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. Author manuscript; available in PMC: 2021 Sep 1.
Published in final edited form as: Pharmacol Ther. 2020 May 29;213:107591. doi: 10.1016/j.pharmthera.2020.107591

Table 1.

Oncogenic or Tumor-Suppressive Long Non-coding RNAs involved in cancer immunity regulation

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.