Identification of MicroRNAs Involved in Resistance to Sunitinib in Renal Cell Carcinoma Cells

Yamaguchi, Noriya; Osaki, Mitsuhiko; Onuma, Kunishige; Yumioka, Tetsuya; Iwamoto, Hideto; Sejima, Takehiro; Kugoh, Hiroyuki; Takenaka, Atsushi; Okada, Futoshi

doi:10.21873/anticanres.11652

Cited by 30 publications

(43 citation statements)

References 21 publications

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“… 6 – 8 miR-431 is located on chromosome 14q32.2; 9 Pan et al found that miR-431 is a possible novel marker for renal cancer, lung cancer, and melanoma, even at the primary stage of cancer. 10 – 13 Meng et al 14 investigated that hsa-miR-431-5p was downregulated in the serum of diffuse large B-cell lymphoma patients. Yamaguchi et al 13 found that miR-431 could contribute to chemotherapy resistance in human cancer.…”

Section: Introductionmentioning

confidence: 99%

“… 10 – 13 Meng et al 14 investigated that hsa-miR-431-5p was downregulated in the serum of diffuse large B-cell lymphoma patients. Yamaguchi et al 13 found that miR-431 could contribute to chemotherapy resistance in human cancer. In addition, Trehanpati et al 15 found that miR-431 was significantly expressed in hepatitis E viral (HEV) infection in liver.…”

Section: Introductionmentioning

confidence: 99%

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miR-431-5p alters the epithelial-to-mesenchymal transition markers by targeting <em>UROC28</em> in hepatoma cells

Kong

Han

Deng

et al. 2018

OTT

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ObjectiveMicroRNA (miR)-431 plays an essential role in various human cancer types, particularly in the process of invasion. However, the function and mechanism of miR-431-5p in the invasion of hepatocellular carcinoma (HCC) remain undefined.MethodsThe expression levels of miR-431-5p and its potential target protein UROC28 in hepatocellular carcinoma cells and tissues were detected, and the levels of EMT markers in vivo and in vitro were also detected.ResultsMiR-431-5p was downregulated in HCC cell lines and tissues and associated with vascular invasion and tumor encapsulation. Furthermore, miR-431-5p was able to influence the epithelialto-mesenchymal transition (EMT) process in HCCLM3 and HUH7 cells. Mechanistically, it was discovered that miR-431-5p repressed invasion by targeting UROC28. Furthermore, miR-431-5p influenced the EMT markers in HCCLM3 and HUH7 cells by downregulating UROC28 expression. Similarly, in vivo assays confirmed that miR-431-5p upregulation in HCC cells remarkably inhibited tumor proliferation and influenced the EMT markers.ConclusionThe current study has demonstrated that the miR-431-5p/UROC28 axis acts possible influence on the EMT in HCC. Upregulation of miR-431-5p could be an original approach for inhibiting tumor invasion.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

miR-431-5p alters the epithelial-to-mesenchymal transition markers by targeting <em>UROC28</em> in hepatoma cells

Kong

Han

Deng

et al. 2018

OTT

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“…One of the primary reasons for the failure of RCC treatments is that patients with advanced RCC often develop resistance to anti-cancer agents [13]. The matrix metalloproteinases (MMPs), crucial proteolytic proteinases that allow malignant cells to access the vasculature, are a family of zinc-dependent endopeptidases with broad substrate specificities for a variety of extracellular matrix (ECM) and basement membrane proteins [14].…”

Section: Introductionmentioning

confidence: 99%

Alpha-Mangostin Suppresses the Metastasis of Human Renal Carcinoma Cells by Targeting MEK/ERK Expression and MMP-9 Transcription Activity

