Furthermore, miR-195-5p inhibitor abrogated the effects of short-interfering BRAF-activated noncoding RNA on PANC-1 and SW1990 cell growth and invasion <i>in vitro</i>.
Subsequently, the expression of LINC00355 and miR-195 was altered to evaluate their effects on viability, invasion, migration, epithelial mesenchymal transition (EMT), and apoptosis of cancer stem cells (CSCs) in HNSCC.
Hsa-miR-195 is a molecule associated with abnormal placental growth mechanisms such as impaired cellular proliferation, inadequate trophoblastic invasion causing defective spiral artery remodeling, and apoptosis.
Moreover, cell migration and invasion were significantly inhibited in the mimic group. miR‑195 specifically targeted IGF1, however, the co‑transfection of IGF1 could partially reverse the inhibitory effects of miR‑195 on rectal cancer cells.
These findings indicated that expression of miRNA-195 in laryngeal carcinoma tissue is down-regulated, and the low expression of miRNA-195 may be related to invasion and metastasis of laryngeal carcinoma, which indicates poor prognosis of patients.
We found that miR-195 directly targets <i>TUBB</i>; knockdown of <i>TUBB</i> sensitizes cells to MTAs, while overexpression confers resistance; high expression of <i>TUBB</i> is correlated with worse survival of lung adenocarcinoma; TUBB is also regulated by CHEK1, which has been shown to regulate chemoresistance; and miR-195 targets <i>BIRC5</i> to repress migration and invasion <i>in vitro</i> and metastasis <i>in vivo</i>.
Exogenous induction of miR-195-5p suppressed multiple mediators of invasion and angiogenesis in colorectal cancer cells and increased the apoptotic cell population in both cell lines.
On the whole, the findings of this study indicate that the inhibitory effects of miR195 on EC cell migration and invasion are associated with the PI3K/AKT signaling pathway and GPER expression.
Our data constitute evidence that miR-195 inhibits lung adenocarcinoma cell proliferation and invasion though targeting apelin and provides novel insight into the mechanism underlying the development of lung adenocarcinoma.
While transfecting miR-195 mimics decreased the proliferation, migration, and invasion of colon cancer cells, miR-195 inhibition exerted opposing effects.
Inhibition of JAK/STAT and NF-κB pathways reversed the effects of miR-195 suppression on propofol-induced MKN 45 cell proliferation, migration and invasion inhibition, as well as apoptosis enhancement.
Our results suggest that MMP14 is a direct target of miR-195-5p, and down-regulated MMP14 and up-regulated miR-195-5p suppressed proliferation and invasion of CC cells by inhibiting TNF signaling pathway.
Additionally, upregulation of miR-195 and knockdown of hepatoma-derived growth factor (HDGF) inhibited proliferation, migration and invasion of cervical cancer cells.
Here we find that miR-195-5p expression is lower in OSCC than in nontumor tissues, while its overexpression in cell lines can lead to the promotion of apoptosis and the reduction of cell growth, migration, and invasion.
In addition, the rescue experiment revealed that overexpression of VEGFA reversed the inhibitory effects of miR‑195 overexpression on the invasion ability and tube formation of HUVECs.
In summary, these data suggest that low expression of miR-195 contributes to the poor prognosis of LSCC and miR-195 regulates the proliferation and invasion ability of LSCC cells in vitro. miR-195 may suppress growth and invasion of LSCC cells possibly through targeting DCUN1D1, which would provide a candidate target for cancer therapy.