Inhibition of Vascular Endothelial Growth Factor Receptor 3 Reduces Migration of Gastric Cancer Cells

Lim, Jae‐Young; Ryu, Jinhyun; Kim, Eun Jin; Ham, Songhee; Kang, Dawon

doi:10.3109/07357907.2015.1047509

Cited by 6 publications

(7 citation statements)

References 37 publications

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“…Furthermore, in our previous study it was demonstrated that SIX1, a developmental transcription factor predicted to represent a potential target gene of miR-23b-3p, may enhance the expression of VEGF-C in OS (2). VEGF-C promotes cervical cancer cell invasion and migration (48), and enhances the metastatic ability of esophageal carcinoma (49), whereas knocking down VEGF-C suppresses gastric cancer cell migration (50). Therefore, VEGF-C was investigated in the present study, and the results demonstrated that miR-23b-3p is associated with decreased expression levels of VEGF-C in U2OS cells.…”

Section: Discussionmentioning

confidence: 84%

miR‑23b‑3p promotes the apoptosis and inhibits the proliferation and invasion of osteosarcoma cells by targeting SIX1

et al. 2018

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Osteosarcoma (OS) is the most common primary malignant bone tumor and the third most common cancer that occurs during childhood and adolescence. Increasing evidence has suggested that microRNA (miR)-23b-3p has an important role in OS tumorigenesis; however, the underlying molecular mechanisms remain unknown. The aim of the present study was to investigate the expression levels of miR-23b-3p and sine oculis homeobox homolog 1 (SIX1) in OS tissues and cell lines (MG-63, SaOS-2 and U2OS), as well as to observe the effects of miR-23b-3p on U2OS cell viability, cell cycle, apoptosis and invasive ability. The results revealed that the expression levels of miR-23b-3p were significantly decreased in OS tissues and cell lines compared with tumor-adjacent normal tissues and a non-cancerous human fetal osteoblastic cell line (hFOB1.19). To investigate the underlying mechanisms of miR-23b-3p in OS tumorigenesis and progression, human U2OS cell lines over-or under expressing miR-23b-3p were established. The effects of miR-23b-3p on U2OS cell viability, cell cycle, apoptosis and invasion properties were determined by performing Cell Counting Kit-8, flow cytometry and Transwell invasion assays. miR-23b-3p was revealed to suppress cell viability, proliferation and invasion, and to enhance the levels of cell apoptosis. Furthermore, SIX1 mRNA and protein expression levels in OS tissues and cell lines were significantly upregulated when compared with tumor-adjacent normal tissues and hFOB 1.19 cells, which suggested that SIX1 expression levels may be inversely associated with miR-23b-3p levels in OS. Luciferase reporter system analysis demonstrated that miR-23b-3p binds to the SIX1 3'-untranslated region. miR-23b-3p downregulation contributed to SIX1 upregulation, which facilitated the potentiation of cyclin D1 and vascular endothelial growth factor-C expression levels, as well as the inhibition of caspase-3 expression. Collectively, these results suggested that miR-23b-3p is downregulated and SIX1 is upregulated in OS cells, and that miR-23b-3p inhibition may suppress the proliferation and invasion of OS cells, and contribute to cell apoptosis via negative regulation of SIX1. miR-23b-3p/SIX1 may therefore represent a potential target for the treatment of OS.

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Section: Discussionmentioning

confidence: 84%

miR‑23b‑3p promotes the apoptosis and inhibits the proliferation and invasion of osteosarcoma cells by targeting SIX1

et al. 2018

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“…ZNF684 (zinc finger protein 684) was increased 2.08‐fold of gene expression, and zinc finger protein X‐linked represents the prominent role in the progression of prostate cancer and may be a promising therapy target for prostate cancer . VEGFB (vascular endothelial growth factor B) was down‐regulated 2.06‐fold of gene expression and VEGFR3 could be a therapeutic target for reducing the metastasis of gastric cancer cells . CDK10 (cyclin‐dependent kinase 10), was down‐regulated 3.22‐fold of gene expression, and the association of low levels of CDK10 with methylation of the CDK10 promoter have been suggested to be a mechanism by which CDK10 expression is reduced in tumors .…”

