Overexpression of miR-145 showed no significant effects on Erbb4-IR expression, but played an opposite role on cancer cell proliferation and apoptosis.
Overexpression of BRE-AS1 and miR-145-5p led to inhibited proliferation and promoted apoptosis of PC cells. miR-145-5p inhibitor attenuated the effects of BRE-AS1 overexpression on cancer cell behaviors.
Overexpression of miR‑145‑3p significantly reduced cancer cell proliferation, migration and invasive abilities, and further increased apoptotic abilities.
We conclude that miR-145 is a potential marker for use in the early diagnosis and prognostic evaluation of patients with cancer, has a role as a tumor suppressor, and is a promising cancer treatment target candidate.
Acting as an important tumor-related miRNA, the clinical significance and underlying mechanisms of miR-145 in various malignant tumors have been investigated by numerous studies.
To mimic in vivo cancer microenvironment, hypoxia and serum deprivation were used to induce metastasis in breast (MCF-7, MDA-MB-231, MDA-MB-453), prostate (PC3, LNCaP, DU145), lung (A549, NCIH82,) cancer cell lines and noncancerous cell lines of the coresponding tissues (MCF10A, RWPE-1, MRC-5). miR-145-3p expression levels were determined by qRT-PCR.
Collectively, our findings elucidated the role of miR-145-5p as an important regulator of drug resistance in prolactinoma by controlling TPT1, and implicated the potential application of miR-145-5p in cancer therapy as well.
Hepatocellular carcinoma (HCC) is a malignant cancer with a high fatality rate, and the expression of microRNA-145 (miR-145) is significantly low in HCC tissue.
MicroRNA-145 (miR-145) is commonly down-regulated and has been identified as a tumor-suppressive miRNA in multiple types of cancers, as well as in esophageal squamous cell carcinoma (ESCC).
To test discrimination of cancer from non-cancer, the area under the receiver operating characteristic curves determined for cancer antigen 125 (CA125), miR-145, miR-200c, miR-21, and miR-93 were 0.801 (<i>p</i><0.001), 0.910 (<i>p</i><0.001), 0.802 (<i>p</i><0.001), 0.585 (<i>p</i>=0.303), and 0.755 (<i>p</i>=0.002), respectively.
This distinctive role of miR-145 in the regulation of metastasis-related gene expression may introduce miR-145 as an ideal candidate for controlling of cancer metastasis by miRNA replacement therapy.
miR-145 is a tumor suppressive miRNA which is abnormally reduced in different cancers. miR-145 overexpression reduces cancer migration, invasion, and cell adhesion.
Further target-gene prediction and pathway enrichment analysis indicated that deregulated miRNAs in F-CAFs showed significant associations with "pathways in cancer" (miR-145-3p, miR-299-3p and miR-410-3p), "Wnt signaling pathway" (miR-410-3p and miR-505-3p), and "TGF-beta signaling pathway" (miR-410-3p).
The tumor suppressor miR‑145 has been reported to be lowly expressed in numerous types of human cancer; in the present study, the expression levels of miR‑145 were decreased in patients with NSCLC.