Chen

Hsieh

Lin

et al. 2017

Cell Physiol Biochem

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Background/Aims: α-mangostin has anti-carcinogenic effects against several cancers. We investigated the molecular mechanism of this compound on the metastasis of human renal carcinoma cells. Methods: Cell viability was measured using the MTT assay, and cell cycle distribution using flow cytometry. A Matrigel-based assay was used to measure in vitro cell migration and invasion. MAPK-related proteins and matrix metalloproteinase (MMP)-9 and MMP-2 expression were measured by western blotting, and MMP2/-9 activities were determined by gelatin zymography. RT-qPCR and a luciferase assay were used to examine the transcriptional activity of MMP-9. Results: α-mangostin inhibited the migration and invasion of RCC cells in a dose-dependent manner, but had no evident cytotoxic effects. Treatment of 786-O cells with α-mangostin inhibited activation of MEK and ERK. Treatment with a specific MEK inhibitor (U0126) enhanced the inhibitory effects of α-mangostin on cell migration and invasion, and the phosphorylation of ERK and MEK. Moreover, α-mangostin inhibited the expression of the MMP-9 mRNA levels as well as the activity of MMP-9 promoter, and these suppressive effects were further enhanced by U0126. Conclusions: Our results suggest that α-mangostin suppresses cell migration and invasion via MEK/ERK/MMP9 pathway, and might be a promising anti-metastatic agent against human renal cell carcinoma.

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“…miRNAs play an important role as regulators of gene expression in tumorigenesis, tumor progression, drug resistance, and metastasis ( 13 , 14 ). Thus, we previously generated a sunitinib-resistant RCC cell line, SR-ACHN (sunitinib-resistant ACHN), by continuous treatment with sunitinib to detect candidate miRNAs implicated in the regulation of sunitinib resistance ( 15 ). The aim of this study was to identify miRNAs that suppressed sunitinib resistance via LAMP2 expression using ACHN and SR-ACHN cells.…”

Section: Introductionmentioning

confidence: 99%

Lysosome‑associated membrane protein 2 (LAMP‑2) expression induced by miR‑194‑5p downregulation contributes to sunitinib resistance in human renal cell carcinoma cells

et al. 2017

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Sunitinib is a tyrosine kinase inhibitor that is used as the primary treatment in metastatic renal cell carcinoma (RCC). The main difficulty associated with its use is the development of drug resistance. In the present study, ACHN cells, a human renal cell carcinoma cell line, were used to establish sunitinib-resistant (SR) cells. Microarray analysis and reverse transcription-quantitative polymerase chain reaction revealed that miR-194-5p expression was significantly decreased in SR-ACHN cells when compared with that observed in ACHN cells (P<0.05). Transfection of miR-194-5p, though not with negative control miR, in SR-ACHN cells could significantly inhibit cell proliferation following sunitinib treatment (2.5–40 µM; P<0.05). Western blotting demonstrated that the expression of lysosome-associated membrane protein-2 (LAMP-2), which attenuates the anti-proliferative effect of sunitinib, was significantly higher in SR-ACHN than in ACHN cells (P<0.01). In addition, LAMP-2 expression was suppressed by miR-194-5p transfection in SR-ACHN cells. These data suggested that miR-194-5p downregulation may be associated with sunitinib resistance via the induction of LAMP-2 expression in human RCC.

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Identification of MicroRNAs Involved in Resistance to Sunitinib in Renal Cell Carcinoma Cells

Abstract: These miRNAs may contribute to sunitinib resistance in humans.

Cited by 30 publications

References 21 publications

miR-431-5p alters the epithelial-to-mesenchymal transition markers by targeting <em>UROC28</em> in hepatoma cells

miR-431-5p alters the epithelial-to-mesenchymal transition markers by targeting <em>UROC28</em> in hepatoma cells

Alpha-Mangostin Suppresses the Metastasis of Human Renal Carcinoma Cells by Targeting MEK/ERK Expression and MMP-9 Transcription Activity

Lysosome‑associated membrane protein 2 (LAMP‑2) expression induced by miR‑194‑5p downregulation contributes to sunitinib resistance in human renal cell carcinoma cells

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