MicroRNA-10b Promotes Apoptosis via JNK Pathway in Clear Cell Renal Cell Carcinoma

Qin, Jianyang; Zhou, Jia; Han, Ying

doi:10.1159/000486017

Cited by 6 publications

(2 citation statements)

References 25 publications

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“…A study also showed that ABCC3 was able to contribute to hepatic cell growth (Fernandez‐Barrena et al, ). Consistently, miR‐10b has been investigated to be negatively associated with proliferation but positively correlated with apoptosis in clear cell renal cell cancer via the JNK pathway (Qin, Zhou, Teng, & Han, ). These supporting findings can help us explain why lung fibroblasts produced a lower degree of proliferation yet strengthened apoptosis in groups where miR‐448 expression was forced and ABCC3 expression was decreased.…”

Section: Discussionmentioning

confidence: 91%

MicroRNA‐448 overexpression inhibits fibroblast proliferation and collagen synthesis and promotes cell apoptosis via targeting ABCC3 through the JNK signaling pathway

Xie

et al. 2019

Journal Cellular Physiology

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Idiopathic pulmonary fibrosis (IPF) is a condition that results in the progressive deterioration of lung function with poor prognosis. The current study is aimed at exploring how microRNA-448 (miR-448) targeting ABCC3 affects fibroblast proliferation, apoptosis, and collagen synthesis of mice with IPF via the Jun N-terminal kinase (JNK) signaling pathway. Bioinformatics and dual-luciferase polymerase chain reaction were used to predict the relationship of miR-448 and ABCC3. The expression of miR-448 and ABCC3 was detected in IPF tissues. Using IPF mouse models, lung fibroblasts for the experiments were treated with miR-448 mimic, miR-448 inhibitor, si-ABCC3, or SP600125 (inhibitor of JNK) to evaluate the cell proliferation and apoptosis in response to miR-448. Reverse transcription quantitative polymerase chain reaction and western blot analysis were used to identify the expression of miR-448, ABCC3, and the activation of the JNK signaling pathway. ABCC3 was targeted and downregulated by miR-448 based on bioinformatics prediction and dual-luciferase reporter gene assay.Additionally, miR-448 was found to be highly expressed in IPF lung tissues with low expression levels of ABCC3. In response to the treatment of miR-448 mimic or si-ABCC3, lung fibroblasts exhibited decreased cell proliferation and increased apoptotic rates, whereas the miR-448 inhibitor reversed the conditions. Notably, we also found that miR-448 mimic inhibited the JNK signaling pathway. In conclusion, by using miR-448 to target and downregulate ABCC3 to block the JNK signaling pathway in mice with IPF, we found an increase in fibroblast apoptosis, inhibited cell proliferation, and decreased collagen synthesis of fibroblasts.

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Section: Discussionmentioning

confidence: 91%

MicroRNA‐448 overexpression inhibits fibroblast proliferation and collagen synthesis and promotes cell apoptosis via targeting ABCC3 through the JNK signaling pathway

Xie

et al. 2019

Journal Cellular Physiology

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“…Studies have found that the activation of JNK signaling pathway can promote the production of vascular endothelial growth factor (VEGF) and matrix metalloproteinases (MMPs) by renal hyaluronic cell cancer cells, thus promoting tumor angiogenesis and remodeling of tumor microenvironment [30,31] , and these changes are conducive to the nutrient supply and metastasis of renal hyaluronic cell cancer cells. In addition, the activation of JNK can lead to the inhibition of apoptosis pathway, making renal hyaluronic cell cancer cells resistant to radiotherapy and chemotherapy [32,33] . Inhibition of JNK signaling pathway has become a research focus in the treatment of renal hyaluronic cell carcinoma [34] .…”

Section: Introductionmentioning

confidence: 99%

Acetyltransferase Tip60 inhibits the invasion and migration of renal cell carcinoma through JNK signaling

