Exploring the regulatory role of lncRNA in cancer immunity

Imbalanced immune homeostasis in cancer microenvironment is a hallmark of cancer. Increasing evidence demonstrated that long non-coding RNAs (lncRNAs) have emerged as key regulatory molecules in directly blocking the cancer immunity cycle, apart from activating negative regulatory pathways for restraining tumor immunity. lncRNAs reshape the tumor microenvironment via the recruitment and activation of innate and adaptive lymphoid cells. In this review, we summarized the versatile mechanisms of lncRNAs implicated in cancer immunity cycle, including the inhibition of antitumor T cell activation, blockade of effector T cell recruitment, disruption of T cell homing, recruitment of immunosuppressive cells, and inducing an imbalance between antitumor effector cells (cytotoxic T lymphocytes, M1 macrophages, and T helper type 1 cells) versus immunosuppressive cells (M2 macrophages, T helper type 2 cells, myeloid derived suppressor cells, and regulatory T cells) that infiltrate in the tumor. As such, we would highlight the potential of lncRNAs as novel targets for immunotherapy.

Automated summary

Long non-coding RNAs (lncRNAs) play diverse roles in regulating the cancer immunity cycle, including inhibiting antitumor T cell activation, blocking effector T cell recruitment, disrupting T cell homing, recruiting immunosuppressive cells, and inducing an imbalance between antitumor effector cells and immunosuppressive cells. Thus, lncRNAs have the potential to be novel targets for immunotherapy.