EMP1 regulates cell proliferation, migration, and stemness in gliomas through PI3K‐AKT signaling and CD44

Wang, Junxiang; Li, Xuetao; Wu, Haibin; Wang, Hao; Lin, Yu; Deng, Zhitong

doi:10.1002/jcb.28974

Cited by 33 publications

(24 citation statements)

References 22 publications

(52 reference statements)

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“…11 Studies have shown that EMP1 plays a crucial part in cell adhesion, proliferation, apoptosis, differentiation, tumor formation and metastasis. 12,13 Li et al found that in glioblastoma, highly expressed EMP1 promotes tumor cell proliferation, invasion and metastasis by activating PI3K/AKT/mTOR signaling pathway. 14 Ogita et al found that EMP1 binding with copine-III promoted the expression of Src, Vav2 and Rac1 in prostate cancer, leading to enhanced migration and metastasis of prostate cancer cells, indicating that EMP1 may take a part in the positive regulation of metastasis.…”

Section: Introductionmentioning

confidence: 99%

<p>EMP1 Promotes the Proliferation and Invasion of Ovarian Cancer Cells Through Activating the MAPK Pathway</p>

Liu¹,

Ding²,

Nie³

et al. 2020

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Introduction: Epithelial membrane protein 1 (EMP1), a member of the EMP family, is overexpressed in a large number of tumors and is thought to be a cellular connexin on the cell membrane and is involved in proliferation, invasion, metastasis of tumor cells, and epithelial-mesenchymal transition (EMT). Nevertheless, its biomedical function in ovarian cancer is still unclear. Methods: EMP1 was detected in ovarian cancer cell lines by whole transcriptome resequencing. The mRNA of EMP1 was examined by qRT-PCR. The relationship between expression of EMP1 and clinical classification, metastasis, and shortened survival time in ovarian cancer specimens was analysed by immunohistochemical (IHC). The mechanism of EMP1 enhanced proliferation and invasion of ovarian cancer cells was determined by siRNA interference, colony formation, migration and invasion experiments, and Western blot. Results: EMP1 was up-regulated in ovarian cancer cell lines and ovarian cancer tissues in comparison with non-cancerous ovarian specimens. High expression of EMP1 in ovarian cancer specimens was obviously related to high clinical classification, metastasis, and shortened survival time. High expressed EMP1 facilitates cell proliferation, invasion and EMT in ovarian cancer cells. Over-expressed EMP1 increased the protein levels of RAS/ RAF/MAPK/c-JUN. Conclusion: Over-expressed EMP1 in ovarian cancer promotes tumor cell proliferation, invasion, and EMT by the MAPK signaling pathway.

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Section: Introductionmentioning

confidence: 99%

<p>EMP1 Promotes the Proliferation and Invasion of Ovarian Cancer Cells Through Activating the MAPK Pathway</p>

Liu¹,

Ding²,

Nie³

et al. 2020

OTT

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“…It has been demonstrated that EMP1 mediates PRD resistance induced by the interaction of leukemic cells with mesenchymal stem cells (16). EMP1 is upregulated in glioblastoma multiforme and its inhibition decreases proliferation and invasiveness of tumor (28)(29)(30). In contrast, in carcinoma of the nasopharynx, stomach, breast, urothelium, and prostate, EMP1 reduces cell migration and invasion and increases apoptosis and caspase-9 expression (27,(31)(32)(33)(34).…”

Section: Discussionmentioning

confidence: 99%

Prognostic Relevance of Expression of EMP1, CASP1, and NLRP3 Genes in Pediatric B-Lineage Acute Lymphoblastic Leukemia