Section: Discussionmentioning

confidence: 99%

Quercetin induced cell apoptosis and altered gene expression in AGS human gastric cancer cells

Shang

Lee

et al. 2018

Environmental Toxicology

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Quercetin is one of the natural components from natural plant and it induces cell apoptosis in many human cancer cell lines. However, no available reports show that quercetin induces apoptosis and altered associated gene expressions in human gastric cancer cells, thus, we investigated the effect of quercetin on the apoptotic cell death and associated gene expression in human gastric cancer AGS cells. Results indicated that quercetin induced cell morphological changes and reduced total viability via apoptotic cell death in AGS cells. Furthermore, results from flow cytometric assay indicated that quercetin increased reactive oxygen species (ROS) production, decreased the levels of mitochondrial membrane potential (ΔΨ ), and increased the apoptotic cell number in AGS cells. Results from western blotting showed that quercetin decreased anti-apoptotic protein of Mcl-1, Bcl-2, and Bcl-x but increased pro-apoptotic protein of Bad, Bax, and Bid. Furthermore, quercetin increased the gene expressions of TNFRSF10D (Tumor necrosis factor receptor superfamily, member 10d, decoy with truncated death domain), TP53INP1 (tumor protein p53 inducible nuclear protein 1), and JUNB (jun B proto-oncogene) but decreased the gene expression of VEGFB (vascular endothelial growth factor B), CDK10 (cyclin-dependent kinase 10), and KDELC2 (KDEL [Lys-Asp-Glu-Leu] containing 2) that are associated with apoptosis pathways. Thus, those findings may offer more information regarding the molecular, gene expression, and signaling pathway for quercetin induced apoptotic cell death in human gastric cancer cells.

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“…CDK2, a member of protein kinase family, significantly modulated abundant events of eukaryotic cell division cycle [ 92 ]. VEGF was known to take a great part in the progression and metastasis of cancers through inducing angiogenesis [ 93 ]. Thus it can be seen that miR-29a adjusted these biological and significant genes and participated in tumorigenesis.…”

Section: Discussionmentioning

confidence: 99%

MiR-29a: a potential therapeutic target and promising biomarker in tumors

et al. 2018

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MiRNAs, small non-coding RNA molecules, were recognized to be associated with the incidence and development of diverse neoplasms. MiRNAs were small non-coding RNAs that could regulate post-transcriptional level by binding to 3′-UTR of target mRNAs. Amongst which, miR-29a was demonstrated that it had significant impact on oncogenicity in various neoplasms through binding to critical genes which enhanced or inhibited the progression of cancers. MiR-29a participated in kinds of physiological and pathological processes, including virus replication, cell proliferation, differentiation, apoptosis, fibrosis, angiogenesis, tumorigenicity, metastasis, drug-resistance, and so on. According to its sufficient sensitivity and specificity, many studies showed that miR-29a might serve as a potential therapeutic target and promising biomarker in various tumors. In this review, we discussed the functions of miR-29a and its potential application in the diagnosis, treatment and stages of carcinoma, which could provide additional insight to develop a novel therapeutic strategy.

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Inhibition of Vascular Endothelial Growth Factor Receptor 3 Reduces Migration of Gastric Cancer Cells

Cited by 6 publications

References 37 publications

miR‑23b‑3p promotes the apoptosis and inhibits the proliferation and invasion of osteosarcoma cells by targeting SIX1

miR‑23b‑3p promotes the apoptosis and inhibits the proliferation and invasion of osteosarcoma cells by targeting SIX1

Quercetin induced cell apoptosis and altered gene expression in AGS human gastric cancer cells

MiR-29a: a potential therapeutic target and promising biomarker in tumors

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