&lt;p&gt;EFEMP2 Inhibits Breast Cancer Invasion And Metastasis In Vitro And In Vivo&lt;/p&gt;

Kang, Ning; Zhou, Jiyin; Xu, Jia; Zhou, Dongsheng; Shi, Weichen

doi:10.2147/ott.s221219

Cited by 5 publications

(3 citation statements)

References 48 publications

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“…Another report showed that DDR2 mediates stromal and cancer cell interaction in mesenchymal stem cells and metastasis growth in breast cancer (17,18). EFEMP2 significantly inhibits the invasion and metastasis of tumor cells and the process of epithelial-mesenchymal transition (EMT) through the Wnt/bcatenin pathway in lung, bladder, and breast cancers (19)(20)(21). Similarly, ITGBL1 is involved in tumor cell invasion and metastasis through the KRAS/EMT pathway (22).…”

Section: Discussionmentioning

confidence: 99%

A Weighted Gene Co-Expression Network Analysis–Derived Prognostic Model for Predicting Prognosis and Immune Infiltration in Gastric Cancer

et al. 2021

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BackgroundGastric cancer (GC) is a major public health problem worldwide. In recent decades, the treatment of gastric cancer has improved greatly, but basic research and clinical application of gastric cancer remain challenges due to the high heterogeneity. Here, we provide new insights for identifying prognostic models of GC.MethodsWe obtained the gene expression profiles of GSE62254 containing 300 samples for training. GSE15459 and TCGA-STAD for validation, which contain 200 and 375 samples, respectively. Weighted gene co-expression network analysis (WGCNA) was used to identify gene modules. We performed Lasso regression and Cox regression analyses to identify the most significant five genes to develop a novel prognostic model. And we selected two representative genes within the model for immunohistochemistry staining with 105 GC specimens from our hospital to verify the prediction efficiency. Moreover, we estimated the correlation coefficient between our model and immune infiltration using the CIBERSORT algorithm. The data from GSE15459 and TCGA cohort validated the robustness and predictive accuracy of this prognostic model.ResultsOf the 12 gene modules identified, 1,198 green-yellow module genes were selected for further analysis. Multivariate Cox analysis was performed on genes from univariate Cox regression and Lasso regression analysis using the Cox proportional hazards regression model. Finally, we constructed a five gene prognostic model: Risk Score = [(-0.7547) * Expression (ARHGAP32)] + [(-0.8272) * Expression (KLF5)] + [1.09 * Expression (MAMLD1)] + [0.5174 * Expression (MATN3)] + [1.66 * Expression (NES)]. The prognosis of samples in the high-risk group was significantly poorer than that of samples in the low-risk group (p = 6.503e-11). The risk model was also regarded as an independent predictor of prognosis (HR, 1.678, p < 0.001). The observed correlation with immune cells suggested that this risk model could potentially predict immune infiltration.ConclusionThis study identified a potential risk model for prognosis and immune infiltration prediction in GC using WGCNA and Cox regression analysis.

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Section: Discussionmentioning

confidence: 99%

A Weighted Gene Co-Expression Network Analysis–Derived Prognostic Model for Predicting Prognosis and Immune Infiltration in Gastric Cancer

et al. 2021

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“…reported that EFEMP2 increases the invasive ability of cervical cancer cells by promoting EMT via the Raf/MEK/ERK signaling pathway. In contrast, Kang et al 29 . reported that EFEMP2 inhibited breast cancer invasion and metastasis in vitro and in vivo .…”

Section: Discussionmentioning

confidence: 90%

Fibulin‐4 as a potential extracellular vesicle marker of fibrosis in patients with cirrhosis

Kumagai,

Tsuchiya,

Yang

et al. 2024

FEBS Open Bio

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Chronic liver injury leads to decreased liver function and increased fibrosis. Fibrosis is not only associated with the development of portal hypertension and carcinogenesis, but with the occurrence of events and a poor prognosis, highlighting the importance of non‐invasive fibrosis assessment in patients. In the present study, we searched for markers related to liver fibrosis via proteomic analysis of small extracellular vesicles (sEVs). In the discovery cohort, proteomic analysis was carried out in the sEVs extracted from the sera of 5 patients with decompensated cirrhosis, 5 patients with compensated cirrhosis, and 5 controls without liver disease. Interestingly, in this cohort, fibulin‐4 was significantly associated with cirrhosis while in the validation cohort [formed by 191 patients: 7 patients without disease, 16 patients without liver disease (other diseases), 38 patients with chronic liver disease (CLD), 75 patients with cirrhosis of Child–Pugh class A (36 without hepatocellular carcinoma [HCC], 29 with HCC), and 65 patients with cirrhosis of Child–Pugh class B–C (39 without HCC, 26 with HCC)], fibulin‐4/CD9 levels increased with cirrhosis progression. Furthermore, the fibulin‐4/CD9 ratio was significantly higher in patients with varices. Immunostaining also revealed strong fibulin‐4 expression in cholangiocytes within the fibrous areas and mesothelial cells in liver tissue blood vessels. Taken together, our results suggest that fibulin‐4, essential for lysyl oxidase activation, might be a new liver fibrosis marker found in the sEVs of patients with cirrhosis.

