From: Long non-coding RNAs as the critical regulators of doxorubicin resistance in tumor cells
Cancer type | DOX response | LncRNA | Target | Samples | Function | References |
---|---|---|---|---|---|---|
Breast cancer (BC) | ||||||
BC | Resistance | XIST | miR-200c-3p /ANLN | MDA-MB-231/ADM and MDA-MB-231 cell lines | XIST up regulated ANLN by sponging miR-200c-3p and inhibited cell proliferation as well as promoted apoptosis | [34] |
BC | Resistance | Linc00152 | - | 40 NT* MDA-MB-231 and MCF-7 cell lines | Knockdown of Linc00152 suppressed tumor growth, cell migration, invasion, and chemo-resistance | [41] |
BC | Resistance | Linc00518 | miR-199a/MRP1 | 30 NT MCF-10A, MCF-7/ADR and MCF-7 cell lines | Linc00518 Knockdown suppressed MRP1 expression and induced cell apoptosis | [44] |
BC | Resistance | HOTAIR | PI3K/AKT | MCF-7 and DOXR-MCF-7 cell lines | HOTAIR suppressed PI3K/AKT pathway, reduced cell survival and promoted apoptosis | [48] |
BC | Resistance | Linc00668 | SND1 | HMEC-hTERT, MCF-10A, MCF-7, T47D, MDA-MB-231, HS578t, and 293T, SUM149, and SUM159 cell lines | Linc00668 interacted with SND1 and regulated SMAD2/3/4 expression, and also decreased invasion, self-renewal, and chemo-resistance | [54] |
BC | Resistance | DCST1-AS1 | ANXA1 | MDA-MB-231, BT-549, T-47D, and MCF7 cell lines | DCST1-AS1 targeted ANXA1 and induced EMT | [61] |
BC | Resistance | LINC00160 | C/EBPβ/TFF3 | 47 NT MCF‐7, MCF‐7/Tax, BT474, BT474/Dox and MCF10A cell lines | LINC00160 knockdown reduced cell migration and invasion | [64] |
BC | Resistance | LINP1 | CASP9/BAX | MDA-MB-231, MDA-MB-231/5FU, MDA-MB-231/DOX, MDA-MB-468 and MCF7 cell lines | LINP1 knockdown suppressed tumor growth and metastasis as well as promoted apoptosis | [65] |
BC | Resistance | H19 | CUL4A /ABCB1/MDR1 | MCF-7 cell lines | H19 up regulated CUL4A and ABCB1/MDR1 genes | [69] |
BC | Resistance | H19 | PARP-1 | 63 NT MCF-7 and MCF-7/Dox cell lines | Knockdown of H19 increased PARP-1 expression and induced cell death | [71] |
Osteosarcoma (OS) | ||||||
OS | Resistance | TUG1 | AKT | Saos-2 and MG-63 cell line | Polydatin inhibited TUG1/AKT axis and proliferation and promoted apoptosis | [83] |
OS | Resistance | FOXC2-AS1 | FOXC2 | 68 NT MG63, SaoS2 and HOS cell lines | FOXC2-AS1 facilities ABCB1 expression by increasing FOXC2 expression | [86] |
OS | Resistance | FOXC2-AS1 | ABCB1 | MG63, SaoS2 and U-2OS cell lines | Silencing of FOXC2-AS1 and ABCB1 repressed tumor growth | [89] |
OS | Resistance | OIP5-AS1 | miR-137-3p | 56 tumor tissues and 16 normal tissues hFOB1.19, MG63, and MG63/DOX cell lines | OIP5-AS1 knockdown inhibited proliferation and metastasis | [93] |
OS | Resistance | OIP5‐AS1 | miR‐200b‐3p | 80 patients MG63, KHOS and U2OS cell lines | OIP5‐AS1 sponged miR‐200b‐3p and regulated FN1 expression. Overexpression of FN1 contributed to the sensitivity of OS cells to doxorubicin | [97] |
OS | Resistance | SNHG12 | miR-320a / MCL1 | 32 doxorubicin-resistant patients and 32 doxorubicin-sensitive patients MG-63, U2OS, HOS, SAOS-2 and hFOB cell lines | SNHG12 modulated Wnt/β-catenin pathway, so inhibited miR-320a expression and promoted MCL1 expression | [103] |
OS | Resistance | LINC00426 | miR-4319 | MG63, KHOS, U2OS, MG63/DXR, and KHOS/DXR cell lines | Knockdown of LINC00426 significantly decreased cell viability and proliferation | [104] |
OS | Sensitivity | CTA | miR-210 | 30 patients Saos-2, U-2OS, MG-63 and MG-63/DOX cell lines | Overexpression of CTA reduced autophagy and promoted apoptosis | [105] |
OS | Sensitivity | FENDRR | ABCB1/ ABCC1 | 80 patients MG63, SaoS2, HOS and MG63/DXR cell lines | FENDRR down regulated ABCB1 and ABCC1 as well as suppressed DOX resistance and induced cells apoptosis | [108] |
Gastric cancer (GC) | ||||||
GC | Resistance | HOTAIR | miR-217 | 30 NT BGC-823, SGC-7901, KATO-3, MGC-803, and GES1 | Knockdown of HOTAIR inhibited cell proliferation and migration | [116] |
GC | Sensitivity | UCA1 | PARP | 77 NT GES-1, BGC-823 and SGC7901 cell lines | Knockdown of UCA1 caused repression of proliferation in cancerous cells | [120] |
GC | Resistance | UCA1 | miR-27b | 28 patients SGC-7901, SGC-7901/ADR, SGC-7901/DDP and SGC-7901/FU | Knockdown of UCA1 induced the expression of miR-27b, resulting in reduction of Bcl2 expression and promotion of CASP3 expression | [123] |
