Table 1 Roles of AIMPs in cancer.
From: Roles of aminoacyl-tRNA synthetase-interacting multi-functional proteins in physiology and cancer
AIMPs | Cancer type | Cell/tissue type | Effects | Mechanisms | References |
|---|---|---|---|---|---|
AIMP1 | LSCC | Hep2 and TU-177 | Promoted the proliferation, migration and invasion of LSCC cells | AIMP1 and LTA4H were upregulated in LSCC tissues and interacted with FSCN1 | |
| Â | GBM | Tumor tissue samples were obtained from glioma patients | Defined as an immune-related gene with prognostic value in GBM | Â | |
| Â | Melanoma | B16F10 and B16F0-OVA | Impaired BMDC vaccine-mediated protection against melanoma | The absence of AIMP1 in BMDCs reduced downstream Th1 polarization by impairing p38 MAPK signaling | |
| Â | Melanoma | B16F1 | Inhibited lung metastasis of melanoma cells | Activated NK cells through macrophages | |
|  | Breast cancer | 4T1 | Suppressed tumor growth in breast cancer‑bearing mice | Negatively regulated MDSC functions by weakening the activation of STATs, Akt and ERK | |
|  | Stomach cancer | MKN45 | The cells exhibiting an active cell cycle progression were reduced in AIMP1-treated mice | Induced tumor-suppressing cytokines, such as TNF-α and IL-1β | |
EMAP II | Lung cancer and breast cancer | LLC and MDA-MB 468 | Inhibited the primary and metastatic tumor growth and facilitated apoptosis in growing capillary endothelial cells | Â | |
| Â | GBM | U87-MG | Inhibited tumor growth | Inducing defective autophagy and G2/M arrest in GSCs by PI3K/Akt/FoxO1 | |
| Â | GBM | U87 | Inhibited GBM-induced angiogenesis | Induced autophagy by downregulating miR-96 in GECs | |
| Â | GBM | U-87 and U-251 | Inhibited the viability, migration and invasion of glioma cells | Negatively regulated the expression of ATG5 and ATG7 by downregulating miR-20a | |
|  | Melanoma | Pmel, 883, Smel and 1286 | Sensitized human melanoma to TNF-α | Induced TNF-R1 redistribution from Golgi storage pools to cell membranes and mobilization and membrane expression of TRADD | |
|  | GBM | U87 | Increased permeability of BTB | Upregulated the expression of PKC-α and increased its activity by inhibiting miR-330-3p | |
| Â | GBM | U87 | Increased permeability of BTB | Reduced the expression of TJ-related proteins by upregulating miR-429 | |
| Â | GBM | C6 | Increased permeability of BTB | Associated with caveolae-mediated transcellular pathway | |
| Â | Colorectal cancer | HT29, DLD-1, LS513 and HCT-15 | Induced apoptosis in PBMCs and Jurkat cells | Suppressed DNA synthesis and cell division in PBMCs and activated caspase 8 in Jurkat cells | |
| Â | Colorectal cancer | DLD-1 and HT29 | Mediated the apoptosis of tumor-infiltrating lymphocytes induced by hypoxia | Associated with active caspase-3 and cleaved PARP | |
AIMP2 | Â | NCI-H157, A549 and NCI-H460 | Functioned as a proapoptotic factor in response to DNA damage | Interacted with tumor suppressor p53 | |
|  |  | HeLa | Mediated the pro-apoptotic activity of TNF-α | Promoted the ubiquitin-dependent degradation of TRAF2 | |
|  | Colorectal cancer | HCT116 and HeLa | Controlled ISC compartments and tumorigenesis | Inhibited Wnt/β-catenin signaling | |
| Â | Â | A549 | Participated in lung cell differentiation and suppressed proliferation of the epithelial carcinoma cells | Downregulated FBP and c-Myc | |
|  |  | WI-26, 293 T and HeLa | Inhibited tumor formation | Bound to Smurf2 and thus enhanced the ubiquitination of FBP | |
| Â | NPC | CNE2, HK1 and S26 | Induced CSC-like properties | RARS-MAD1L1 fusion protein interacted with AIMP2 to increase the expression of FBP | |
AIMP2-DX2 | Lung cancer | A549, NCI-H460, H322 and H157 | Increased susceptibility to carcinogen-induced lung tumorigenesis | AIMP2-DX2 impaired the pro-apoptotic activity of AIMP2 through binding to p53 | |
|  | Ovarian cancer | A2780, SKOV3 and HeyA8 | Contributed to the chemoresistance of ovarian cancer | Reduced the pro-apoptotic activity of TNF-α by competitively inhibiting the binding of AIMP2 to TRAF2 | |
| Â | Lung cancer | H522, H1435, H460, etc. | Led to an increase in AIMP2-DX2 levels | HSP70 blocked the Siah1 binding and ubiquitination of AIMP2-DX2 | |
| Â | NPC | 5-8F, CNE-1 and CNE-2Z | Promoted the proliferation, migration and invasion of NPC cells | AIMP2-DX2 upregulated MMP-2 and MMP-9 | |
| Â | Lung cancer | H460 | Inhibited the growth of cancer cells | Targeted and replaced the AIMP2-DX2 RNA with a new transcript by a trans-splicing ribozyme | |
| Â | Lung cancer | NCI-H23, NCI-H322, NCI-H358 and NCI-H460 | Reduced the viability of small cell lung cancer cells | SLCB050 inhibited the interaction between AIMP2-DX2 and p14/ARF | |
AIMP3 | Â | HCT116, A549 and H460 | The AIMP3 heterozygous mice showed high susceptibility to tumors | Upregulated p53 by directly interacting with ATM/ATR, thereby responding to DNA damage | |
| Â | Â | HeLa | The dissociated AIMP3 translocated to the nucleus and participated in the DNA damage response | MRS was phosphorylated by GCN2, causing a conformational change in MRS and the subsequent dissociation of AIMP3 from MRS | |
| Â | Liver cancer | HepG2, Hep3B and PLC/PRF/5 | HULC promoted the proliferation of liver cancer cells | Downregulated the expression of AIMP3 | |
| Â | MIBC | T24, 253J, RT112 and RT4 | The reduction of AIMP3 increased the resistance of cancer cells to ionizing radiation | Associated with impaired Tp53 transactivity and genomic instability |
