Next, SGC-7901 cells presenting with the lowest LINC00319 expression and the highest <i>miR-335-5p</i> expression were transfected with LINC00319, <i>miR-335-5p</i> inhibitor or <i>ADCY3</i> vector to examine their roles in growth and metastasis of GC cells, which was further ascertained by <i>in vivo</i> experiments.
In conclusion, our data suggest that miR-335 plays a significant role in the tumorigenesis and metastasis of OS and may serve as a therapeutic target for OS treatment.
Our previous study has indicated that miR-335-5p expression was significantly down-regulated and acted as a vital player in the metastasis of non-small cell lung cancer (NSCLC), however the underlying mechanism remained unclear.
Rho-associated coiled-coil forming protein kinase l (ROCK1) is characterized as pivotal downstream effectors of the small GTPase RhoA and reported to participate in tumor metastasis. miR-335-5p acts as tumor suppressor microRNA and is identified to be downregulated in tumor tissues. miR-335-5p/ROCK1 axis has been demonstrated to promote cell proliferation and metastasis in gastric cancer, hepatocellular carcinoma and so on.
Further cellular behavioral experiments demonstrated that DNACR promoted ROCK1-meidated proliferation and metastasis through decoying both miR-335-5p and miR-1972.
In multivariate survival analysis, clinical stage (P=0.002 for DFS, P=0.015 for OS), distant metastasis (P=0.024 for DFS, P=0.002 for OS), low expression of miR-335 (P<0.001 for DFS, P=0.002 for OS) and combined depressed miR-335 and elevated Rock1 (P=0.021 for DFS, P=0.050 for OS) expression remained as the independent prognostic factors for DFS and OS.
Moreover, cells were co-transfected with miR-335 inhibitor and Twist1 siRNA, and then cell growth and metastasis were re-evaluated. miR-335 overexpression inhibited cell viability, migration and invasion, and promoted apoptotic cells rate. miR-335 overexpression up-regulated E-Cadherin, while down-regulated N-Cadherin, Vimentin and Snail.
Performing a PCR array on cells transfected with miR-335, 19 (30.6%) out of 62 genes involved in metastasis and tumor invasion showed decreased transcription levels.
In conclusion, our results suggest that miR-335-5p and miR-15b-5p down-regulation results in TRIM29 over-expression, which induces proliferation, EMT and metastasis of NPC through the PTEN/AKT/mTOR signaling pathway.
In conclusion, our results demonstrate that miR-335 functions as a tumor suppressor and play a role in inhibiting metastasis of CRC cells through targeting ZEB2.
The aim of the paper was to study the expression of miR335 in non-small cell lung cancer (NSCLC) and miR335's relation to the metastasis, invasion, and apoptosis in lung cancer cells A549 and H1299. qRT-PCR was used to identify the miR-335 expression.
Turning to its clinical significance, the low expression of miR-335 was significantly associated with high Gleason Score (P = 0.04), advanced clinical stage (P = 0.04), and positive metastasis (P = 0.02), but not with prognosis in PCa patients.
Furthermore, the expression levels of miR-335 were significantly lower in HCC tumors with distant metastasis compared to those without distant metastasis (P=0.02).
Specific miRNAs (mir-10, mir-21, mir-155, mir-373, mir-30b, mir-126, mir-17p, mir-335) are associated with tumor metastasis and other clinical characteristics for BC, facilitating identification of individuals who are at risk.
Overexpression of miR-335 suppressed gastric cancer cell invasion and metastasis in vitro and in vivo, but has no significant effects on cell proliferation.
Of these microRNAs, miR-126 restoration reduces overall tumour growth and proliferation, whereas miR-335 inhibits metastatic cell invasion. miR-335 regulates a set of genes whose collective expression in a large cohort of human tumours is associated with risk of distal metastasis. miR-335 suppresses metastasis and migration through targeting of the progenitor cell transcription factor SOX4 and extracellular matrix component tenascin C. Expression of miR-126 and miR-335 is lost in the majority of primary breast tumours from patients who relapse, and the loss of expression of either microRNA is associated with poor distal metastasis-free survival. miR-335 and miR-126 are thus identified as metastasis suppressor microRNAs in human breast cancer.