| Gene information | Literature | Expression | lncRNA | Mutation | Homolog |
Basic Information | |
|---|---|
Gene ID | 768216 |
Name | MIR454 |
Synonymous | microRNA 454;MIR454;microRNA 454 |
Definition | - |
Position | 17q22 |
Gene type | ncRNA |
Title | Abstract |
| The oncogenic role of microRNA-130a/301a/454 in human colorectal cancer via targeting Smad4 expression. | Transforming growth factor (TGF)-beta/Smad signaling plays an important role in colon cancer development, progression and metastasis. In this study we demonstrated that the microRNA-130a/301a/454 family is up-regulated in colon cancer tissues compared to paired adjacent normal mucosa, which share the same 3 -untranslational region (3 -UTR) binding seed sequence and are predicated to target Smad4. In colorectal cancer HCT116 and SW480 cells, overexpression of miRNA-130a/301a/454 mimics enhances cell proliferation and migration, while inhibitors of these miRNAs affect cell survival. The biological function of miRNA-130a/301a/454 on colon cancer cells is likely mediated by suppression of Smad4, and the up-regulation of the miRNAs is correlated with Smad4 down-regulation in human colon cancers. Collectively, these results suggest that miRNA-130a/301a/454 are novel oncogenic miRNAs contributing to colon tumorigenesis by regulating TGF-beta/Smad signaling, which may have potential application in cancer therapy. |
| miR-454 functions as an oncogene by inhibiting CHD5 in hepatocellular carcinoma. | Previous studies showed that miR-454 acted as an oncogene or tumor suppressor in cancer. However, its function in HCC remains unknown. In this study, we found that miR-454 expression was upregulated in HCC cell lines and tissues. Knockdown of miR-454 inhibited HCC cell proliferation and invasion and epithelial mesenchymal transition (EMT), whereas overexpression of miR-454 promoted HCC cell proliferation and invasion and EMT. Furthermore, we identified the CHD5 as a direct target of miR-454. CHD5 was downregulated in HCC tissues and cell lines and the expression level of CHD5 was inversely correlated with the expression of miR-454 in HCC tissues. In addition, knockdown of miR-454 inhibited the growth of HepG2-engrafted tumors in vivo. Taken together, these results indicated that miR-454 functioned as an oncogene in HCC. |
| MicroRNA-454 functions as an oncogene by regulating PTEN in uveal melanoma. | MicroRNAs (miRNAs) regulate gene expression by targeted repression of transcription and translation, and are involved in carcinogenesis. In this study, we demonstrated that the expression of miR-454 was up-regulated in uveal melanoma tissues compared to normal tissues. Ectopic expression of miR-454 resulted in significant promotion of cell proliferation, colony formation, invasion and induction of cell cycle in uveal melanoma cells. Furthermore, we identified PTEN as a direct target of miR-454. Our data revealed that ectopic expression of PTEN restored the effects of miR-454 on cell proliferation and invasion in uveal melanoma cells. These findings support an oncogene role of miR-454 in development of uveal melanoma. |