MicroRNA-107 Targets IKBKG and Sensitizes A549 Cells to Parthenolide

Moeng, Sokviseth; Seo, Hyun Ah; Hwang, Cho Yean; Cipolla, Gabriel Adelman; Lee, Dong Jin; Kuh, Hyo-Jeong; Park, Jong Kook

doi:10.21873/anticanres.12987

Cited by 6 publications

(3 citation statements)

References 28 publications

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“…Further, this poor prognosis could be overcome by allo-HSCT but not by chemotherapy. Previous studies have reported the role of miR-107 in regulating chemo-drug sensitivity among several cancer types, such as colorectal cancer ( 28 ), breast cancer ( 29 , 30 ), and non-small cell lung cancer ( 31 , 32 ). In addition, the level of miR-107 could be modulated by small-molecule drugs, including CDK inhibitor SNS-032 ( 33 ), all-trans-retinoic acid ( 34 ), Agrimonia pilos polysaccharide ( 35 ), 6-hydroxydopamine ( 36 ), and skullcapflavone I ( 37 ).…”

Section: Discussionmentioning

confidence: 99%

High expression of miR-107 and miR-17 predicts poor prognosis and guides treatment selection in acute myeloid leukemia

Liu¹,

Cao²,

Yang³

et al. 2023

Transl Cancer Res

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Background:The prognostic significance of miR-107 and miR-17 in patients with acute myeloid leukemia (AML) remains unclear.Methods: A total of 173 patients with de novo AML from the Cancer Genome Atlas database were enrolled in this study and further divided into a chemotherapy group (98 cases) and an allogeneic hematopoietic stem cell transplantation (allo-HSCT) group (75 cases) according to their therapy regimen.Results: In the chemotherapy cohort, high miR-107 or miR-17 expression was associated with poorer overall survival (OS) and event-free survival (EFS). On the other hand, there were no significant differences in OS and EFS between the high-and low-expression subgroups in the allo-HSCT group. Next, we stratified the total number of patients with AML into high-and low-expression groups according to the median expression levels of miR-107 or miR-17. In the high miR-107 or miR-17 expression group, patients treated with allo-HSCT had longer OS than those treated with chemotherapy. In the low miR-107 or miR-17 expression group, no significant differences in OS and EFS were observed between the two therapy subgroups. When patients were further clustered into three groups (both low miR-107 and low miR-17, either high miR-107 or high miR-17, and both high miR-107 and high miR-17), patients with both high miR-107 and high miR-17 expression had the worst OS and EFS of the entire group and of the chemotherapy group. On the other hand, there were no significant differences in OS and EFS among the three subgroups in the allo-HSCT group. Cox regression confirmed the concurrence of high expression of miR-107 and miR-17 might act as an independent prognostic factor for EFS and OS in the entire group and the chemotherapy group. Bioinformatics analysis showed differentially expressed genes (DEGs) associated with miR-107 and miR-17 expression were mainly enriched in multiple metabolic processes. Conclusions:The combination of miR-107 and miR-17 provides prognostic significance for patients with AML and should be considered in the clinical selection of the optimal treatment regimen when deciding between chemotherapy and allo-HSCT.

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Section: Discussionmentioning

confidence: 99%

High expression of miR-107 and miR-17 predicts poor prognosis and guides treatment selection in acute myeloid leukemia

Liu¹,

Cao²,

Yang³

et al. 2023

Transl Cancer Res

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“…Cells were maintained in Dulbecco's modified Eagle's medium (DMEM) supplemented with 10% fetal bovine serum (FBS) in a humidified 5% (v/v) CO 2 atmosphere at 37˚C. For antisense oligonucleotide (ASO) control (ASO-control), ASO-miRNA-301a-3p, ASO-miRNA-301b-3p, miRNA mimic control (miRNA-control), miRNA-301a-3p mimic, and miRNA-301b-3p mimic transfection (GE Healthcare, Chicago, IL, USA), cells were exposed to indicated concentrations using siRNA transfection reagent (RNAiMAX; Invitrogen, Carlsbad, CA, USA) and Opti-MEM medium (Invitrogen) as previously described (28).…”

Section: Methodsmentioning

confidence: 99%

Luteolin-regulated MicroRNA-301-3p Targets Caspase-8 and Modulates TRAIL Sensitivity in PANC-1 Cells

