miR-200b inhibits CD133+ glioma cells by targeting the AKT pathway

Liu, Ai Qun; Yu, Qingyun; Peng, Zhongxing; Huang, Yeqing; Diao, Sheng-Peng; Cheng, Jing; Wang, Wentao; Hong, Ming‐Fan

doi:10.3892/ol.2017.6055

Cited by 16 publications

(9 citation statements)

References 26 publications

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“…A mutant insert was also generated in which the first four nucleotides of the miR-124 binding site the SP1 gene (AUGT-GCAC; predicted by TargetScan) were mutated using a QIAGEN XL-site directed Mutagenesis kit (Qiagen, Inc. Valencia, CA, USA). SGC-7901 and MKN-28 cells were cotransfected by nucleoporation (Amaxa Nucleofector™; Lonza Group, Ltd., Basel, Switzerland) ( 16 ) with 5 µg firefly luciferase reporter vector (Promega Corporation) and 0.5 μg control vector containing Renilla luciferase (pRL-TK; Promega Corporation). For each nucleoporation, 50 nM of the miR-124-3p mimic, miR-124-LNA (inhibitor), miR-ctr or miR-LNA was used.…”

Section: Methodsmentioning

confidence: 99%

miR‑124‑3p acts as a potential marker and suppresses tumor growth in gastric cancer

Liu

Zhao

et al. 2018

biom rep

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miR-124-3p has been implicated in a variety of cancers. The purpose of the present study was to investigate the expression, prognostic roles and functions of miR-124-3p in gastric cancer. Functional studies indicated that ectopic overexpression of miR-124-3p in gastric cancer cells suppressed cell viability and plate colony formation in vitro and tumor growth in vivo. In situ hybridization analysis demonstrated that decreased expression of miR-124-3p was associated with clinical stage and lymph node metastasis, as well as shorter overall survival and disease-free survival rates. Furthermore, it was observed that miR-124-3p repressed the carcinogenesis of gastric cancer by targeting Ras-related C3 botulinum toxin substrate 1 (Rac1) and specificity protein 1 (SP1). Collectively, these results indicate a potential underlying mechanism for the regulation of gastric cancer by miR-124-3p involving targeting of Rac1 and SP1. Thus, miR-124-3p may be an independent indicator of survival and treatment strategy for patients with gastric cancer.

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Section: Methodsmentioning

confidence: 99%

miR‑124‑3p acts as a potential marker and suppresses tumor growth in gastric cancer

Liu

Zhao

et al. 2018

biom rep

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“…The suppression of the PI3K/AKT signaling pathway has been reported to lead to the inhibition of TNF-α-induced inflammation [68]. The PI3K/AKT signaling pathway has been reported to be indirectly suppressed by miR-200c and miR-200b [69,70]; thus, we may assume that miR-200a decreases the levels of IL-4, IL-6, IL-8, TNF-α and IgE by inhibiting the PI3K/AKT signaling pathway to inhibit lung inflammation.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-200a Affects the Proliferation of Airway Smooth Muscle Cells and Airway Remodeling by Targeting FOXC1 via the PI3K/AKT Signaling Pathway in Ovalbumin-Induced Asthmatic Mice

