Table II.
OncomiRs in action.
| miR | Targets | Tumor | Impact on metastasis | Description |
|---|---|---|---|---|
| miR-106a ∼ 363, miR-106b ∼ 25 | BIM, p21 | Gastric cancer | The miR-106b-25 cluster is involved in E2F1 post-transcriptional regulation and may play a key role in the development of TGFβ resistance in gastric cancer | |
| E2F1 | Prostate cancer | microRNA expression becomes altered with the development and progression of prostate cancer. Some of these microRNAs regulate the expression of cancer-related genes in prostate cancer cells | ||
| PTEN | Prostate cancer | Proto-oncogenic miRNA-dependent network for PTEN regulation | ||
| miR-21 | PTEN | Cholangiocarcinoma | Promotes | miR-21 modulates gemcitabine-induced apoptosis by phosphatase and the tensin homolog deleted on chromosome 10 (PTEN)-dependent activation of PI3-kinase signaling |
| TPM1 | Breast cancer | Suppression of miR-21 can inhibit tumor growth | ||
| PDCD4 | Breast cancer | The tumor suppressor protein programmed cell death 4 (PDCD4) is regulated by miR-21, and it has been demonstrated that PDCD4 is a functionally important target for miR-21 in breast cancer cells | ||
| SPRY1 | miR-21-null mice show a significant reduction in papilloma formation compared with wild-type mice due to the up-regulation of its tumor-suppressor targets | |||
| RECK, TIMP3 | Glioblastoma | The inhibition of miR-21 provides a novel therapeutic approach for ‘physiological’ modulation of multiple proteins whose expression is deregulated in cancer | ||
| p63, JMY, TOPORS, TP53BP2, DAXX, HNRPK, TGFβRII | Glioblastoma | miR-21 targets multiple important components of p53, transforming growth factor-β (TGFβ), and mitochondrial apoptosis tumor-suppressive pathways | ||
| MARKS | Prostate cancer | miR-21 could promote apoptosis resistance, motility, and invasion in prostate cancer cells | ||
| ANP32A, SACA4 | Prostate cancer | |||
| miR-10a/10b | HOXB1, HOXB3 | Pancreatic cancer | Promotes | miR-10a is a key mediator of metastatic behavior in pancreatic cancer that regulates metastasis via suppression of HOXB1 and HOXB3 |
| HOXD10 | Breast cancer | TWIST transcription factor induces expression of a specific microRNA that suppresses its direct target and in turn activates another pro-metastatic gene, leading to tumor cell invasion and metastasis | ||
| KLF4 | Esophageal cancer | A significant correlation of miR-10b level with cell motility and invasiveness | ||
| TIAM1 | Breast cancer | A mechanism for the regulation of Tiam1-mediated Rac activation in breast cancer cells | ||
| Nf1 | Ewing's sarcoma | miR-10b may play an important role in NF1 tumorigenesis through targeting neurofibromin and RAS signaling | ||
| miR-107/103 | DICER | Breast cancer | Promotes | Dicer inhibition drifts epithelial cancer toward a less-differentiated, mesenchymal fate to foster metastasis |
| miR-9 | PRDM1/Blimp-1 | Lymphomas | Promotes | miRNA-mediated down-regulation of PRDM1/Blimp-1 may contribute to the phenotype maintenance and pathogenesis of lymphoma cells by interfering with normal B-cell terminal differentiation |
| CDH1 | Breast cancer | |||
| CAMTA | Glioblastoma | miR-9 is highly expressed in glioblastoma cancer stem cells and reduces the levels of CAMTA tumor-suppressor | ||
| miR-17–92 | TSP-1, CTGF | Colon | Promotes | Up-regulated in colonocytes coexpressing K-Ras, c-Myc and p53 impaired activity |
| E2F2, E2F3 | Prostate/Burkitt lymphoma/testis carcinoma/ | Presence of an autoregulatory feedback loop between E2F factors and miR-17/92 | ||
| BIM, PTEN | c-Myc-induced lymphoma | Transgenic mice with higher expression of miR-17/92 in lymphocytes | ||
| HIF1α | Lung cancer | Intricate and finely tuned circuit involving c-myc, miR-17/92, and HIF1α | ||
| PTPRO | Cervix tumor cell line | PTPRO gene is co-regulated by both E2F1 and miR-17/92 at transcriptional and post-transcriptional level, respectively | ||
| p63 | Myeloid cells | miR-92 increases cell proliferation by negative regulation of an isoform of the cell cycle regulator p63 | ||
| BIM, PTEN, PRKAA1, PPP2R5e | T-cell acute lymphoblastic leukemia | Functional genomics approach reveals a co-ordinate clamp-down on several regulators of phosphatidylinositol-3-OH kinase-related survival signals by the leukemogenic miR-19 | ||
| JAK1 | Endothelial cells | The miR-17/92 family may provide an interesting therapeutic perspective specifically to enhance therapeutic angiogenesis | ||