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“…Early studies have shown that EFEMP2 is a product of a candidate oncogene, in mutant p53-independent or dependent mutants, it can exhibit its oncogenic activity [7]. In recent years, the expression of EFEMP2 in different types of cancers has been controversial, in that, in cancers, such as breast, lung, and endometrial cancers, EFEMP2 plays a protective role [8][9][10][11][12]. On the contrary, in cancers, such as ovarian cancer, glioma, osteosarcoma, and aneurysm, EFEMP2 is highly expressed, considered a candidate oncogene, and associated with poor prognosis of the tumors [13][14][15][16][17][18].…”

Section: Introductionmentioning

confidence: 99%

EFEMP2 upregulates PD-L1 expression via EGFR/ERK1/2/c-Jun signaling to promote the invasion of ovarian cancer cells

Shen

Jin

Fang³

et al. 2023

Cell Mol Biol Lett

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Background Fibulin-like extracellular matrix protein 2 (EFEMP2) has been reported to be related to the progression of various cancers. We have previously reported that EFEMP2 was highly expressed in ovarian cancer and was strongly associated with poor prognosis in patients. This study intends to further explore its interacting proteins and possible downstream signaling pathways. Method The expression of EFEMP2 was detected by RT-qPCR, ICC and western blot in 4 kinds of ovarian cancer cells with different migration and invasion ability. Cell models with strong or weak EFEMP2 expression were constructed by lentivirus transfection. The effects of the down-regulation and up-regulation of EFEMP2 on the biological behavior of ovarian cancer cells were studied through in-vitro and in-vivo functional tests. The phosphorylation pathway profiling array and KEGG database analyses identified the downstream EGFR/ERK1/2/c-Jun signaling pathway and the programmed death-1 (PD-L1) pathway enrichment. Additionally, the protein interaction between EFEMP2 and EGFR was detected by immunoprecipitation. Result EFEMP2 was positively correlated with the invasion ability of ovarian cancer cells, its down-regulation inhibited the migrative, invasive and cloning capacity of cancer cells in vitro and suppressed the tumor proliferation and intraperitoneal diffusion in vivo, while its up-regulation did the opposite. Moreover, EFEMP2 could bind to EGFR to induce PD-L1 regulation in ovarian cancer, which was caused by the activation of EGFR/ERK1/2/c-Jun signaling. Similar to EFEMP2, PD-L1 was also highly expressed in aggressive cells and had the ability to promote the invasion and metastasis of ovarian cancer cells both in vitro and in vivo, and PD-L1 upregulation was partly caused by EFEMP2 activation. Afatinib combined with trametinib had an obvious effect of inhibiting the intraperitoneal diffusion of ovarian cancer cells, especially in the group with low expression of EFEMP2, while overexpression of PD-L1 could reverse this phenomenon. Conclusion EFEMP2 could bind to EGFR to activate ERK1/2/c-Jun pathway and regulate PD-L1 expression, furthermore PD-L1 was extremely essential for EFEMP2 to promote ovarian cancer cells invasion and dissemination in vitro and in vivo. Targeted therapy against the source gene EFEMP2 is our future research direction, which may better inhibit the invasion and metastasis of ovarian cancer cells.

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<p>EFEMP2 Inhibits Breast Cancer Invasion And Metastasis In Vitro And In Vivo</p>

Cited by 5 publications

References 48 publications

A Weighted Gene Co-Expression Network Analysis–Derived Prognostic Model for Predicting Prognosis and Immune Infiltration in Gastric Cancer

A Weighted Gene Co-Expression Network Analysis–Derived Prognostic Model for Predicting Prognosis and Immune Infiltration in Gastric Cancer

Fibulin‐4 as a potential extracellular vesicle marker of fibrosis in patients with cirrhosis

EFEMP2 upregulates PD-L1 expression via EGFR/ERK1/2/c-Jun signaling to promote the invasion of ovarian cancer cells

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