Liu¹,

Miao²,

Gào³

et al. 2018

Cell Physiol Biochem

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Background/Aims: The etiology of asthma, which is a complicated disorder with various symptoms, including wheezing, coughing, and airflow obstruction, remains poorly understood. In addition, the effects of microRNAs (miRs) have not been explored. This study explored the effect of microRNA-200a (miR-200a) on airway smooth muscle cells (ASMCs) and airway remodeling in asthmatic mice. Furthermore, we speculated that miR-200a achieves its effect by targeting FOXC1 via the PI3K/AKT signaling pathway based on differentially expressed gene screening, target miR predictions and a bioinformatics analysis. Methods: Eighty mice were assigned to a saline group or an ovalbumin (OVA) group, and the OVA group was transfected with a series of inhibitors, activators, and siRNAs to test the established mouse model. Airway reactivity and the ratio of eosinophils (EOSs) to leukocytes were detected. An ELISA was adopted to measure the levels of interleukin (IL)-4, IL-6, IL-8, tumor necrosis factor (TNF)-α, and immunoglobulin E (IgE). Reverse transcription quantitative polymerase chain reaction (RT-qPCR) and western blotting were used to determine the expression of FOXC1, PI3K, AKT, NF-κB, cyclin D1, TGF-β1 and p-AKT in ASMCs. Finally, CCK-8 assays were performed to detect cell proliferation and flow cytometry to detect apoptosis and cell cycle entry. Results: The bioinformatics analysis indicated that miR-200a mediated the PI3K/AKT signaling pathway by targeting FOXC1. In addition, mouse models of asthma were established. An elevated expression of miR-200a, a decreased mRNA and protein expression of FOXC1, PI3K, AKT, NF-κB, cyclin D1 and TGF-β1, a decreased expression of p-AKT, suppressed cell proliferation, accelerated apoptosis, and an increased number of cells at the G0/G1 phase were observed following the upregulation of miR-200a and downregulation of FOXC1. Conclusion: The overexpression of miR-200a may downregulate FOXC1, thereby inhibiting the activation of the PI3K/AKT signaling pathway and ultimately suppressing ASMC proliferation and airway remodeling in asthmatic mice. This evidence supports the potential that miR-200a represents a new approach to treating asthma.

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“…AKT serine–threonine kinase 1 (AKT) serves as a target and effector of phosphatidylinositol 3-kinase (PI3K) downstream. 17 The PI3K/AKT signaling pathway is recognized to regulate the cell growth and fate decisions in tumors. 18 For example, PI3K/AKT signaling pathway was activated in the progression of glioma.…”

Section: Introductionmentioning

confidence: 99%

Inhibition of CD133 Overcomes Cisplatin Resistance Through Inhibiting PI3K/AKT/mTOR Signaling Pathway and Autophagy in CD133-Positive Gastric Cancer Cells

Zhao

Yang

et al. 2019

Technol Cancer Res Treat

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Cisplatin is widely used as the standard gastric cancer treatment, but the relapse and metastasis are common as intrinsic or acquired drug resistance. CD133 has been widely known to be associated with chemoresistance in various cancer cells. In this study, we focused on investigating the function and mechanism of CD133 underlying cisplatin resistance in gastric cancer cell line KATO-III. We detected CD133 expression by using quantitative real-time polymerase chain reaction and Western blot and found that expression of CD133 was upregulated in cisplatin resistance of KATO-III cells (Cis-KATO-III) compared with KATO-III cells, indicating the role of CD133 in regulating cisplatin resistance of KATO-III cells. Then we sorted the Cis-KATO-III cells into CD133-positive (CD133+) pools and measured the proliferation and apoptosis after the cell is transfected with pc-CD133 and sh-CD133 by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide assay and flow cytometry. The results showed that the inhibition of CD133 inhibited the cell viability and promoted the cell apoptosis after cisplatin treatment. Furthermore, we found that inhibition of CD133 downregulated the expression of PI3K/AKT and promoted the expression of mammalian target of rapamycin, thus inhibited the autophagic activity in the Cis-KATO-III cells after cisplatin treatment. Besides, we also verified the effects of CD133 in vivo. The results indicated that inhibition of CD133 enhanced the Cis-KATO-III cell sensitivity to cisplatin by regulating PI3K/AKT/mTOR signaling pathway. In summary, our data provide new insight that CD133 activates the PI3K/AKT/mTOR signaling transduction pathway, resulting in activation of autophagy and cisplatin resistance of Cis-KATO-III cells. These results may offer a novel therapeutic target in cisplatin-resistant gastric cancer.

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miR-200b inhibits CD133+ glioma cells by targeting the AKT pathway

Cited by 16 publications

References 26 publications

miR‑124‑3p acts as a potential marker and suppresses tumor growth in gastric cancer

miR‑124‑3p acts as a potential marker and suppresses tumor growth in gastric cancer

MicroRNA-200a Affects the Proliferation of Airway Smooth Muscle Cells and Airway Remodeling by Targeting FOXC1 via the PI3K/AKT Signaling Pathway in Ovalbumin-Induced Asthmatic Mice

Inhibition of CD133 Overcomes Cisplatin Resistance Through Inhibiting PI3K/AKT/mTOR Signaling Pathway and Autophagy in CD133-Positive Gastric Cancer Cells

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