Ectopic expression of miR-34a in MBC cell-line BT-549 significantly inhibits cell migration and invasion, but exhibits no clear effect on BC cell growth.
miR-34a expression was significantly decreased in human EHCC tissues and CC cell lines when compared with the adjacent non-tumor tissues and normal bile duct tissues. miR-34a was found correlated with the migration and invasion in EHCC patients.
A vast number of miRNAs, including the well-studied miR-21, miR-155 and miR-34, has been shown to regulate PDAC growth, invasion and metastasis in vitro and in vivo by targeting members of key signaling pathways.
Transwell assays, and Matrigel and wound healing assays were used to detect the effects of miR-34a expression on HCC cell invasion and migration, respectively.
Human papillomavirus-18-positive HeLa cervical cancer cells and HPV-16-positive SiHa cells were used to explore the effect of miR-34a on cell viability and invasion.
Therefore, it can be concluded that through the inhibition of CD44 expression levels, miR-34a plays a significant role in the migration and invasion of osteosarcoma cells.
With univariate analysis, statistically significant prognostic factors for RFS in adenocarcinoma patients were miR-34a expression (Relative risk (RR), 8.14; P = 0.049), TNM stage (RR, 13.55; P = 0.001), LN metastasis (RR, 4.19; P = 0.043), and the presence of lymphatic invasion (RR, 7.05; P = 0.015).
Our data suggest that GKN1 may inhibit gastric cancer cell migration and invasion by downregulating RhoA expression in a miR-185- and miR-34a-dependent manner.
Then, effects of ANRIL suppression on cell proliferation, apoptosis, migration and invasion of U251 cells as well as expression of miR-34a were assessed.
The studies in vitro revealed that SNHG7 directly binds to miR-34a and negatively regulates miR-34a expression, and SNHG7 enhances gastric cancer cell migration and invasion through suppressing miR-34a-Snail-EMT axis.
In this study, we investigated the expression of miR-34 family members, miR-34b and miR-34c, in different PCa cell lines, and discussed the molecular mechanism of miR-34b in the invasion and migration of PCa cells in vitro.
We showed that miR-34a directly binds to the 3'-untranslated region of <i>eEF2K</i> and <i>FOXM1</i> mRNAs and suppresses their expression, leading to inhibition of TNBC cell proliferation, motility, and invasion.
Our results demonstrate that miR-34a/c functions as a metastasis suppressor to regulate breast cancer migration and invasion through targeting Fra-1 oncogene and suggest a therapeutic application of miR-34 in breast cancer.
Moreover, TPD52 was demonstrated as one of miR-34a direct targets in human breast cancer cells. miR-34a was further found significantly repress epithelial-mesenchymal transition (EMT) and inhibit breast cancer cell migration and invasion via TPD52.
The miR‑34a mimic significantly reduced CRC invasion and migration abilities, while the miR‑34a inhibitor enhanced CRC invasion and migration activity.
While there is significant downregulation of tumor suppressor microRNA-34a (miR-34a), which targets many oncogenes related to proliferation, apoptosis, and invasion, high expression level of Polo-like kinase 1 (PLK1) is closely associated with short survival rates of pancreatic cancer patients.