2024

FMSR

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Cancer is one of the major diseases affecting human health, and statistics show that about 90% of cancer patients die from tumor migration rather than primary tumor growth. The mechanism of tumor migration is still unclear, and most of the current studies are in vitro cell experiments, which can not fully reflect the real situation in vivo, so it is particularly important to use in vivo models for research. In vivo models of Drosophila melanogaster, we found that Tip60 inhibited cell migration induced by down-regulating the cell polar gene scrib and tumor invasion induced by lgl -/-/Ras V12 . However, the deletion of acetyltransferase activity in Tip60 can induce cell migration through activation of JNK signaling pathway. We found that Tip60 inhibited JNK signals-mediated cell migration and tumor invasion through the acetylation of downstream transcription factor Fos, and inhibited the expression of downstream migration molecules such as MMP1. In this study, the role of Tip60-Fos in cell migration and tumor invasion was investigated, and the molecular mechanism of Tip60-Fos was elucidated, and corresponding validation was carried out in the samples of kidney cancer patients. These studies will further improve the regulatory network of tumor migration and provide new ideas for the treatment and drug target research of kidney cancer.

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Methylenetetrahydrofolate Dehydrogenase 1 (MTHFD1) is Underexpressed in Clear Cell Renal Cell Carcinoma Tissue and Transfection and Overexpression in Caki-1 Cells Inhibits Cell Proliferation and Increases Apoptosis

Liu

et al. 2018

Med Sci Monit

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BackgroundThe aims of this study were to investigate the expression of methylenetetrahydrofolate dehydrogenase 1 (MTHFD1) in human tissue containing clear cell renal cell carcinoma (CCRCC) compared with normal renal tissue, and the effects of upregulating the expression of MTHFD1 in the human CCRCC cell line, Caki-1.Material/MethodsTumor and adjacent normal renal tissue were obtained from 44 patients who underwent radical nephrectomy for CCRCC. Caki-1 human CCRCC cells were divided into the control group, the empty vector (EV) group, and the plasmid-treated group that overexpressed MTHFD1. MTHFD1 mRNA and protein levels were measured by quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot, respectively. The cell counting kit-8 (CCK-8) assay measured cell viability. Flow cytometry evaluated apoptosis and the cell cycle. Western blot measured the protein levels of MTHFD1, Bax, Bcl-2, Akt, p53, and cyclin D1, and qRT-PCR determined the gene expression profiles.ResultsMTHFD1 mRNA and protein levels in CCRCC tumor tissues were significantly lower compared with adjacent normal renal tissue. MTHFD1 over-expression in Caki-1 cells inhibited cell proliferation, arrested cells in the G1 phase, increased cell apoptosis, and upregulated gene and protein expression of Bax/Bcl-2 and p53, and inhibited p-Akt, and cyclin D1.ConclusionsMTHFD1 was underexpressed in CCRCC tissue when compared with normal renal tissue. MTHFD1 transfection of human CCRCC Caki-1 cells in vitro inhibited cell proliferation and promoted apoptosis, associated with reduced expression of cyclin D1, reduced Akt phosphorylation, and increased expression of Bax/Bcl-2 and p53.

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MicroRNA-10b Promotes Apoptosis via JNK Pathway in Clear Cell Renal Cell Carcinoma

Cited by 6 publications

References 25 publications

MicroRNA‐448 overexpression inhibits fibroblast proliferation and collagen synthesis and promotes cell apoptosis via targeting ABCC3 through the JNK signaling pathway

MicroRNA‐448 overexpression inhibits fibroblast proliferation and collagen synthesis and promotes cell apoptosis via targeting ABCC3 through the JNK signaling pathway

Acetyltransferase Tip60 inhibits the invasion and migration of renal cell carcinoma through JNK signaling

Methylenetetrahydrofolate Dehydrogenase 1 (MTHFD1) is Underexpressed in Clear Cell Renal Cell Carcinoma Tissue and Transfection and Overexpression in Caki-1 Cells Inhibits Cell Proliferation and Increases Apoptosis

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