GC | Resistance | D63785 | miR-422a | 21 patients GES-1, SGC7901, MGC803, BGC823, NCI-N87, HEK293 and HEK293T cell lines | Reduced lncR-D63785 expression repressed proliferation, invasion, and metastasis | [128] |
GC | Resistance | NEAT1 | – | 76 NT SGC790, GES-1, SGC7901/ADR cell lines | NEAT1 repressed cell proliferation, apoptosis, and invasion | [131] |
GC | Resistance | MRUL | P-gp | SGC7901/ADR, SGC7901/VCR, SGC7901/ADR, and SGC7901 cell lines | MRUL depletion induced apoptosis | [132] |
Leukemia and lymphoma | ||||||
AML | Resistance | KCNQ1OT1 | miR-193a3p / Tspan3 | 74 patients and 37 healthy subjects HS-5, HL60, HL60/ADR, K562, and K562/ADR cell lines | KCNQ1OT1 knockdown suppressed the cell proliferation and invasion | [139] |
AML | Resistance | TUG1 | miR-34a | 36 patients and 23 healthy subject HS-5, HL60, and HL60/ADR | TUG1 knockdown overcame ADR resistance of AML by epigenetically enhancing miR-34a expression | [141] |
AML | Resistance | HOXA-AS2 | miR-520c-3p / S100A4 | 48 patients U937, U937/ADR, THP-1, and THP-1/ADR cell lines | HOXA-AS2 acted as ceRNA of miR-520c-3p and induced S100A4 expression. Knockdown of HOXA-AS2 expression significantly suppressed cell proliferation | [144] |
AML | Resistance | Linc00239 | PI3K/ATK/mTOR | HL-60 and KG-1 cell lines | Linc00239 activated PI3K/ATK/mTOR pathway. Linc00239 knockdown suppressed the cell proliferation and migration | [147] |
CML | Sensitivity | FENDRR | HuR | K562 and KCL22 cell lines | FENDER overexpression promoted cell apoptosis and suppressed cell proliferation | [155] |
BL | Resistance | MCM3AP-AS1 | miR-15a/EIF4E | 41 patients B-NHL cell line | MCM3AP-AS1 knockdown decreased cell viability and increased apoptosis | [160] |
Hepatocellular carcinoma (HCC) | ||||||
HCC | Resistance | MALAT1 | miR-216b | BEL-7402 and BEL-7402/5-FU cell lines | MALAT1 knockdown decreased proliferation and migration | [169] |
HCC | Resistance | lncARSR | miR-34/ miR-449/ PTEN | 92 NT SMMC-7721 and HepG2 cell lines | lncARSR promoted PTEN mRNA degradation and modulated PTEN-PI3K/Akt pathway | [177] |
HCC | Resistance | MALAT1 | miR-3129-5p / Nova1 | 36 patients Huh-7 and Hep3B cell lines | MALAT1 knockdown suppressed proliferation, migration, invasion, and promoted apoptosis | [174] |
HCC | Resistance | NEAT1 | – | HepG2, PLC/PRF/5, and Huh7 cell lines | NEAT1 up regulation in DOX resistant HCC cells | [175] |
HCC | Sensitivity | GAS5 | miR-21/PTEN | HepG2 and HepB3 cell lines | GAS5 regulated PTEN expression through binding to miR-21 and reduced cell proliferation | [178] |
HCC | Sensitivity | H19 | – | 32 NT | H19 inhibited HCC cell proliferation following the doxorubicin treatments | [179] |
Colorectal cancer (CRC) | ||||||
CRC | Resistance | XIST | miR-124 | 31 patients HCT116 and LoVo cell lines | XIST inhibited miR-124 expression through sponging. XIST knockdown enhanced the anti-tumor effect of DOX | [187] |
CRC | Resistance | BANCR | miR-203 | 32 NT HCT116, LoVo, NCM460 and HEK293T cell lines | BANCR knockdown suppressed tumor growth | [191] |
CRC | Resistance | GASS | NODAL | HCT116 cell line | GASS knockdown suppressed proliferation of cancer stem cells | [194] |
Thyroid and gallbladder cancers | ||||||
ATC | Sensitivity | PTCSC3 | STAT3/ INO80 | 20 FTC tissues and 20 ATC tissues 8505C, FTC 238, and FTC 133 cell lines | PTCSC3 regulated STAT3/ INO80 pathway and inhibited drug resistance | [203] |
GBC | Resistance | GBCDRlnc1 | ATG5-ATG12 | 45 NT NOZ and GBC-SD cell lines | GBCDRlnc1 knockdown inhibited autophagy | [205] |
Prostate and urothelial cancers | ||||||
RCC | Resistance | LINC-PINT | EZH1/ EZH2 | 98 tumor tissues and 16 healthy tissues HKC, 786-O, A498, 769P, Caki-2, Caki-1, ACHN, OS-RC-2, and SN12-PM6 cell lines | LINC-PINT knockdown decreased proliferation, cell progression, and promoted apoptosis | [208] |
BCa | Sensitivity | GAS5 | BCL2 | 82 tumor tissues and 37 healthy tissues BTCC T24, J82, CCC-HB-2, and T24/DOX cell lines | GAS5 knockdown increased BCL2 expression and apoptosis | [212] |
TCC | Resistance | HOTAIR | – | 35 TCC tissues and 16 healthy tissues TCC T24, J82, and SV-HUC-1 cell lines | HOTAIR knockdown inhibited cell proliferation and promoted apoptosis | [213] |
PCA | Resistance | LOXL1-AS1 | miR-let-7a-5p | DU-145 and DU-145/DOX cell lines | LOXL1-AS1 knockdown inhibited cell proliferation and migration as well as promoted apoptosis | [219] |