Table 1.
LncRNAs that modulate the response of glioblastoma/glioma to chemotherapy.
| lncRNA | Samples | Cell Lines | Target/pathway | Function | Kaplan Meier Analysis | Ref |
|---|---|---|---|---|---|---|
| RP11-838N2.4 | – | U87, U251, U87/TMZ, U251/TMZ, | miR-10a, TGFB 1, TGFBR1, Smad-2/3/4 | RP11-838N2.4 by inhibiting the functions of miR-10a could increase temozolomide cytotoxic effect in GBM. | – | (32) |
| MALAT1 | Mouse | U251, U87, U251/TMZU87/TMZ | ZEB1, Snail, SLUG | MALAT1 by regulating ZEB1 could decrease the sensitivity of resistant GBM. | – | (15) |
| MALAT1 | Mouse | LN-229, LN-428,LN-319, LN-18, | p-MKK3/6, p-p38,P-ERK, WNT/Ca2+ | WIF1 could increase the migratory possibility of GBM via WNT5A that activates the WNT/Ca2+ pathway and MALAT1. | – | (16) |
| MALAT1 | Human | U87, U251, U87/TMZ, U251/TMZ | miR-203, TS | MALAT1 could induce chemoresistance to TMZ by suppressing miR-203 and promoting thymidylate synthase expression. | – | (17) |
| MALAT1 | Human | U251, U251/TMZ | miR-101, MRP1, MGMT, p-gp | Knockdown of MALAT1 by promoting miR-101 could inhibit resistance to TMZ. | – | (18) |
| MALAT1 | Human,Mouse | U87, T98G, LN-18,U87/TMZ, T98G/TMZ, LN-18/TMZ | AERG, CCL2, CXCL4 | MALAT1 silencing could sensitize glioblastoma to TMZ. | – | (33) |
| MALAT1 | U87, A172, U251, U87/TMZ,A172/TMZ, U87/TMZ | p53, NF-kB | p50 and p52 are primary regulators of this ncRNA. | – | (19) | |
| TUSC7 | Human | U87, U87TMZ | miR-10a, MDR1 | TUSC7 by targeting miR-10a could inhibit TMZ resistance in GBM. | – | (29) |
| NEAT1 | Human | U87, U251, U87/TMZ, U251/TMZ | let-7g-5p, MAP3K1, E-cadherin, N-cadherin | NEAT1 by regulating the let-7g-5p/MAP3K1 axis could promote malignant phenotypes and TMZ resistance in GBM. | – | (20) |
| NEAT1 | Human | U87, U87/R, U251, U251/R | MGMT | NEAT1 by regulating MGMT could be involved in TMZ resistance in GBM multiforme. | – | (21) |
| H19 | Human | A172, LN229, U87MG, LN18, T98G | NKD1 | H19 could contribute to NKD1 repression via the recruitment of EZH2 on its promoter. | – | (22) |
| H19 | Human | U87, U251 U87/TMZ U251/TMZ |
PARP, MDR, MRP, ABCG2 |
Knockdown of H19 could enhance the sensitivity of human glioma cells to TMZ. | – | (34) |
| H19 | – | U251, LN229 U251/TMZ LN229/TMZ |
Caspase-3, NF-kB | H19 By activating NF-kB signaling could confer TMZ resistance in glioma. | – | (23) |
| H19 | – | U-251, M059J, U251/TMZ, M059J/TMZ |
Wnt/β-catenin, Vimentin,ZEB1, c-myc,E-cadherin, Survivin |
H19 silencing by suppressing EMT via the Wnt/β-catenin pathway could reduce the resistance of human glioma cells to TMZ. | – | (11) |
| UCA1 | Human | U251,U87MG | CXCL4, miR-182, PFKFB2 | UCA1/miR-182/PFKFB2 axis could modify GBM-associated stromal cells-mediated glycolysis and invasion of glioma cells. | – | (35) |
| uc003iax.2, ENST00000443252 | Human | U87, U251, U87/TMZ, U251/TMZ | IL-18, DPP4, ABCB1, TP53, Collagen I, Fibronectin, Laminin | Dysregulated lncRNAs could be involved as novel targets so as to overcome acquired TMZ resistance in GBM chemotherapy. | – | (31) |
| AC023115.3 | Human | U87MG,U251MG | PARP,Caspase-3 | AC023115.3 could suppress the chemoresistance of GBM by decreasing autophagy. | – | (36) |
| AC003092.1 | Human | U87, U251, U87/TMZ, U251/251 | TFPI-2,miR-195 | AC003092.1 could help TMZ chemosensitivity via the miR-195/TFPI-2 axis modulation in GBM. | – | (37) |
| TP73-AS1 | Human | G26, G7, G26/TMZG7/TMZ | ALDH1A1 | TP73-AS1 is involved in aggressiveness and could promote TMZ resistance in GBM cancer stem cells. | – | (38) |
