Table 1 The information of OS
From: MicroRNA-143 expression inhibits the growth and the invasion of osteosarcoma
References | Genes/proteins affected | Functions |
|---|---|---|
Zhang [41] | LncRNA FOXD2-AS1┤ miR-143 | LncRNA FOXD2-AS1 knockdown inhibits the resistance of human osteosarcoma cells to cisplatin by inhibiting miR-143 expression |
Li [42] | lncRNA MALAT1/miR-143/NRSN2/Wnt/β-Catenin | Bone marrow mesenchymal stem cells-derived extracellular vesicles promote proliferation, invasion and migration of osteosarcoma cells via the lncRNA MALAT1/miR-143/NRSN2/Wnt/β-Catenin Axis |
Bi [43] | Long non-coding RNA colon cancer-associated transcript 2┤ miR-143 | Long non-coding RNA colon cancer-associated transcript 2 knockdown proliferation and metastasis of osteosarcoma cells by inhibiting miR-143 expression |
Yang [44] | – | MiR-143-3p function as diagnostic and prognostic markers for osteosarcoma |
Han [14] | miR-143-3p ┤KIAA1429 | Knockdown of KIAA1429 or ectopic overexpression of miR143-3p could repress stemness cell properties and the inhibition could be partly abolished by overexpression of KIAA1429 |
Wu [39] | LncRNA- PCAT6┤miR-143-3p /ZEB1 | LncRNA-PCAT6 Aggravates Osteosarcoma Tumorigenesis via the MiR-143-3p/ZEB1 Axis |
Wen [1] | LncRNA-SARCC → miR-143┤ Hexokinase 2 | LncRNA-SARCC sensitizes OS to cisplatin through the miR-143-mediated glycolysis inhibition by targeting Hexokinase 2 |
Yu [5] | TGF-β → LncRNA-TUG1 ┤miR-143-5p┤HIF-1α → VEGF | Long non-coding RNA Taurine upregulated gene 1 promotes OS cell metastasis by mediating HIF-1α via miR143-5p |
Jerez [24] | – | MiRNAs (miR-21-5p, miR-143-3p, miR-148a-3p and 181a-5p) present in EVs may regulate the metastatic potential of OS cell lines by potentially inhibiting a network of genes (MAPK1, NRAS, FRS2, PRCKE, BCL2 and QKI) involved in apoptosis and/or cell adhesion |
Zhao [25] | – | The expression of miR-143 was significantly lower in low-grade OS compared to high-grade OS. The expression of miR-143 was significantly lower in OS with lung metastasis compared to OS without lung metastases |
Hou [6] | miR-143-3p┤MAPK7 | Mechanism of miR-143-3p inhibiting proliferation, migration and invasion of OS cells by targeting MAPK7. |
Sun [7] | miR-143 ┤ FOSL2 | MiR143-3p directly and negatively targets FOSL2 to affect OS characteristics |
Dong [15] | miR-143-3p ┤MAPK7 | MiR-143 suppress the proliferation, migration and invasion ability of OS cells via downregulating the MAPK7 expression |
Zhang [26] | CircRNA-UBAP2 ┤miR-143┤Bcl-2 | Circular-RNA UBAP2 was found to inhibit the expression of microRNA-143 (miR-143), thus enhancing the expression and function of anti-apoptotic Bcl-2 |
Li [27] | Low dosage cisplatin → miR-143 | Under low dosage cisplatin treatment, miR-143 may be activated in induce the expression of Bcl-2, which further impede the cell proliferation |
WH Li [28] | miR-143┤Bcl-2 miR-143 → Caspase-3 | MiR-143 could inhibit Bcl-2 expression, causing Caspase-3 activation, thus inducing apoptosis in OS cells |
Hirahata [4] | miR-143-3p ┤PAI-1 → MMP-13 | PAI-1, a target gene of miR-143, regulates invasion and lung metastasis via enhancement of MMP-13 expression and secretion in human OS cells |
Liu [29] | miR-143┤Bcl-2 | mRNA and protein levels of Bcl-2 were depressed after over-expression of miR-143. Meanwhile, the inhibition of miR-143 potentiated intracellular Bcl-2 level |
Zhou [30] | H2O2 → p53, miR-143 ┤ATG2B, Bcl-2, and LC3-I | The chemoresistance of OS tumor cells to doxorubicin is associated with the downregulation of miR-143 expression, activation of ALDH1+CD133+cells, activation of autophagy, and inhibition of cell death |
Fang [31] | Negative correlation between COX-2 and miRNA-143 | COX-2 expression in the tumor tissue and blood samples of patients with OS increases significantly along with the degree of tumor malignancy, and this is accompanied by a decreased expression of miRNA-143; A negative correlation between COX-2 and miRNA-143 may exist in the progression of OS |
Shimbo [3] | – | Exosome-formed miR-143 was easily transferred into recipient cells and suppressed the migration of the 143B OS cell line |
Li [32] | TGF-β1(Smad 2/3 pathway)┤miR-143 | TGF-β1 suppressed miR-143 expression through a Smad 2/3-dependent pathway |
Wang [33] | miR-143┤EGFR → ERK/MAPK → MMP9 | MiR-143 inhibits EGFR signaling through its downstream ERK/MAPK signaling cascades to control MMP9 expression in OS. Thus, miR-143, EGFR, and MMP9 are therapeutic targets for inhibiting OS invasion |
Ye [34] | Propofol → miR-143 ┤MMP-13 | Propofol may have antitumor potential in OS, which is partly due to the downregulation of MMP-13 expression by miR-143 |
Li [35] | Notch-1┤miR-143 | Diallyl trisulfide could be useful for inhibiting OS development and progression via suppression of Notch-1 signaling, accompanied by downregulation of Hes-1, VEGF, MMP-2 and MMP-9, as well as upregulation of specific tumor-suppressive miRNAs (miR34a, miR-143, miR-145 and miR-200b/c) |
Ouyang [8] | – | The circulating levels of miR-143 were significantly decreased in patients with OS compared with controls |
Hu [36] | – | The differential expression profiles of miRNAs between OS and osteoblast cell lines were investigated by miRNA microarrays and real-time quantitative PCR (RT-qPCR). A total of 268 miRNAs were identified that were significantly dysregulated in OS compared with the osteoblast cell line, including miR-9, miR-99, miR-195, miR-148a and miR-181a, which had been validated as overexpressed, and miR-143, miR-145, miR-335 and miR-539, which were confirmed to be downregulated |
Osaki [37] | miR-143 ┤MMP-13 | The downregulation of miR-143 correlates with the lung metastasis of human OS cells by promoting cellular invasion, probably via MMP-13 upregulation |
Zhang [38] | miR-143┤Bcl-2 | Bcl-2, an important antiapoptotic molecule, was identified to be a novel direct target of miR-143, and the proapoptotic function of miR-143 is further suggested to be mainly through the targeting of Bcl-2 expression |