Table 1.
LncRNAs involved in the crosstalk between stromal cells and tumor cells.
| LncRNA | Cancer type | Stromal cells | Mechanisms of action | Reference |
|---|---|---|---|---|
| LncRNA-CAF | Oral squamous cell carcinoma | CAFs | Lnc-CAF up-regulates IL-33 expression to reprogram CAFs, promoting tumor development. | (36) |
| LINC00092 | Ovarian cancer | CAFs | CAFs-secreted CXCL14 induces LINC00092 upregulation which promotes ovarian cancer metastasis by enhancing PFKFB-2 translation. | (37) |
| LncRNA-ZEB2NAT | bladder cancer | CAFs | TGFβ1 secreted by CAFs induces epithelial-mesenchymal transition and invasion of bladder cancer cells via lncRNA-ZEB2NAT. | (34) |
| HOTAIR | Breast cancer | CAFs | TGFβ1 secreted by CAFs induces epithelial-mesenchymal transition and metastasis of breast cancer through HOTAIR. | (35) |
| LncRNA H19 | Glioma | endothelial cells | Knockdown of H19 suppresses proliferation and migration of glioma-associated endothelial cells through upregulating miR-29a. | (39) |
| LncRNA-APC1 | Colorectal carcinoma | endothelial cells | LncRNA-APC1 suppresses the MAPK pathway overactivation in endothelial cells and further inhibits tumor angiogenesis by increasing exosome production in colorectal carcinoma cells. | (40) |
| LncRNA CCAT1 | Prostate cancer | TAMs | LncRNA CCAT1 knockdown enhances macrophages polarization to M2 and promotes prostate cancer cell migration and invasion through upregulating the expression of miR-148a. | (45) |
| LncRNA NIFK-AS1 | Endometrial cancer | TAMs | LncRNA NIFK-AS1 suppresses the M2 macrophages polarization by inhibiting miR-146a, thus reducing the endometrial cancer cell proliferation, migration and invasion. | (46) |
| LncRNA-MM2P | – | TAMs | LncRNA-MM2P promotes M2 polarization of macrophages via reducing phosphorylation on STAT6, then affecting macrophage- mediated tumorigenesis and tumor growth. | (47) |
| LncRNA LNMAT1 | Bladder cancer | TAMs | LncRNA LNMAT1-induced CCL2 recruits TAMs, leading to lymphatic metastasis of bladder cancer. | (51) |
| Lnc-BM | Breast cancer | TAMs | Lnc-BM induces STAT3-dependent expression of CCL2 to attract macrophages, thus enhancing breast cancer brain metastasis. | (52) |
| Lnc-chop | – | MDSCs | Lnc-chop upregulates the production of ROS and NO to enhance immunosuppression and promots tumor growth. | (56) |
| Lnc-C/EBPβ | – | MDSCs | Lnc-C/EBPβ suppresses the immunosuppressive capacity of MDSCs by suppressing the expression of NO and ROS. | (57) |
| LncRNA Pvt1 | – | MDSCs | LncRNA Pvt1 knockdown suppresses G-MDSC-mediated immunosuppression in vitro by decreasing the level of ROS and ARG1, and delays tumor progression in tumor-bearing mice. | (61) |
| Lnc-Tim3 | Hepatocellular carcinoma | CD8+ T cells | Lnc-Tim3 binds to Tim-3 and induces nuclear translocation of Bat3 in hepatocellular carcinoma, which compromises anti-tumor immunity by promoting CD8 + T cell exhaustion. | (64) |
| Lnc-sox5 | Colorectal cancer | CD8+ T cells | Lnc-sox5 regulates the CD8+T cells infiltration and cytotoxicity through modulating the expression of IDO, further affecting the progression of colorectal cancer. | (65) |
| Lnc-EGFR | Hepatocellular carcinoma | Tregs | Lnc-EGFR specially binds to EGFR, enhances AP-1/NF-AT1/Foxp3 signaling, leading to Treg differentiation, and hepatocellular carcinoma progression | (68) |
| LncRNA SNHG1 | Breast cancer | Tregs | Knockdown of lncRNA SNHG1 suppresses Treg differentiation by increasing the expression of miR-448 and reducing level of IDO, further alleviating the immune escape in breast cancer. | (69) |
| Flicr | – | Tregs | Flicr modulates the expression of Foxp3 and enhances the immunosuppressive function of Tregs. | (70) |
CAFs, cancer-associated fibroblasts; TAMs, tumor-associated macrophages; MDSCs, myeloid-derived suppressor cells; Tregs, regulatory T cells.