Poor-differentiation group has lower miR-143/-4636 levels in serum (P < .05). miR-4636 level was correlated gross tumor volume and the depth of invasion (P < .0001).
LncRNA-H19 knockdown repressed cell viability, migration and invasion while promoted apoptosis in Y79 cells. miR-143 was a downstream factor of lncRNA-H19, and its inhibition reversed the effects of lncRNA-H19 silence on Y79 cells.
Restoration experiments disclosed that CTNND1 upregulation weakened the inhibitory effects of miR-143-3p on CRC cell proliferation, migration and invasion.
Furthermore, miR‑143 inhibited glioma cells migration and invasion through cytoskeletal rearrangement in vitro and in vivo through matrigel invasion assay, scratch assay, cellular F‑actin measurement, chemotaxis assay and intracranial brain tumor xenografts.
Rescue assays showed that miR-143-3p inhibitors or ITGA6 overexpression could reverse the inhibitory effects of OIP5-AS1 suppression on the proliferation and invasion in CC cells.
The aim of this study was to investigate the effect of miR-31 and miR-143 inhibition on metastasis and invasion in both MDA-MB231, MDA-MB468 as well as the MCF-7 breast cancer cell lines and 5-week old female mice.
Secondly, we indicated that the up-regulation of miR-143-3p in the ovarian cancer cell lines SKOV3, ES2, and OVCAR3 significantly reduced their proliferation, migration, and invasion.
The LncRNA UCA1 was also found to upregulate the expression of miR-143, and overexpression of miR-143 could also suppress the proliferation, migration, and invasion of the SK-MES-1 lung cancer cells.
We had earlier shown that the microRNA-143 (miR-143) replenishment not only chemosensitizers CRC cell line with mutant KRAS instead of wild-type KRAS gene, to paclitaxel-mediated cytotoxicity, but also inhibits cell migration and invasion ability.
GATA6 was identified as the downstream target of miR-143 in HCC, and overexpressing GATA6 was able to counter the tumor-suppressive effect of miR-143 on HCC in HepG2 and Bel7402 cells by significantly increasing proliferation and invasion rates (P<0.05).
Finally, our results indicated that increased expression of MMP7 reversed the potential influence of miR-143 on CRC cell proliferation and invasion ability.
Using gain- and loss-of-function experiments in vitro, we demonstrate that miR-143-3p negatively regulated cell growth, apoptosis, migration and invasion.
Loss-of-function and rescue experiments revealed that hsa_circ_0001982 knockdown suppressed breast cancer cell proliferation and invasion and induced apoptosis by targeting miR-143.