et al. 2021

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Glucocorticoid (GC), such as prednisolone, is an essential component of multidrug chemotherapy regimen for pediatric acute lymphoblastic leukemia (ALL). Resistance to GC in leukemia cells is associated with disease progression and poor prognosis. Despite the extensive use of GC for many years, molecular mechanisms underlying its resistance in ALL have not been fully uncovered. Recent studies have shown a potential role of EMP1, CASP1, and NLRP3 genes in prednisolone response. In this study on 148 pediatric B-ALL patients, we studied these three genes to assess their association with prednisolone response measured by day 8 blast count after 7 days of induction therapy with prednisolone. Intriguingly, ALL samples exhibited higher expression of EMP1 along with a low expression of CASP1 and NLRP3 compared to disease free normal bone marrow collected from patients with solid tumors. Among the three analyzed genes, only EMP1 was found to be overexpressed in prednisolone poor responders (p=0.015). Further, a comparison of gene expression between cytogenetic subtypes revealed higher expression of EMP1 in BCR-ABL subtype. Expression of EMP1 in multiple gene expression datasets was used for gene set enrichment analysis, which revealed TNF-α, IL-2-STAT5 signaling, inflammatory responses and hypoxia as the major positively associated pathways and E2F targets as negatively associated pathways. Interestingly, the clinical remission rate was higher in CASP1 high patients (p=0.048). In univariate survival analysis, higher EMP1 expression was associated with poor prognostic measures while higher expression of NLRP3 and CASP1 was associated with better prognostic measures in our data. Further, multivariate analysis revealed an independent association of high CASP1 and NLRP3 with a better prognosis. This study strengthens the available evidence that mRNA expression of EMP1, CASP1, and NLRP3 may serve as potential biomarkers for risk stratification of pediatric B-ALL patients.

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“…EMP1 belongs to the peripheral myelin protein 22-kDa (PMP22) gene family. It promotes glioblastoma progression through the PI3K/AKT/mTOR signaling pathway 6 , and the unusual expression of EMP1 has been revealed in most tumor types 12 . TPM1 gene is a member of a tumor-associated protein family (the tropomyosin family) -it plays an important role in tumor-specific variations of actin filament aggregation via stress fiber modulation and actin cytoskeleton modification 7 .…”

Section: Discussionmentioning

confidence: 99%

The prognostic value of six survival-related genes in bladder cancer

et al. 2020

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This study was conducted to identify genes that are differentially expressed in paracancerous tissue and to determine the potential predictive value of selected gene panel. Gene transcriptome data of bladder tissue was downloaded from UCSC Xena browser and NCBI GEO repository, including GTEx (the Genotype-Tissue Expression project) data, TCGA (The Cancer Genome Atlas) data, and GEO (Gene Expression Omnibus) data. Differentially Expressed Genes (DEGs) analysis was performed to identify tumor-DEGs candidate genes, using the intersection of tumorparacancerous DEGs genes and paracancerous-normal DEGs genes. The survival-related genes were screened by Kaplan-Meier (KM) survival analysis and univariable Cox regression with the cutoff criteria of KM < 0.05 and cox pvalue < 0.05. The risk model was developed using Lasso regression. The clinical data were analyzed by univariate and multivariate Cox regression analysis. Gene Ontology (GO) and KEGG enrichment analysis were performed in the DEGs genes between the high-risk and low-risk subgroups. We identified six survival-related genes, EMP1, TPM1, NRP2, FGFR1, CAVIN1, and LATS2, found in the DEG analyses of both, tumor-paracancerous and paracancerous-normal differentially expressed data sets. Then, the patients were classified into two clusters, which can be distinguished by specific clinical characteristics. A three-gene risk prediction model (EMP1, FGFR1, and CAVIN1) was constructed in patients within cluster 1. The model was applied to categorize cluster 1 patients into high-risk and low-risk subgroups. The prognostic risk score was considered as an independent prognostic factor. The six identified survival-related genes can be used in molecular characterization of a specific subtype of bladder cancer. This subtype had distinct clinical features of T (topography), N (lymph node), stage, grade, and survival status, compared to the other subtype of bladder cancer. Among the six identified survival-related genes, three-genes, EMP1, FGFR1, and CAVIN1, were identified as potential independent prognostic markers for the specific bladder cancer subtype with clinical features described.

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EMP1 regulates cell proliferation, migration, and stemness in gliomas through PI3K‐AKT signaling and CD44

Cited by 33 publications

References 22 publications

<p>EMP1 Promotes the Proliferation and Invasion of Ovarian Cancer Cells Through Activating the MAPK Pathway</p>

<p>EMP1 Promotes the Proliferation and Invasion of Ovarian Cancer Cells Through Activating the MAPK Pathway</p>

Prognostic Relevance of Expression of EMP1, CASP1, and NLRP3 Genes in Pediatric B-Lineage Acute Lymphoblastic Leukemia

The prognostic value of six survival-related genes in bladder cancer

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