Table 2.
ncRNAs and tumor microenvironment.
| ncRNA | Microenvironment component and its activity | References |
|---|---|---|
| CANCER-ASSOCIATED FIBROBLASTS (CAFs) | ||
| miR-149 | Inhibits fibroblast activation by targeting IL-6. It is suppressed in gastric cancer. | Li et al., 2015b |
| miR-424 | Regulates IDH3α expression in melanoma and colon cancer cell line models triggering the metabolic switch from oxidative phosphorylation to glycolysis in CAFs. | Zhang et al., 2015 |
| miR-133b | In prostate cancer (PCA), its overexpression modulates IL6-activation, and other miRNAs, including miR-210, miR-143, and miR-590-5p, that coherently up-modulate CAF activation. miR-133b is also released into the media and its incorporation into PCa cells, may contribute to the establishment of mesenchymal phenotype. | Doldi et al., 2015 |
| ZEB2NAT | In bladder cancer, CAFs induces EMT and invasion through the TGFβ1-ZEB2NAT-ZEB2 axis. | Zhuang et al., 2015 |
| IMMUNOLOGICAL ENVIRONMENT | ||
| miR-21 | It suppresses antitumor T-cell-mediated immunity and density in colorectal carcinoma. | Mima et al., 2016 |
| miR-142 | Regulates proliferative responses and maturation of T cell cycling by mediating E2F transcription factors (Sun Y. et al., 2015). In hepatic and colon cancer, miR-142 is down modulated, while in breast cancer it is over-expressed. | Shen et al., 2013; Chai et al., 2014; Isobe et al., 2014 |
| miR-101 and 26a | In ovarian tumors, the overexpression of the miRNAs imposed glucose restriction on T cells, limiting the expression of the methyltransferase EZH2. | Zhao et al., 2016 |
| lnc-DILC | IL-6 autocrine signal in hepatome depends on lnc-DILC and consequently, its expression enhances the activation of IL-6/STAT3 pathway. | Wang et al., 2016 |
| ADIPOCYTES | ||
| miR-27a | Its excretion from adipose tissue leads liver cancer cells to proliferate through the down-regulation of the transcription factor FOXO1. FOXO1 in particular, plays a significant role in regulating energy metabolism and gluconeogenic enzymes (Gross et al., 2008). | Sun B. et al., 2015 |
| miR-143 | Its down-modulation promotes adipocyte differentiation in cancer cell lines. Its expression level may be a cause or a consequence of the undifferentiated state of the tumor cells. | Esau et al., 2004 |
| lncRNA SRA | It responds to insulin, and its altered expression in tumor cells may allow both glucose uptake and phosphorylation of Akt and FOXO1 in adipocytes. | Xu et al., 2010 |