Mechanistic investigations demonstrated that MALAT1, as a competing endogenous RNA (ceRNA), regulated osteosarcoma proliferation and metastasis through competitively binding to miR-34a/c-5p and miR-449a/b.
Here, we provide an overview of the function of miR-34a in tumor-associated EMT. ceRNA hypothesis plays an important role in miR-34a regulation in EMT, cancer progression, and metastasis.
Moreover, miR‑34 has been identified as a tumour‑suppressor in GC. p53‑induced miR‑34 regulates several different target genes and signalling pathways, inducing apoptosis, senescence, and cell cycle arrest and repressing GC cell proliferation, migration and metastasis, thus contributing to the suppression of carcinogenesis and GC cancer progression.
Notably, blocking LIN28B/MYC/miR-34a-5p signaling pathway by LIN28B-specific inhibitor causes dramatic inhibition of tumor growth and metastasis in immunodeficient orthotopic mouse models of human breast cancer cell MDA-MB-231.
High miR-34a expression was associated with better survival of patients. miR-34a showed lower expression levels in male patients with lymph node involvement, and a trend towards decreased expression in male patients with distant metastases.
Downregulation of miR-34a distinguished between patients with bladder cancer and the healthy controls. miR-34a expression was associated with tumor metastasis; however, not with tumor size.
Luciferase activity assay showed that <i>miR-34a-5p</i> directly target Smad family member 4 (Smad4), which is associated with cancer cell invasiveness and metastasis.
According to the results, this work uncovers a previously unappreciated ZDHHC8P1/miR-34a regulatory axis in controlling progression and metastasis of CRC and suggests that interfering with lncRNA-ZDHHC8P1 and miR-34a could be a viable approach to treat late-stage metastatic CRC patients.
Collectively, these findings suggested a plausible role of CD44v/SYNE1/miR34a axis as non-invasive salivary biomarkers to diagnose this disease at an early stage and predict the early onset of metastasis.
Combined inactivation of the microRNA 34a gene (MIR34A, by methylation) and the TP53 gene (by mutation or deletion) is observed in 50% of colorectal tumors that progress to distant metastases.
Further results indicated that SNHG7 facilitated the proliferation and metastasis as a competing endogenous RNA to regulate GALNT7 expression by sponging miR-34a in CRC cell lines.
The low expression of miR-34a in patients with cervical cancer is related to the degree of tumor differentiation as well as invasion and metastasis, and the low expression of miR-218 is related to the degree of tumor differentiation, invasion and metastasis and clinical staging. miR-34a and miR-218 in the serum can be used as markers for the diagnosis of cervical cancer and reference indicators for the evaluation of prognosis.
The expression of shrimp miR-34 in breast cancer cells and in mice suppressed the growth and metastasis of breast cancer by targeting human CCND1, CDK6, CCNE2, E2F3, FOSL1, and MET genes in a cross-phylum manner.
Here, we studied miR-34a-5p expression, and Met-receptor expression and localization in bone metastases from ductal breast carcinomas, and in ductal carcinomas without history of metastasis (20 cases). miR-34a-5p was elevated in non-metastatic breast carcinoma, intermediate in the adjacent tissue and practically absent in bone metastases, opposite to pair-matched carcinoma.
The expressions of miR-34a/34b/34c were significantly lower in TNBC patients than in HC (p<0.001, p=0.027, p<0.001, respectively). miR-34a was correlated with tumor grade (p=0.038), lymph node positive (p=0.027), distant metastasis (p=0.004), and surgery (p=0.023); miR-34b was correlated with lymph node positivity (p=0.027); and miR-34c was correlated with tumor grade (p=0.017) and distant metastasis (p<0.001).
Taken together, the results of the present study suggested that the overexpression of miR-34a may have suppressed HCC metastasis via inhibited cell migration and invasion.
Here, the potential association between aberrant miR-34 expression and promoter methylation and distant metastases formation in lung adenocarcinoma (LAC) is investigated.