In addition, the downregulated miRNA hsa-mir-204 promotes invasion and proliferation of gastric cancer cells by regulating the abnormal expression of mRNAs (CHRDL1 and NPTX1) and lncRNAs (ADAMTS9-AS2, NKX2-1-AS1, TLR8-AS1, and VCAN-AS1).
The research attempted to uncover the impacts of miR-204-3p on colon cancer cells growth, migration, and invasion. miR-204-3p expression level in colon cancer tissues and diverse colon cancer cell lines were testified by the quantitative real-time polymerase chain reaction.
In conclusion, BCYRN1 acts as a promising prognostic predictor in GC patients and regulated GC cell proliferation, cell cycle, migration and invasion through targeting miR-204-5p.
<b>Conclusion:</b> Therefore, lncRNA MIR100HG promoted cancer cell proliferation, migration and invasion in LSCC possibly through the downregulation of miR-204-5p.
Conversely, the overexpression of PCNA‑1 in A549 cells transfected with miR‑204 mimics promoted the proliferation, migration and invasion of lung cancer cells.
In addition, overexpression of miR-204-5p resulted in increase of osteosarcoma cell apoptosis and decrease of osteosarcoma cell migration and invasion.
The ERβ-modulated HOTAIR is able to function via antagonizing several microRNAs, including miR-138, miR-200c, miR-204, or miR-217 to impact various oncogenes, including ADAM9, CCND2, EZH2, VEGFA, VIM, ZEB1, and ZEB2, to promote RCC proliferation and invasion.
The results showed that overexpression of miR-204 dramatically suppressed cell proliferation, migration, and invasion, caused cell cycle arrest at the G0/G1 phase, promoted cell apoptosis in vitro, and inhibited tumor growth in vivo.
Finally, it was identified that miR-204 was downregulated in glioblastoma and that its overexpression inhibited proliferation, migration and invasion in glioblastoma cells.
Subsequently, we demonstrated that ARNILA functioned as a competing endogenous RNA (ceRNA) for miR-204 to facilitate expression of its target gene Sox4, which is known to induce EMT and contribute to breast cancer progression, thereby promoting EMT, invasion and metastasis of TNBC.
Application of miR-204-5p mimics or inhibitors resulted in a decrease or increase, respectively, in melanoma cell proliferation and colony formation. miR-204-5p mimics hindered invasion, whereas miR-204-5p inhibitors stimulated cancer cell migration.
Long Non-Coding RNA MALAT1 Interacts With miR-204 to Modulate Human Hilar Cholangiocarcinoma Proliferation, Migration, and Invasion by Targeting CXCR4.
After transfection for 24 h and 48 h, c-met expression in miR-204 over-expression group gradually decreased (p<0.05 compared to control group), accompanied with reducing cell migration or invasion potency in a time dependent manner (p<0.05).
We also identified that upregulation of Six1 could downregulate miR-204-5p expression, affecting the migration and invasion of breast cancer cell lines.