Table 1.
The lncRNAs involved in cancer stemness
| Cancer type | Function | Mechanisms | Ref. | |
|---|---|---|---|---|
| LncRNA-LET | Bladder cancer | Inhibition of cancer stemness and gemcitabine resistance | Down-regulation of lncRNA-LET increased the protein expression of NF90 which in turn inhibited miRNA-145 expression and promoted cancer stemness. | [23] |
| NEAT1 | Triple-negative breast cancer | Induction of cancer stemness | NEAT1 increased CD44+/CD24-, ALDH+, and SOX2+ stem cell populations. | [24] |
| NSCLC | Induction of cancer stemness and cisplatin resistance | NEAT1 was overexpressed and activated wnt signaling pathway. | [46] | |
| AFAP1-AS1 | Laryngeal cancer | Induction of cancer stemness | AFAP1-AS1 negatively regulated the expression of miR-320a, resulting in overexpression of RBPJ and Notch signaling activation. | [26] |
| BC200 | Glioblastoma | Induction of cancer stemness and temozolomide resistance | BC200 up-regulated stemness related markers and multidrug resistance proteins through interfering with miR-218-5P expression. | [27] |
| Lnc00963 | Oral cancer | Induction of cancer stemness | By up-regulating ABCB5, a known drug efflux transporter, lnc00963 conferred oral cancer cells stemness-like traits. | [28] |
| TALNEC2 | Glioblastoma | Induction of cancer stemness and radioresistance | Inhibition of TALNEC2 inhibited cancer stemness partly through the recovery of miR-21 and miR-11 expression. | [30] |
| LincRNAp21 | Glioblastoma | Inhibition of cancer stemness and radioresistance | LincRNAp21 negatively regulates β-catenin, which is a critical activator of wnt/β-catenin signaling pathway. | [31] |
| FENDRR | Lung cancer | Inhibition of cancer stemness | FENDRR bound to 3’UTR of MDR1, prevent the binding of RNA binding protein HuR to MDR1 3’UTR and thus inhibit MDR1 expression. | [32] |
| LINC01567 | Lung cancer | Inhibition of cancer stemness | LINC01567 acted as a sponge to competitively bind to miRNA-93, increasing target genes expressions including HDAC8, TLE4, stratifin and MSI1. | [33] |
| DLX6-AS1 | Osteosarcoma | Induction of cancer stemness | DLX6-AS1 competitively bind to miR-129-5p and increased DLK1 expression, resulting in wnt signaling activation. | [34] |
| Linc-DYNC2H1-4 | Pancreatic cancer | Induction of cancer stemness and gemcitabine resistance | Linc-DYNC2H1-4 competitively bound to miRNA-145 and inhibited EMT and the expressions of cancer stemness markers. | [35] |
| FOXD2-AS1 | Thyroid cancer | Induction of cancer stemness | FOXD2-AS1 interacted with miR-7-5p as a sponge and induced overexpression of miR-7-5p target gene telomerase reverse transcriptase (TERT). | [36] |
| HOTAIR | Prostatic cancer | Induction of cancer stemness and docetaxel resistance | HOTAIR sequestered miR-590-5p as a sponge and induced overexpression of IL-10, which initiated the activation of STAT3 signaling. | [37] |
| ASB16-AS1 | Gastric cancer | Induction of cancer stemness and cisplatin resistance | ASB16-AS1 interacted with miR-3918 and miR-4676-3 and increased the expression of TRIM37. Furthermore, ASB16-AS1 cooperated with ATM kinase, facilitated TRIM37 phosphorylation and promoted the activation of NF-κB pathway. | [38] |
| DGCR5 | NSCLC | Induction of cancer stemness | DGCR5 inhibited the expression of miR-330-5p, which negatively regulated cancer stemness marker CD44 expression, by interaction with it as a sponge. | [39] |
| LBCS | Bladder cancer | Inhibition of cancer stemness | LBCS formed a scaffold complex with hnRNPK and EZH2, which suppressed SOX2 expression by mediating H3K27me3 of SOX2 promoter. | [40] |
| LncZic2 | Liver cancer | Induction of cancer stemness | LncZic2 interacted with BRG1 and directed it to MARCKS and MARCKSL1 promoter, promoting the expressions of MARCKS/MARCKSL1. | [41] |
| LncGPR107 | Liver cancer | Induction of cancer stemness | LncGPR107 recruited SRCAP complex to GPR107 promoter and initiated its transcription activation. | [43] |
| CCAT1 | NSCLC | Induction of cancer stemness | CCAT1 inhibited let-7c, one suppressor of wnt signaling pathway, resulting in the activation of wnt signaling pathway. | [47] |
| H19 | Breast cancer | Induction of cancer stemness | H19 inhibited let-7c by which oestrogen receptor activated Wnt signaling was released. | [48] |
