Table 1.
LncRNA | O/T | Cell type | Localization | Immunity-Related Mechanisms | Reference |
---|---|---|---|---|---|
LINK-A | O | Tumor cell | Cytoplasm | Inhibits breast cancer cell antigen presentation and decrease CTL cells infiltration | (Q. Hu, et al., 2019) |
HOTAIR | O | Tumor cell, macroph age and MDSC | Nuclear | Promotes gastric cancer cell (HLA)-G expression via inhibiting miR-152 and miR-148a, also facilitates macrophage and MDSC activity in liver cancer through transcriptional upregulation of chemokine (C-C motif) ligand 2 | (Fujisaka, et al., 2018; Song, et al., 2015) |
MALAT1 | O | Tumor cell and MDSC | Nuclear | Increase the expression of PD-L1 by sponging miR-195 and modulating miR-200a, promotes infiltration of MDSC in lung cancer | (Q. M. Wang, et al., 2019; Wei, et al., 2019; Q. Zhou, et al., 2018) |
LncRNA-C ox2 | O | Macrop hages | Nuclear | Regulates the inflammatory gene expression in the macrophages via interacts with heterogeneous nuclear ribonucleoprotein A/B and A2/B1, assembles into the switch/sucrose nonfermentable (SWI/SNF) complex and regulating the NF-κb signaling axis | (Bian, Yang, Zhang, Li, Wang, Jiang, Chen, Li, et al., 2019; Carpenter, et al., 2013; Elling, et al., 2018) |
CASC2c | T | Macrop hages | Nuclear | Inhibits of M2 polarization and decreased proliferation of tumor cells via downregulating the expression and extracellular production of coagulation factor X (FX) | (Y. Zhang, et al., 2018) |
TUC339 | O | Macrop hagy | Nuclear | Upregulates the expression of M2 markers after IFN-γ + LPS treatment | (X. Li, et al., 2018) |
Morrbid | T | T cell | Nuclear | Controls the expansion, survival, and effector function of CD8+ T cells by regulating the expression of the pro-apoptotic factor Bcl2111 and the strength of the PI3K-AKT signaling pathway | (Kotzin, et al., 2019) |
Lnc-CD56 | T | NK Cell | Nuclear | Promotes the expression of CD56 and differentiation of NK cells from human CD34 + hematopoietic progenitor cells | (R. Zhang, et al., 2016) |
GAS5 | T | NK Cell | Nuclear | Enhances the killing effect of NK cell on liver cancer through regulating miR-544/RUNX3 | (Fang, et al., 2019) |
Linc-MAF-4 | T | T Cell | Nuclear | Facilitates the differentiation of T cells toward the TH2 phenotype through regulating MAF transcriptional activities by recruiting chromatin modifiers | (Ranzani, et al., 2015) |
Lnc-DC | T | DC Cell | Cytoplasm | Promotes the DC differentiation by activating the transcription factor STAT3 and increase the ability of DCs to stimulate T cell activation | (P. Wang, et al., 2014) |
Flatr | O | T Cell | Nuclear | Modulates chromatin accessibility of the FoxP3 gene loci, leading to impaired Treg activity and autoimmunity | (Brajic, et al., 2018) |
NKILA | T | T Cell | Regulates T cell sensitivity to AICD by inhibiting NF-κB activity | (Huang, et al., 2018) | |
Lnc-EGFR | O | T Cell | Cytoplasm | Stimulates the differentiation of Treg cells, thereby inhibiting CTL activity in the tumor area and enhancing the growth of HCC | (R. Jiang, et al., 2017) |
Lnc-CHOP | O | MDSC | Nuclear | Promotes MDSC differentiation by interacting with CHOP and C / EBPβ isoforms to encourage C / EBPβ activation and regulate a large number of target transcripts in MDSC | (Gao, Wang, et al., 2018) |
Lnc-C/EBP beta | O | MDSC | Nuclear | Controls immune-suppressive function and differentiation of MDSCs by regulating a set of target transcripts, such as Arg-1, NOS2, NOX2, and COX2 | (Gao, Sun, et al., 2018) |
PVT1 | O | MDSC | Nuclear | Promotes the immunosuppressive function of G-MDSCs in vitro and in vivo | (Zheng, et al., 2019) |
Olfr29-ps1 | O | MDSC | Nuclear | Regulates the differentiation and function of MDSCs through a m6A-modified Olfr29-ps1/miR-214–3p/MyD88 regulatory network | (Shang, et al., 2019) |
HOXA | T | MDSC | Nuclear | delay tumor progression and enhance the antitumor immune response by downregulating the immunosuppression of MDSCs | (Tian, et al., 2018) |
O/T represents the role of lncRNA as Oncogenic or Tumor-Suppressive Long Non-coding RNAs regulating cancer immunity, respectively.