Table 3.
Summary of possible role and potential mechanism of miRs entered this study in bladder cancer.
| microRNA | Role | Mechanism | Reference |
|---|---|---|---|
| miR-155 | Proto-oncogene | Zhang: miR-155 overexpression promotes some tumor cell growth via Wnt/β-catenin signaling activation which is also a vital pathway in bladder cancer tumorigenesis. | 14, 19 |
| Wang: Oncogenic properties of miR-155 are attributed to its antiapoptotic function through a blockade of caspase-3 activity or suppression of proapoptotic genes such as TP53BP1 and promote cell proliferation by down-regulating the SOCS1 gene, or activate PKB signaling via downregulation of tumor suppressors, including PTEN, PDCD4, and SHIP1. | |||
| miR-203 | Tumor suppressor | miR-203 simultaneously suppressed antiapoptotic factors Bcl-w and Survivin. | 15 |
| miR-21 | Proto-oncogene | Zhang: miR-21 functions through regulation of maspin and VEGF-C, suggesting a miR-21/maspin/VEGF-C pathway in bladder cancer. | 16, 25 |
| Zaravinos: miR-21 represses the tumor suppressors PTEN deleted on chromosome 10, tropomyosin 1 and the PDCD4. | |||
| miR-424 | Tumor suppressor | miR-424 regulates multiple cellular biological behaviors, such as retarding growth, inducing apoptosis, and reducing invasion, by directly targeting EGFR in bladder cancer. | 36 |
| miR-214 | Tumor suppressor | Wang: miR-214 could exert tumor-suppressive effects in bladder cancer by directly down-regulating oncogene PDRG1. | 17, 24 |
| Kim: miR-214 could be related to the inhibition of angiogenesis, to cell proliferation, and to tumor recurrence. | |||
| miR-152 | Proto-oncogene | miR-152 acts through upregulation of DNA hypermethylation in bladder cancer. | 30 |
| miR-27a-3p | Tumor suppressor | miR-27a-3p as a target of mutant p53–273 H and uncovered a novel mutant p53–273 H/miR-27a-3p/EGFR pathway which played an important role in tumorigenesis. | 30 |
| miR-143 | Tumor suppressor | miR-143 can suppress cell proliferation and migration as well as promote apoptosis in bladder cancer by inhibiting PI3K/Akt and MAPK signaling. | 21 |
| miR-224 | Proto-oncogene | The upregulation of miR-224 levels has been observed to promote cell migration and tumor growth by targeting the tumor suppressors. | 21 |
| miR-34a | Tumor suppressor | miR-34a expression can inhibit cell migration and invasion by antagonizing Notch1 signaling. | 39 |
| miR-101 | Tumor suppressor | Abnormal down-regulation of miR-101 could frequently lead to the overexpression of EZH2 in cancer, which increased cell proliferation in bladder cancer cells and retarded transition of G phase to S phase. | 34 |
| miR-222 | Proto-oncogene | miR-222 decreased the tumor suppressor PTEN, which was considered to enhance angiogenesis, tumor cell proliferation, EMT and activation of metastasis in bladder cancer. | 67 |
| miR-26a | Tumor suppressor | miR-26a functions through regulation of HMGA1 in bladder cancer. | 35 |
| miR-29c | Tumor suppressor | miR-29c regulates the apoptotic protein MCL1 and thereby regulating apoptosis as well as DNA de novo methyltransferases DNMT3A and DNMT3B, key enzymes that are frequently up-regulated in cancer. | 29 |
| miR-210 | Proto-oncogene | miR-210 over expression activates VEGF and leads to the formation of capillary structures under hypoxic conditions during the early steps of tumor development. | 25 |
| miR-200 | Tumor suppressor | Higher levels of miR-200 might inhibit EMT and prevent non-muscle invasive bladder cancer recurrence through the silencing of various target genes. | 26 |
| miR-27a | Tumor suppressor | miR-27a functions through regulation of cystine/glutamate exchanger SLC7A11 in bladder cancer. | 38 |
| miR-129 | Proto-oncogene | miR-129 simultaneously repressed the tumor suppressors SOX4 and GALNT1 in bladder cancer. | 29 |
| miR-29c* | Tumor suppressor | miR-29c* acts through downregulation of DNA methyltransferases as well as upregulation of demethylating genes to keep the normal methylation pattern. | 37 |
| miR-9 | Proto-oncogene | miR-9 directly targeted the CDH-1 gene encoding E-cadherin, a regulator of EMT, considered to be an important initiating step for tumor metastasis. | 23 |
TP53BP1: tumor protein p53 binding protein 1; SOCS1: suppressor of cytokine signaling 1; PKB: protein kinase B; PTEN: phosphatase and tensin homolog; PDCD4: programmed cell death 4; VEGF-C: vascular endothelial growth factor-C; EGFR: epidermal growth factor receptor; PDRG1: p53 and DNA-damage regulated 1; EZH2: enhancer of zeste homologue 2; HMGA1: high mobility group AT-hook 1; MCL1: myeloid cell leukemia 1; DNMT3A: DNA-methyltransferase 3 alpha; DNMT3B: DNA-methyltransferase 3 beta; EMT: epithelial-to-mesenchymal transition; SLC7A11: solute carrier family 7 member 11; SOX4: SRY-box 4; GALNT1: polypeptide N-acetylgalactosaminyltransferase 1; CDH1: cadherin 1.