| ADAMTS9-AS2 | Human | T98G, U118, T98G/TMZU118/TMZ | FUS/MDM2, Tubulin | ADAMTS9-AS2 by upregulating the FUS/MDM2 ubiquitination axis could help TMZ resistance in GBM. | – | (39) |
| SNHG15 | Human | HMC3, HMC3/TMZ | miR-627, EGFR, CDK6, Sox2, β-catenin | Modulating SNHG15/CDK6/miR-627 axis by palbocicli could reduce M2-polarization of glioma-associated microglia in GBM multiforme and finally could overcome TMZ resistance. | – | (40) |
| SNHG12 | Mouse | N3S, N3T3rd, U251, U251T3rd | PARP, Caspase-3, RB, CDK4, CDK6, Cyclin-D1, P-MEK, DNMT1, DNMT3a, DNMT3b, MAPK1, E2F7, P-ERK1/2 | Knockdown of SNHG12 by increasing MAPK1 and E2F7 expression and activating the MAPK-ERK could restore TMZ sensitivity in GBM. | SNHG12 expression is associated with poor prognosis in GBM. | (41) |
| NONHSAT163779 | Human | U87, U87/TMZ | hsa_circ_0043949, MDR1, MRP1, BCRP, MGMT | NONHSAT163779 and hsa_circ_0043949 could be involved as prognostic biomarkers for the treatment of GBM. | – | (42) |
| SBF2-AS1 | Human | U87, LN229, A172, T98, U251 | XRCC4, y-H2AX, Pro-caspase-3, Cleaved-caspase 3 | Knockdown of SBF2-AS1 could increase sensitivity to TMZ in GBM. | SBF2-AS1 expression is associated with poor prognosis in GBM. | (43) |
| OKN-007 | Rat | U138, LN18, T98, U251 | TGFβ1 | OKN-007 could enhance TMZ sensitivity and suppresses TMZ-resistant GBM. | – | (44) |
| SOX2OT | Human | U87, U251, U87/TMZ, U251/TMZ | MDR1, BCRP1, MRP1, SOX2, ALKBH5, TCF1, Caspase-3/7/8/9, Wnt5a/β-catenin, Cyclin-D1, C-Myc, LEF1 | SOX2OT by elevating SOX2 expression via ALKBH5-mediated epigenetic regulation could promote TMZ resistance. | Elevated SOX2OT expression is associated with poor prognosis in GBM. | (45) |
| 00021 | BALB/c | U87, U251, A172, and SHG44 | P21, Notch1, Hes1, Hes5 | Long intergenic noncoding RNA 00021 by epigenetically silencing p21 via the Notch pathway could promote GBM TMZ resistance. | LINC00021 expression is associated with the poor prognosis of GBM patients. | (46) |
| MIR22HG | Mouse | U87MG, LN229, LN1 | Wnt/β-catenin, P21, P27, c-Muc, p-GSK3B, Cyclin-D1, LEF1 | MIR22HG via suppressing the Wnt/β-catenin pathway could inhibit GBM progression. | MIR22HG expression is associated with poor prognosis in GBM | (12) |
| HOTAIR | Mouse | A172, LN229, A172/TMZ, LN229/TMZ | miR-519a-3p, RRM1, Vimentin, E-cadherin, CD63, N-cadherin, MAP3K1 | Knockdown of HOTAIR by miR-519a-3p/RRM1 axis could regulate TMZ resistance. | – | (24) |
| HOTAIR | Human | U87, A172, U87/TMZ, A172/TMZ | miR-125, Cyt C, Caspase-3, HK2 | HOTAIR by targeting miR-125 could promote chemoresistance in human GBM. | – | (25) |
| MIR155HG | Mouse, databases | A172, U251, A172/TMZ, U251/TMZ |
Wnt/β-catenin, c-Myc, PTBP1, Cyclin-D1 |
Knockdown of MIR155HG by inhibiting the Wnt/β-catenin pathway via downregulation PTBP1 could increase glioma sensitivity to TMZ. | MIR155HG Upregulation was associated with poor prognosis | (13) |
| KCNQ1OT1 C | Mouse | U251, U87, U251/TMZ, U87/TMZ |
miR-761, c-MYC, Pim-1L, p-MDR1, MDR1, Survivin |
KCNQ1OT1 C by retrieving PIM1 From miR-761 could confer gliomas resistance to TMZ. |
– | (47) |
| NCK1-AS1 | Human | U251, A172, U251/TMZ, A172/TMZ |
TRIM1, miR-137, TRIM24 |
NCK1-AS1 by modulating the miR-137/TRIM24 axis could increase the resistance of glioma cells to TMZ. | – | (48) |
| NCK1-AS1 | Human | A172, LN229 A172/TMZ LN229/TMZ |
miR-22-3p, IGF1R | NCK1-AS1 via miR-22-3p/IGF1R axis could enhance chemoresistance in glioma. | – | (49) |
