High expression of miR-25 predicts favorable chemotherapy outcome in patients with acute myeloid leukemia

Niu, Mingshan; Yuan, Feng; Zhang, Ninghan; Shao, Tingting; Zhang, Huihui; Wang, Rong; Yao, Yao; Yao, Ruosi; Wu, Qingyun; Cao, Jiang; Liu, Xuejiao; Liu, Yubo; Xu, Kailin

doi:10.1186/s12935-019-0843-9

Cited by 9 publications

(6 citation statements)

References 36 publications

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“…S 3 A). Research has shown that activation of miR-25-3p can overcome chemotherapy resistance [ 25 ]. qRT-PCR analysis showed that miR-25-3p expression was downregulated in MCF-7/ADR cells (Fig.…”

Section: Resultsmentioning

confidence: 99%

LncRNA CBR3-AS1 regulates of breast cancer drug sensitivity as a competing endogenous RNA through the JNK1/MEK4-mediated MAPK signal pathway

Zhang

Wang

Jiang

et al. 2021

J Exp Clin Cancer Res

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Background Adriamycin (ADR) resistance is one of the main obstacles to improving the clinical prognosis of breast cancer patients. Long noncoding RNAs (lncRNAs) can regulate cell behavior, but the role of these RNAs in the anti-ADR activity of breast cancer remains unclear. Here, we aim to investigate the imbalance of a particular long noncoding RNA, lncRNA CBR3 antisense RNA 1 (CBR3-AS1), and its role in ADR resistance. Methods Microarray analysis of ADR-resistant breast cancer cells was performed to identify CBR3-AS1. CCK-8 and colony formation assays were used to detect the sensitivity of breast cancer cells to ADR. Dual-luciferase reporter, RNA pulldown, IHC and western blot analyses were used to verify the relationship between the expression of CBR3-AS1, miRNA and target genes. For in vivo experiments, the effect of CBR3-AS1 on breast cancer resistance was observed in a xenograft tumor model. The role of CBR3-AS1 in influencing ADR sensitivity was verified by clinical breast cancer specimens from the TCGA, CCLE, and GDSC databases. Results We found that CBR3-AS1 expression was significantly increased in breast cancer tissues and was closely correlated with poor prognosis. CBR3-AS1 overexpression promoted ADR resistance in breast cancer cells in vitro and in vivo. Mechanistically, we identified that CBR3-AS1 functioned as a competitive endogenous RNA by sponging miR-25-3p. MEK4 and JNK1 of the MAPK pathway were determined to be direct downstream proteins of the CBR3-AS1/miR-25-3p axis in breast cancer cells. Conclusions In summary, our findings demonstrate that CBR3-AS1 plays a critical role in the chemotherapy resistance of breast cancer by mediating the miR-25-3p and MEK4/JNK1 regulatory axes. The potential of CBR3-AS1 as a targetable oncogene and therapeutic biomarker of breast cancer was identified.

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Section: Resultsmentioning

confidence: 99%

LncRNA CBR3-AS1 regulates of breast cancer drug sensitivity as a competing endogenous RNA through the JNK1/MEK4-mediated MAPK signal pathway

Zhang

Wang

Jiang

et al. 2021

J Exp Clin Cancer Res

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“…Identifying new prognostic markers is of great importance in adult AML, because currently available molecular stratification approaches do not completely capture the heterogeneity of such cases (21–23). The significance of miRNAs as predictive biomarkers in AML patients remains mostly unclear.…”

Section: Discussionmentioning

confidence: 99%

MiR-340 Is a Biomarker for Selecting Treatment Between Chemotherapy and Allogeneic Transplantation in Acute Myeloid Leukemia

