Silencing MARCH1 suppresses proliferation, migration and invasion of ovarian cancer SKOV3 cells via downregulation of NF-κB and Wnt/β-catenin pathways

Meng, Ying; Hu, Jianguo; Chen, Yuhong; Yu, Tinghe; Hu, Lina

doi:10.3892/or.2016.5076

Cited by 37 publications

(33 citation statements)

References 39 publications

(41 reference statements)

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“…13 Previous studies have demonstrated that pathway. 13 Previous studies have demonstrated that pathway.…”

Section: Discussionmentioning

confidence: 97%

“…8 Ubiquitination was recently identified as an important and specific process, participating in several protein degradation and cell signalling pathways through the close cooperation of three enzymes: the ubiquitin-activating enzyme E1, the ubiquitin-conjugating enzyme E2 and the ubiquitin-ligase enzyme E3. 13 These data suggest that MARCH1 may be a proto-oncogene that promotes tumour progression and, hence, a potential molecular target for cancer therapy. 11,12 Previous studies have focused on the role of MARCH1 in the immune system.…”

Section: Introductionmentioning

confidence: 97%

“…Recently, a study demonstrated that MARCH1 was overexpressed in ovarian cancer tissues, silencing MARCH1 inhibits the proliferation, migration and invasion of the ovarian cancer cells by down-regulating the NF-κB and Wnt/β-catenin pathways. 13 These data suggest that MARCH1 may be a proto-oncogene that promotes tumour progression and, hence, a potential molecular target for cancer therapy.…”

mentioning

confidence: 97%

“…demonstrated that MARCH1 silencing by siRNA suppressed cell development and progression via the down-regulation of the Wnt/β-catenin pathway in ovarian cancer 13. To explain how downregulated MARCH1 inhibited HCC cell proliferation, migration and invasion and promoted cell apoptosis, we explored the underlying molecular changes downstream of the MARCH1 perturbation.Here, we addressed the molecular effects of the down-regulatedMARCH1 by using western blotting assay.…”

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confidence: 99%

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MARCH1 encourages tumour progression of hepatocellular carcinoma via regulation of PI3K‐AKT‐β‐catenin pathways

Xie

Dai

et al. 2019

J Cellular Molecular Medi

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Membrane‐associated RING‐CH‐1 (MARCH1) is a membrane‐anchored E3 ubiquitin ligase that is involved in a variety of cellular processes. MARCH1 was aberrantly expressed as a tumour promoter in ovarian cancer, but the signalling about the molecular mechanism has not yet been fully illuminated. Here, we first determined that MARCH1 was obviously highly expressed in human hepatocellular carcinoma samples and cells. In addition, our findings demonstrated that the proliferation, migration and invasion of hepatocellular carcinoma were suppressed, but the apoptosis was increased, as a result of MARCH1 knockdown by either siRNA targeting MARCH1 or pirarubicin treatment. Conversely, the proliferation, migration and invasion of hepatocellular carcinoma were obviously accelerated, and the apoptosis was decreased, by transfecting the MARCH1 plasmid to make MARCH1 overexpressed. Moreover, in vivo, the results exhibited a significant inhibition of the growth of hepatocellular carcinoma in nude mice, which were given an intra‐tumour injection of siRNA targeting MARCH1. Furthermore, our study concluded that MARCH1 functions as a tumour promoter, and its role was up‐regulated the PI3K‐AKT‐β‐catenin pathways both in vitro and in vivo. In summary, our work determined that MARCH1 has an important role in the development and progression of hepatocellular carcinoma and may be used as a novel potential molecular therapeutic target in the future treatment of hepatocellular carcinoma.

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“…13 Previous studies have demonstrated that pathway. 13 Previous studies have demonstrated that pathway.…”

Section: Discussionmentioning

confidence: 97%

Section: Introductionmentioning

confidence: 97%

mentioning

confidence: 97%

mentioning

confidence: 99%

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MARCH1 encourages tumour progression of hepatocellular carcinoma via regulation of PI3K‐AKT‐β‐catenin pathways

Xie

Dai

et al. 2019

J Cellular Molecular Medi

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“…For example, MARCH1 knock out suppresses proliferation, migration, and invasion of ovarian cancer cells by suppressing the NF-κB and Wnt/β-catenin pathways [12]. Similarly, MARCH2 silencing inhibits the growth of colon cancer cells via induction of endoplasmic reticulum stress [13].…”