et al. 2020

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Background/Aim: MicroRNAs (miRNAs) play regulatory roles in pancreatic ductal adenocarcinoma (PDAC). However, it is still required to identify the function of miRNA-301-3p in pancreatic cancer cells. Materials and Methods: Effects of luteolin on cell growth, TRAIL cytotoxicity, and miR-301-3p levels were evaluated. The role of miRNA-301-3p in regulating cell proliferation, target gene expression, and TRAIL cytotoxicity were studied. Results: The levels of miR-301-3p were down-regulated in PANC-1 cells exposed to luteolin, which inhibits the growth of PANC-1 cells and sensitizes cells to TRAIL. The knockdown of miR-301-3p attenuates cell proliferation and enhances TRAIL cytotoxicity. In addition, caspase-8 was directly targeted by miR-301-3p. Conclusion: Our findings unveil a critical biological function of miR-301-3p in regulating cell proliferation and elevating an antiproliferative effect of TRAIL on cancer cells. Our observation of miR-301-3p/caspase-8 relationship can also serve to clarify the role of miR-301-3p in other cancer types and related diseases.Pancreatic ductal adenocarcinoma (PDAC) is the most common form of pancreatic cancer and a highly fatal malignancy with lymph node or distant metastases upon diagnosis. PDAC is predicted to be the second principal cause of cancer-related deaths by the year 2030 (1). Despite much progress on pancreatic cancer research over the past decades, surgery is the only attempt towards a curative outcome (2). Insufficient clinical efficacy of chemotherapy and radiation therapy has been reported and attributed to drug resistance in PDAC (3-6). Several signaling pathways, including nuclear factor kappa light chain enhancer of activated B cells (NF-ĸB) signaling, are activated, leading to cell growth and metastasis in PDAC. Mutations in tumor suppressor genes are also detected in PDAC (5, 7-9). A better understanding of the molecular characteristics of PDAC can lead to development of novel treatment strategies to combat PDAC.Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) is a member of the TNF superfamily. TRAIL has been known to inhibit cell growth by inducing cell-cycle arrest (10,11). In addition, anticancer effects of TRAIL can occur through death receptors 4 and 5, which generally regulate the activation of caspases, a family of cysteine proteases (12-14). Upon TRAIL binding, activation of caspase-8 cleaves executioner caspases, such as caspase-3 and -7, by which effective caspases contribute to chromatin condensation and nuclear fragmentation with the formation of apoptotic bodies (12-15). Indeed, TRAIL-induced apoptosis is impeded by the low expression of death receptors and caspases (16-18). Moreover, TRAIL resistance is associated with FADD-like ICE inhibitory proteins (FLIP) and inhibitor of apoptosis (IAP) family, such as cIAP, XIAP, and survivin, which inhibit the activation of caspases (19). Accumulating evidence has shown that combination of TRAIL with cancer therapeutic agents is effective to subdue TRAIL resistance. For instance, trea...

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“…As reported, miR-107 is a modulator of cell proliferation and apoptosis in lung cancer through modi cation of its target gene, TP53 regulated inhibitor of apoptosis 1 [9]. Besides, from another perspective, miR-107 serves to facilitate lung cancer cells to be sensitive to parthenolide through inhibiting cell proliferation and inducing apoptosis [10]. Also, low miR-107 advances the development of NSCLC [11].…”

Section: Introductionmentioning

confidence: 99%

Long Non-Coding RNA NEAT1 Accelerates Lung Cancer Development Via MicroRNA-107/FOXK1 Axis

Cao

Kong

et al. 2021

Preprint

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Objective: Studies have abstracted the partial mechanism of long non-coding RNA nuclear enriched abundant transcript 1 (NEAT1) in lung cancer, but its reciprocal with microRNA-107/Forkhead box k1 (miR-107/FOXK1) is not disclosed clearly. Hence, the mechanism of NEAT1/miR-107/FOXK1 was delved out in lung cancer.Methods: NEAT1, miR-107 and FOXK1 expression in clinical cancer tissues were determined, along with their interactions. The relation between the survival of lung cancer patients and NEAT1 expression was determined. NEAT1 and/or miR-107-related lentivirus or plasmid were transfected into A549 cells, after which cell biological functions were tested. Tumors were xenografted in mice to observe tumor formation and cell apoptosis.Results: High NEAT1 and FOXK1 and low miR-107 levels were tested in lung cancer tissues. High NEAT1 was connected with low overall survival of lung cancer patients. Depleting NEAT1 or augmenting miR-107 inhibited the biological functions of lung cancer cells. Depleted NEAT1 suppressed tumor-forming ability of A549 cells in vivo. Inhibited miR-107 antagonized depleted NEAT1-mediated effects on A549 cells. NEAT1 regulated FOXK1 by competitively binding miR-107.Conclusion: Silenced NEAT1 suppresses lung cancer development through elevating miR-107 and reducing FOXK1 expression, which supplies a plan to treat lung cancer.

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MicroRNA-107 Targets IKBKG and Sensitizes A549 Cells to Parthenolide

Cited by 6 publications

References 28 publications

High expression of miR-107 and miR-17 predicts poor prognosis and guides treatment selection in acute myeloid leukemia

High expression of miR-107 and miR-17 predicts poor prognosis and guides treatment selection in acute myeloid leukemia

Luteolin-regulated MicroRNA-301-3p Targets Caspase-8 and Modulates TRAIL Sensitivity in PANC-1 Cells

Long Non-Coding RNA NEAT1 Accelerates Lung Cancer Development Via MicroRNA-107/FOXK1 Axis

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