levels of MALAT1 often affect the tumor size, stage, lymph node metastasis, and distant invasion.
In addition, reciprocal abolishment of the effects of miR663a overexpression and MALAT1 activation on the proliferation, migration, and invasion of cancer cells was also observed, while miR663a upregulation and MALAT1 activation alone inhibited and promoted the behaviors of these CC cell lines, respectively.
In addition, miR-124 suppression inhibited cell apoptosis and remarkably abolished the inhibitory effects of MALAT1 silence on cell viability, migration, and invasion (<i>p</i> < 0.05, <i>p</i> < 0.01, or <i>p</i> < 0.001).