Section: Introductionmentioning

confidence: 99%

MARCH9 Suppresses Lung Adenocarcinoma Progression by Downregulating ICAM-1

Shen

Wang

2018

Cell Physiol Biochem

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Background/Aims: To investigate the clinical significance and functional mechanisms of membrane-associated RING-CH protein 9 (MARCH9) in lung adenocarcinoma (LAC). Methods: Immunohistochemistry staining was performed to explore the expression of MARCH9 in LAC tissues and adjacent normal lung tissues. Patients’ prognosis was evaluated using overall survival. The prognostic role of MARCH9 was tested with univariate and multivariate analyses. To confirm the effect of MARCH9 in cell proliferation and invasion, overexpression of MARCH9 was induced in two LAC cell lines. Cell cycle, apoptosis, migration, invasion, and immunoprecipitation experiments were performed to further explore the signaling pathways involved. Results: Analysis of a series of 143 clinical samples revealed that MARCH9 was down-regulated in tumor tissues compared with normal lung tissues, and this was closely associated with lymph node metastasis (P = 0.004). Univariate and multivariate analyses indicated that MARCH9 was an independent prognostic biomarker for LAC; low MARCH9 expression indicated poor overall survival. Cellular studies with A549 and H1299 cells demonstrated that MARCH9 can attenuate tumor migration and invasion but had little effect on cell cycle or apoptosis. Moreover, an interaction between MARCH9 and ICAM-1 protein was identified, and overexpression of MARCH9 was found to attenuate the oncogenic effect of ICAM-1, suggesting that MARCH9 may inhibit tumor progression by downregulating ICAM-1 signaling. Conclusion: MARCH9 downregulation in LAC tissues correlated with poor clinical outcomes. MARCH9 may serve as a novel biomarker and potential therapeutic target for LAC.

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Osteoglycin silencing exerts inhibitory effects on myocardial fibrosis and epithelial/endothelial‐mesenchymal transformation in a mouse model of myocarditis

Fang

Chang

et al. 2020

BioFactors

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Osteoglycin (Ogn), a class III SLRP member with multiple glycosylation sites, has been proposed to be engaged in cardiac dysfunction and adverse remodeling in human heart failure following myocardial infarction. However, the underlying mechanism remains to be elucidated. Thus, we sought to define the role of Ogn in regulation of the Wnt pathway on myocardial fibrosis and epithelial/endothelial-mesenchymal transformation (EMT/EndMT) in mice with myocarditis. The pathological changes are observed, while hematoxylin-eosin staining and picric acid Sirius red staining were conducted in successfully constructed myocarditis mouse models. Immunohistochemistry and enzymelinked immunosorbent assay were adopted to determine Ogn and β-catenin levels and serum procollagen propeptide concentrations in the mouse myocardial tissues, respectively. Expression of Ogn and Wnt signaling pathway-related factors were measured by reverse transcription quantitative polymerase chain reaction and western blot assay, cell viability by 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, and cell cycle distribution and apoptosis by flow cytometry. We saw indicative pathological changes accompanied by many Ogn and β-catenin positive cells and increased serum procollagen propeptide, in the mouse myocardial tissues. Loss function assays showed reduced levels of Ogn, β-catenin, LRP6, TGF-β1, Twist, FSP-1, α-SMA and higher levels of E-cadherin and VE-cadherin, together with decreased proliferation rate, as well as increased apoptosis rate, indicating that the Wnt signaling pathway, proliferation were inhibited while apoptosis was enhanced with upon gene silencing. Coherently, depletion of Ogn inhibits myocardial fibroblasts

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Silencing MARCH1 suppresses proliferation, migration and invasion of ovarian cancer SKOV3 cells via downregulation of NF-κB and Wnt/β-catenin pathways

Cited by 37 publications

References 39 publications

MARCH1 encourages tumour progression of hepatocellular carcinoma via regulation of PI3K‐AKT‐β‐catenin pathways

MARCH1 encourages tumour progression of hepatocellular carcinoma via regulation of PI3K‐AKT‐β‐catenin pathways

MARCH9 Suppresses Lung Adenocarcinoma Progression by Downregulating ICAM-1

Osteoglycin silencing exerts inhibitory effects on myocardial fibrosis and epithelial/endothelial‐mesenchymal transformation in a mouse model of myocarditis

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