RBMS3 Inhibits the Proliferation and Metastasis of Breast Cancer Cells

Yang, Yuan; Quan, Lingli; Ye, Ling

doi:10.3727/096504017x14871200709504

Cited by 30 publications

(32 citation statements)

References 21 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Similarly, upregulation of MSI2 is an indicator of increased metastatic potential in lung cancer (Kudinov et al 2016) and hepatocellular carcinoma (Kudinov et al 2016), and is proposed to stimulate EMT through stimulation of canonical Wnt signaling . RBMS3 has been shown to reduce EMT and metastatic capacity of lung cancer cells (Liang et al 2015) and reduces EMT in gastric cancer cells through suppression of canonical Wnt signaling (Yang et al 2018). Taken together, these results suggest that the Wnt subnetwork we identified here may mediate cellular transdifferentiation in the SSc lung through regulation of Wnt signaling.…”

Section: Discussionsupporting

confidence: 54%

See 1 more Smart Citation

Genetic Interactions Affect Lung Function in Patients with Systemic Sclerosis

Tyler

Mahoney

Carter

2020

G3 Genes|Genomes|Genetics

View full text Add to dashboard Cite

Scleroderma, or systemic sclerosis (SSc), is an autoimmune disease characterized by progressive fibrosis of the skin and internal organs. The most common cause of death in people with SSc is lung disease, but the pathogenesis of lung disease in SSc is insufficiently understood to devise specific treatment strategies. Developing targeted treatments requires not only the identification of molecular processes involved in SSc-associated lung disease, but also understanding of how these processes interact to drive pathology. One potentially powerful approach is to identify alleles that interact genetically to influence lung outcomes in patients with SSc. Analysis of interactions, rather than individual allele effects, has the potential to delineate molecular interactions that are important in SSc-related lung pathology. However, detecting genetic interactions, or epistasis, in human cohorts is challenging. Large numbers of variants with low minor allele frequencies, paired with heterogeneous disease presentation, reduce power to detect epistasis. Here we present an analysis that increases power to detect epistasis in human genome-wide association studies (GWAS). We tested for genetic interactions influencing lung function and autoantibody status in a cohort of 416 SSc patients. Using Matrix Epistasis to filter SNPs followed by the Combined Analysis of Pleiotropy and Epistasis (CAPE), we identified a network of interacting alleles influencing lung function in patients with SSc. In particular, we identified a three-gene network comprising WNT5A, RBMS3, and MSI2, which in combination influenced multiple pulmonary pathology measures. The associations of these genes with lung outcomes in SSc are novel and high-confidence. Furthermore, gene coexpression analysis suggested that the interactions we identified are tissue-specific, thus differentiating SSc-related pathogenic processes in lung from those in skin.

show abstract

Section: Discussionsupporting

confidence: 54%

“…Like WNT5A, RBMS3 has been linked to transdifferentiation. Upregulation of RBMS3 inhibits EMT in lung cancer through the inhibition of canonical Wnt signaling (Yang et al 2018;Liang et al 2015). By downregulating MMP2 and b-catenin, RBMS3 also inhibits microvessel formation (Chen et al 2012).…”

Section: Discussionmentioning

confidence: 99%

Genetic Interactions Affect Lung Function in Patients with Systemic Sclerosis

Tyler

Mahoney

Carter

2020

G3 Genes|Genomes|Genetics

View full text Add to dashboard Cite

show abstract

“…Similar, Wnt/β-Catenin has also been reported as a pivotal regulator of tumor cells metastasis [33-35]. Thus, to further explore the molecular mechanism via which BRI3 modulated BON1 cells, we monitored the protein levels of main factors in p38/ ERK/AKT and Wnt/β-Catenin signaling pathways in response to the BRI3 silence and BRI3 overexpression.…”

Section: Discussionmentioning

confidence: 99%

MEG3 Suppresses Human Pancreatic Neuroendocrine Tumor Cells Growth and Metastasis by Down-Regulation of Mir-183

Zhang

Feng

2017

Cell Physiol Biochem

View full text Add to dashboard Cite

Background/Aims: Pancreatic neuroendocrine tumors (pNETs) are rare neoplasms which arise from pancreatic islet cells. Recently, lncRNA MEG3 has been reported as a tumor suppressor in variety cancers. This study aimed to reveal the functional effects of MEG3 on pNETs which has not been uncovered previously. Methods: The expression of MEG3, miR-183, and BRI3 in BON1 cells were altered by transfection with their specific vectors/shRNA, or mimic/inhibitor. Thereafter, cell viability, apoptosis, the protein expressions of cell cycle related factors, and apoptosis associated factors, as well as cell migration and invasion were respectively assessed by typan blue staining, flow cytometry, western blotting, and transwell assay. Results: MEG3 was low expressed in BON1 and QGP-1 cells, when compared to three normal cell lines (HEK293, CCL-153, and EC-304). MEG3 overexpression decreased BON1 cells viability, invasion, migration, but significantly induced apoptosis. miR-183 was a direct target of MEG3, and miR-183 up-regulation abolished the anti-growth and anti-metastasis effects of MEG3 overexpression on BON1 cells. Moreover, BRI3 was a target of miR-183, and BRI3 exhibited a tumor-promoting role possibly via activation of p38/ERK/AKT and Wnt/β-Catenin signaling in BON1 cells. Conclusion: This study demonstrated a tumor suppressive effect of MEG3 in BON1 cells that suppresses tumor cells growth and metastasis. A novel regulatory mechanism has been revealed that modulation of MEG3/miR-183/BRI3 axis may be pivotal in pNET.

show abstract

“…Like WNT5A, RBMS3 has been linked to transdifferentiation. Upregulation of 250 RBMS3 inhibits EMT in lung cancer through the inhibition of canonical Wnt 251 signaling [62,63]. By downregulating MMP2 and β-catenin, RBMS3 also inhibits 252 microvessel formation [64].…”

mentioning

confidence: 99%

“…Similarly, 276 upregulation of MSI2 is an indicator of increased metastatic potential in lung 277 cancer [71] and hepatocellular carcinoma [71], and is proposed to stimulate EMT 278 through stimulation of canonical Wnt signaling [72]. RBMS3 has been shown to reduce 279 EMT and metastatic capacity of lung cancer cells [63] and reduces EMT in gastric 280 cancer cells through suppression of canonical Wnt signaling [62]. Taken together, these 281 results suggest that the Wnt subnetwork we identified here may mediate cellular 282 transdifferentiation in the SSc lung through regulation of Wnt signaling.…”

mentioning

confidence: 99%