| EPIC1 | – | SNB19, T98G, U97MG, SNB19/TMZ, T98G/TMZ, U97MG/TMZ |
Cdc20 | Overexpression of EPIC1 via targeting Cdc20 could be useful in glioma treatment. | – | (50) |
| HOXD-AS1 | TCGA dataset | U87, U251, U373, SNB19, U87/DDP, U251/DDP |
miR-204, Caspase-3/9 | Knockdown of HOXD-AS1 by buffering miR-204 could enhance cisplatin sensitivity. | high HOXD-AS1 expression had a poor prognosis |
(51) |
| LINC01198 | Human | U251, SNB-19, LN229, U87, U87/TMZ, U251/TMZ, LN229/TMZ, SNB-19/TMZ |
PTEN, AKT, NEDD4-1 |
Overexpression of LINC01198 by enhancing the NEDD4-1-dependent repression of PTEN could promote glioma cell proliferation and resistance to TMZ. | LINC01198 high elevation was associated with a poor prognosis of glioma. | (52) |
| LINC00174 | Human | U251, U87, U251/TMZ, U87/TMZ |
SOX9, P13K/Akt |
Knockdown of LINC00174 by regulating miR-138-5p/SOX9 axis could decrease chemoresistance to TMZ in glioma. | – | (53) |
| GAS5 | – | U138, LN18 U87MG, U251MG, U138/Cis, LN18/Cis, U87/Cis, U251/Cis |
mTOR, LC3I, LC3II, p-62 |
GAS5 by suppressing excessive autophagy in an mTOR‐dependent manner could facilitate glioma cell sensitivity to cisplatin. | (54) | |
| CASC2 | Human | U257, U87, U257/TMZ, U87/TMZ | mTOR, Beclin1, miR-193a-5p, LC3II/LCI |
Upregulation of CASC2 through autophagy inhibition by buffering miR-193a-5p and regulating mTOR expression could sensitize glioma to TMZ cytotoxicity. | – | (55) |
| CASC2 | Human | U251, U373, SNB19, U118, LN229 SNB19/TMZ, U251/TMZ |
PTEN, AGO2, Akt, miR-181a |
CASC2 by inhibiting miR-181a could increase sensitivity to TMZ in glioma. | CASC2 upregulation was associated with poor prognosis | (56) |
| CCAT2 | Human | U251, U87, A172, SHG44 | miR-424 | CCAT2 by disturbing the normal function of miR-424 could enhance resistance in glioma. | CCAT2 upregulation was associated with a poor prognosis. | (57) |
| DANCR | Mouse | U87MG, LN18, U251MG, U138MG, U87MG/Cis, U251MG/Cis, U138MG/Cis |
AXL, NF-kB, IkBa, PI3K/AKT |
DANCR via activating AXL/PI3K/Akt/NF-κB signaling pathway could mediate cisplatin resistance in glioma cells. | – | (58) |
| MEG3 | – | U87, U87/Cis | p-62, LC3 I/II, PARP |
MEG3 by suppression of autophagy could enhance cisplatin resistance in glioma. | – | (30) |
| MSC-AS1 | Human | LN229, HG-44 LN229/TMZ, SHG-44/TMZ |
miR-373-3p, CPEB4, Bax, MCL-1, MRP-1, P-PIK3, Cyclin-D1, Caspase-3, PI3K/AKT |
Knockdown of MSC−AS1 by regulating miR-373-3p/CPEB4 axis via PI3K/Akt pathway could inhibit cell growth and TMZ resistance in glioma. | MSC−AS1 upregulation was associated with a poor prognosis. | (50) |
| NR5A2 | Mouse | U138, U251, A172, U87, U138/TMZ, U251/TMZ | NR5A2, PARP, NOTCH1, p21, Cyclin-D1, caspase-3, MMP2, E-cadherin |
NR5A2 via regulating notch signal pathway could promote cell growth and resistance to TMZ in glioma. | NR5A2 overexpression was associated with the poor prognosis of glioma patients | (59) |
| ZFAS1 | Human | U87, U251, NHA, A172, LN299, LN299/Cis, U251/Cis, | miR‐432‐5p | Knockdown of ZFAS1 by upregulating miR‐432‐5p could enhance cisplatin cytotoxicity in glioma. | Expression levels of ZFAS1 in clinical tissues is associated with poor prognosis |
(60) |
| XIST | Human | LN229, U251, LN229/TZM, U251/TZM | Ago2, miR-29c | XIST via interacting with miR-29c and through DNA mismatch repair pathway could modulate the chemoresistance of glioma cell to TMZ. | Higher expression of XIST was associated with a lower OS rate. | (61) |