| Liver cancer | Induction of cancer stemness and drug resistance | H19 conferred activated MAPK/Erk pathway and reduction of oxidative stress. | [56] | |
| Breast cancer | Up-regulation of cancer stemness | H19 interacted with miRNA let-7 to release HIFr1α, resulting in upregulation of pyruvate dehydrogenase kinase 1 (PDK1) and increase of glycolysis. | [77] | |
| Colorectal cancer | Up-regulation of cancer stemness | H19 in exosomes secreted by CAFs activated the β-catenin pathway via acting as a competing endogenous RNA sponge for miR-141. | [87] | |
| Hepatocellular carcinoma | Induction of cancer stemness | TAMs induced overexpression of H19 which sequestered miR-193b, increasing MAPK1 expression to activate MAPK signaling pathway. | [92] | |
| RBM5-AS1/LUST | Colon cancer | Induction of cancer stemness | LUST directly interacts with β-catenin, stabilizes the β-catenin/TCF-4 complex and potentiates the transcription of β-catenin target genes. | [49] |
| BCAR4 | Gastric cancer | Induction of cancer stemness and cisplatin resistance | BCAR4 increased the expressions of stem cells markers such as β-catenin, Nanog, Oct3/4, Sox2, c-Myc, and Klf4 due to wnt signaling activation. | [50] |
| THOR | Liver cancer | Induction of cancer stemness and sorafenib resistance | THOR promoted liver cancer stem cells expansion and resistance to sorafenib treatment through activating β-catenin signaling pathway. | [51] |
| Gastric cancer | Induction of cancer stemness and cisplatin resistance | THOR directly bound to SOX9 untranslated region (3’UTR), promoting SOX9 expression. | [64] | |
| LncRNA-cCSC1 | Colon cancer | Induction of cancer stemness and 5-fluorouracil resistance | LncRNA-cCSC1 induced cancer stemness by activation of Hh pathway. | [53] |
| LINC-PINT | Laryngeal carcinoma | Inhibition of cancer stemness | LINC-PINT inhibited cancer stemness of laryngeal carcinoma possibly through inactivating the Hedgehog pathway. | [54] |
| TUSC-7 | Lung adenocarcinoma | Induction of cancer stemness | TUSC-7 inhibited the degradation of NUMB by miR-146 and lead to Notch signaling activation. | [55] |
| LncRNA MAPK6 | Esophageal cancer | Induction of cancer stemness | LncRNA MAPK6 interacted with and recruited RNA polymerase II to MAPK6 promoter, resulting in the activation of MAPK6 transcription. | [57] |
| LncARSR | Liver cancer | Induction of cancer stemness and resistance to cisplatin and sorafenib | lncARSR promoted liver CSCs expansion and resistance to cisplatin and sorafenib by activating STAT3 signaling. | [62] |
| Renal cancer | Induction of cancer stemness | LncARSR interacted with YAP and prompted YAP nuclear translocation while repressed YAP phosphorylation. | [65] | |
| PTCSC3 | Thyroid cancer | Inhibition of cancer stemness and doxorubicin resistance | Overexpression of PTCSC3 inhibited STAT3 signaling and the expression of INO80, which is a positive regulator of thyroid cancer stemness. | [63] |
| MALAT1 | Ovarian cancer | Induction of cancer stemness and cisplatin resistance | By interaction with YAP, MALAT1 inhibited it translocation from nucleus to cytoplasm, stabilized it and increased its activity in ovarian cancer. | [66] |
| Liver cancer | Induction of cancer stemness | MALAT1 increased the expression of YAP1 by sponging miRNA-375, which inhibited YAP1 expression through binding to its 3’-UTR. | [67] | |
| Lnc HOXA10 | Liver cancer | Induction of cancer stemness | Lnc HOXA10 recruited SNF2L to the promoter of HOXA10, resulting in HOXA10 overexpression. | [68] |
| FGF13-AS1 | Breast cancer | Inhibition of cancer stemness | By competitively interacting with IGF2BP proteins, FGF13-AS1 reduced the mRNA stability of c-Myc to suppress glycolysis. | [79] |
| TP73-AS1 | Glioblastoma | Induction of cancer stemness and temozolomide resistance | TP73-AS1 regulated, mitochondria, and nucleotide metabolism, and curbed ROS levels. | [81] |
| HAL | Breast cancer | Induction of cancer stemness | HAL was induced by tumor microenvironment such as hypoxia and acidosis. | [85] |
| HCP5 | Gastric cancer | Up-regulation of cancer stemness | MSCs induced overexpression of HCP5, which interacted with miR-3619-5P and initiated the transcription of CPT1, prompting FAO. | [90] |
| MACC1-AS1 | Gastric cancer | Induction of cancer stemness and resistance to 5-FU and oxaliplatin | TGF-β1 secreted by MSCs induced MACC1-AS1 overexpression which promoted FAO by sequestering miR-145-5p. | [91] |