The effects of miR-145-5p or combined with TLR4 on cell proliferation, colony formation, migration, and invasion abilities were investigated by (4,5-Dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide, colony formation, wound healing, and transwell assays, respectively.
The viability and invasion were suppressed when miR-145-5p was inhibited in trophoblasts cells, while miR-145-5p overexpression promoted the effectiveness.
Down-regulation of long noncoding RNA PVT1 inhibits esophageal carcinoma cell migration and invasion and promotes cell apoptosis via microRNA-145-mediated inhibition of FSCN1.
Furthermore, we found that LINC00491 positively regulates SERPINE1 expression through sponging miR-145 and promoting the proliferation, migration, and invasion of colon adenocarcinoma cells, thus playing an oncogenic role during colon adenocarcinoma pathogenesis.
High expression of miR-21 and low expression of miR-145 are closely related to the development and progression of CRC, especially with the grade of differentiation, invasion, metastasis and clinical stage.
Moreover, miR-145 expression was enhanced by lidocaine; and transfection with miR-145 inhibitor increased cell viability, proliferation, migration, and invasion, but inhibited apoptosis.
<b>Conclusion:</b> These findings suggested that miR-145 can inhibit HOXA1 to inactivate the ERK/MAPK signaling pathway, thereby suppressing OSCC cell proliferation, migration, and invasion to further inhibit the development of OSCC, highlighting a novel therapeutic target for the OSCC treatment.
In addition, miR-145 inhibits the proliferation, cell cycle and invasion, and promotes the apoptosis of fibroblasts by down-regulating the expression of SOX-9.
In this review, we summarized the recent findings regarding miR-145, to elucidate its functional roles in cell invasion and migration of diverse human malignancies, and considered it a potential biomarker for cancer diagnosis, screening, and prognosis.
The lower expression of miR-145 increases <i>pd-l1</i> mRNA stability due to the reduction of its direct binding to 3'-UTR of <i>pd-l1</i> mRNA, in turn leading to increasing in <i>pd-l1</i> mRNA stability and expression, and finally enhancing stem-like property and invasion of BC cells.
Functionally, LncRNA-ROR could induce epithelial-mesenchymal transition (EMT), and regulated ovarian cancer cell migration and invasion by decreasing the expression of tumor suppressive miR-145 and its target gene FLNB.
<b>Conclusion:</b> These results suggested that CDX2 inhibits the expression of miR-145-5p, thereby relieving the inhibitory effect of miR-145-5p on the translation of SENP1 and affecting the invasion and migration of prostate cancer cells.
Treating MIR145-5p with MAP(Aib)-cRGD also revealed various anticancer effects, such as cell viability, invasion inhibition, and apoptosis induction in WiDr cells.
The overexpression of miR-145 could remarkably reduce the expression level of ADAM19 in PC-9/G cells, increase the sensitivity of PC-9/G cells to gefitinib, and inhibit cell invasion and metastasis.
In addition, the protein expression levels of RIOK2 and NOB1 were inhibited in response to miR‑145 overexpression, thus resulting in the suppression of cell viability, migration and invasion.
MYPT1 knockdown by siRNAs reproduced miR-145 effects suggesting miR-145 as a tumor suppressor through MYPT1 targeting, leading to a subsequent increase of pMLC levels with implications for cervical cell viability, migration and invasion.
In adenocarcinoma cell lines, we have previously demonstrated that expression of miR-145, leads to enhanced invasion, resistance to anoikis and better attachment to fibronectin in esophageal adenocarcinoma.
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.