| HBP1 | Breast cancer | The miR-17/92 cluster plays an important role in breast cancer cell invasion and migration by suppressing HBP1 and subsequently activating Wnt/β-catenin | ||
| p21(WAF1) | Ras-induced senescent fibroblasts | Disruption of senescence by miR-17/92 or its miR-17/20a components leads to enhanced oncogenic transformation by activated Ras in primary human cells | ||
| TGFβII SA4 | Glioblastoma | miR-17/92 attenuates the TGFβ signaling pathway to shut down clusterin expression, thereby stimulating angiogenesis and tumor cell growth | ||
| MnSOD, GPX2, TRXR2 | Prostate | miR-17/92 may suppress tumorigenicity of prostate cancer through inhibition of mitochondrial antioxidant enzymes | ||
| miR-221/222 | p27kip1 | Glioblastoma, prostate and thyroid carcinoma | Promotes | Certain cancer cell lines require high activity of miR-221/222 to maintain low p27kip1 levels and continuous proliferation |
| p57kip2 | Normal fibroblast | Up-regulation of miR-221/222 is tightly linked to the initiation of S phase with growth factor signaling pathways that stimulate cell proliferation | ||
| PTEN, TIMP3 | Non-small cell lung cancer and hepatocellular carcinoma | miR-221/222, by targeting PTEN and TIMP3 tumor suppressors, induce TRAIL resistance and enhance cellular migration. The MET oncogene is involved in miR-221/222 activation through the c-Jun transcription factor | ||
| FOXO3A | Breast cancer | The miR-221/222 cluster targets FOXO3A to suppress p27kip1 also at a transcriptional level | ||
| KIT | Endothelial cells | Interaction between miR-222 and c-Kit is likely to be part of a complex circuit that controls the ability of endothelial cells to form new capillaries | ||
| ESR1 | Breast cancer | Modulation of ERα is associated with antiestrogen therapy | ||
| PUMA | Glioblastoma | miR-221/222 directly regulate apoptosis by targeting PUMA in glioblastoma | ||
| TRSP1 | Breast cancer | miR-221/222 promote EMT and contribute to the more aggressive clinical behavior of basal-like breast cancers | ||
| PTPμ | Glioblastoma | miR-221/222 regulate glioma tumorigenesis at least in part through the control of PTPμ protein expression | ||
| DICER | Breast cancer | Dicer is low in ERα-negative breast cancers, since such cells express high miR-221/222 | ||
| APAF1 | Non-small cell lung cancer | miR-221/222 are modulated by both epidermal growth factor (EGF) and MET receptors, and, by targeting APAF1, miR-221/222 are responsible for gefitinib resistance | ||
| miR-155 | SOCS1 | Breast cancer | miR-155 is an oncomiR in breast cancer, and it has been suggested that miR-155 may serve as a bridge between inflammation and cancer | |
| CEBPB, PU.1, CUTL1, PICALM | AML | miR-155 as a contributor to physiological GM expansion during inflammation and to certain pathological features associated with AML | ||
| BACH1, ZIC3 | The induction of miR-155 by EBV contributes to EBV-mediated signaling in part through the modulation of transcriptional regulatory factors | |||
| ETS1, MEIS1 | Human cord blood CD34+ | miR-155 is required for megakaryocytic proliferation and differentiation | ||
| C-MAF | Lymphocytes | bic/microRNA-155 plays a key role in the homeostasis and function of the immune system | ||
| HGAL | Diffuse large B-cell lymphoma | Cell dissemination and aggressiveness is a phenotype of DLBCL typically expressing high levels of miR-155 and lacking HGAL expression | ||
| JMJD1A | Nasopharyngeal carcinoma | Up-regulation of miR-155 is partly driven by LMP1 and LMP2A, and results in down-regulation of JMJD1A, associated with N stage and poor prognosis | ||
| WEE1 | Breast cancer | miR-155 enhances mutation rates by decreasing the efficiency of DNA safeguard mechanisms by targeting of cell cycle regulators such as WEE1 | ||
| TP53INP1 | Pancreatic cancer | TP53INP1 expression is repressed by the oncogenic micro RNA miR-155, which is overexpressed in pancreatic carcinoma cells | ||
| SMAD1, SA5, HIVEP2, CEBPB, RUNX2, MYO10 | Role for miR-155 in controlling BMP-mediated cellular processes | |||
| FOXO3a | Breast cancer | Molecular links between miR-155 and FOXO3a affect cell survival and response to chemotherapy in breast cancer | ||
| hMSH2, hMSH6, and hMLH1 | Colon cancer | Inactivation of mismatch repair is induced by miR-155 | ||
| SMAD5 | Diffuse large B-cell lymphoma | Highlighted a hitherto unappreciated role of SA5 in lymphoma biology and defined a unique mechanism used by cancer cells to escape TGFβ's growth-inhibitory effects |