et al. 2019

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Acute myeloid leukemia (AML) requires refined risk stratification tools to drive decisions concerning effective therapeutic strategies. Here, genome-wide screening was carried out for identifying miRNA molecules capable of predicting treatment outcome in AML patients based on the TCGA dataset. We identified miR-340 as a prognostic factor for selecting treatment between chemotherapy and allogeneic transplantation (allo-HSCT). In multivariable analyses, low miR-340 expression independently predicted reduced OS (HR = 2.07, P = 0.004) and EFS (HR = 1.909, P = 0.01) independent of other well-known prognostic factors. Meanwhile, allo-HSCT overcome deleterious outcomes related to low miR-340. Cases administered allo-HSCT showed markedly improved OS (HR = 0.316, P < 0.0001) and EFS (HR = 0.391, P = 0.002) in comparison with those receiving chemotherapy in the low miR-340 group. Gene expression assessment revealed that elevated miR-340 amounts were negatively correlated with HOXA/HOXB cluster levels, as well as the amounts of the HOX cofactor MEIS1. Strikingly, in silico analysis pointing to HOXA10, HOXB2, and MEIS1 as miR-340 targets. The miR-340 expression may help identify cases requiring strategies for selecting the optimal therapeutic option between chemotherapy and allo-HCST. AML cases showing low miR-340 levels should be strongly considered for early allo-HSCT treatment.

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“…S3A). The research has shown that have shown that activating miR-25-3p can resist the resistance of chemotherapy [25]. qRT-PCR analysis showed that miR-25-3p was down-expressed in MCF-7/ADR cells (Fig.…”

Section: Cbr3-as1 Regulates Mek4 / Jnk1 Expression Through Mir-25-3pmentioning

confidence: 93%

LncRNA CBR3-AS1 Regulates of Breast Cancer Drug Sensitivity as a Competing Endogenous RNA Through the JNK1/MEK4‑Mediated MAPK Signal Pathway

Zhang¹,

Wang²,

Jiang³

et al. 2020

Preprint

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Background: Adriamycin (ADR) resistance is one of the main obstacles to improve the clinical prognosis of breast cancer (BRCA) patients. Long non-coding RNAs (lncRNAs) can regulate cell behavior, but the role of these RNAs in anti ADR of BRCA remains unclear. Here we aim to investigate the imbalance of a particular long noncoding RNA, lncRNA CBR3 antisense RNA 1 (CBR3-AS1), and its role in ADR resistance.Methods: Microarray analysis of ADR-resistant BRCA cells was performed to identify CBR3-AS1. CCK8 assay and colony formation assay were used to detect the sensitivity of BRCA cells to ADR. Dual-luciferase reporter, RNA pull down, IHC and Western blot were used to verify the relationship between CBR3-AS1, miRNA and target genes. In vivo, the effect of CBR3-AS1 on BRCA resistance was observed by xenograft tumor model. The role of CBR3-AS1 in influencing ADR sensitivity was verified by clinical BRCA specimens, TCGA, CCLE, and GDSC databases.Results: Here, we found that lncRNA CBR3-AS1 was significantly increased in BRCA tissues and was closely correlated with poor prognosis. CBR3-AS1 overexpression promoted ADR resistance in BRCA cells in vitro and in vivo. Mechanistically, we identified that CBR3-AS1 functioned as a competitive endogenous RNA by acting as a molecular sponge of miR-25-3p. MEK4 and JNK1 of MAPK pathway were the direct downstream proteins of CBR3-AS1 / miR-25-3p axis in BRCA cells.Conclusions: In summary, our findings demonstrate that CBR3-AS1 plays a critical role in the chemotherapy resistance of BRCA by mediating the miR-25-3p, MEK4/JNK1 regulatory axis. The potential of CBR3-AS1 as an oncogene and therapeutic biomarker of BRCA was identified.

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High expression of miR-25 predicts favorable chemotherapy outcome in patients with acute myeloid leukemia

Cited by 9 publications

References 36 publications

LncRNA CBR3-AS1 regulates of breast cancer drug sensitivity as a competing endogenous RNA through the JNK1/MEK4-mediated MAPK signal pathway

LncRNA CBR3-AS1 regulates of breast cancer drug sensitivity as a competing endogenous RNA through the JNK1/MEK4-mediated MAPK signal pathway

MiR-340 Is a Biomarker for Selecting Treatment Between Chemotherapy and Allogeneic Transplantation in Acute Myeloid Leukemia

LncRNA CBR3-AS1 Regulates of Breast Cancer Drug Sensitivity as a Competing Endogenous RNA Through the JNK1/MEK4‑Mediated MAPK Signal Pathway

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