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.
Furthermore, miR‑34 is a novel prognostic and predictive biomarker in GC, and restoring miR‑34 expression by delivering miR‑34 mimics may be a promising therapeutic strategy for the treatment of GC.
Taken together, our findings support a model in which the KLF5, MYC/LINC00346/miR-34a-5p cross-talk served as critical effectors in GC tumorigenesis and progression, suggesting a new therapeutic direction in the treatment of GC.
The expression of miR-34a showed negative correlation with IGF2BP3 mRNA expression in primary GC samples and more importantly, re-overexpression of IGF2BP3 rescued the inhibitory effect of miR-34a.
Bmi-1 positively regulates stem cell-like properties via upregulating miR-21, and miR-34a negatively regulates stem cell-like characteristics by negative feedback regulation of Bmi-1 in gastric cancer.
Our study found that the expression of miR-34a was significantly decreased in DDP resistance human GC tissues and DDP resistance human GC SGC7901/DDP cells compared with normal GC tissues and cells.
Therefore, we concluded that miR-34a could inhibit tumor invasion and metastasis in gastric cancer by targeting Tgif2 and may be a novel therapeutic candidate for gastric cancer.
The regulative role of miR-335 and miR-34a over GC cell growth, apoptosis, and invasion was studied using Cell Counting Kit-8 (CCK-8) assay, flow cytometry, and transwell assay, respectively.
In conclusion, miR‑34a was associated with the clinicopathological features of gastric cancer and was a valuable predictor of patient prognosis. miR‑34a acted as a tumor suppressor to inhibit gastric cancer proliferation and invasion via the downregulation of MET.
We also showed that HOTAIR recruiting and binding to PRC2 epigenetically represses miR34a, which controls the targets C-Met (HGF/C-Met/Snail pathway) and Snail, thus contributing to GC cell-EMT process and accelerating tumor metastasis.
In conclusion, miR-34a may act as a potential tumour suppressor in gastric cancer and is associated with the mechanisms of gastric cancer metastasis; miR-34a can inhibit gastric cancer tumourigenesis by targeting PDGFR and MET through the PI3K (phosphoinositide 3-kinase)/Akt pathway.
The effects of miR-34a ectopic expression on the AKT and p-AKT expression of cisplatin-induce gastric cancer cells were determined by Western blot and flow cytometry with the PI3K pathway inhibitor Wortmannin.