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REG3A promotes the development of pancreatic cancer by activating EGFR pathway

ABSTRACT: REG3A promotes the development of pancreatic cancer by activating EGFR pathway

PROVIDER: PRJNA1190379 | ENA |

REPOSITORIES: ENA

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REG3A promotes the development of pancreatic cancer by activating EGFR pathway

Project description:REG3A is highly expressed in pancreatic tissues, but its significance is unclear. We found that REG3A overexpressed in paracancerous acinar cells interacted with EGFR on tumor cells to stimulate downstream tumor growth signals and promote the occurrence and development of tumors

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RNA-Seq of flow-sorted Egfr WT or Egfr KO pancreatic stellate cells (PSCs) and flow-sorted pancreatic tumor organoids following co-culture.

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TMPRSS4 promotes cell proliferation and inhibits apoptosis in pancreatic ductal adenocarcinoma by activating ERK1/2 signaling pathway

Project description:Transmembrane protease serine 4 (TMPRSS4) is upregulated in various kinds of human cancers, including pancreatic cancer. However, its biological function in pancreatic ductal adenocarcinoma (PDAC) remains unclear. In the current study, real-time qPCR, immunohistochemical staining, Western blotting, and database (Cancer Genome Atlas and Gene Expression) analysis revealed remarkable overexpression of TMPRSS4 in PDAC tissue as compared to non-tumor tissue. The TMPRSS4 overexpression was associated with poor prognosis of PDAC patients. Moreover, multivariate analysis revealed that TMPRSS4 serves as an independent risk factor in PDAC. We performed gain-and loss-of-function analysis and found that TMPRSS4 promotes cellular proliferation and inhibits apoptosis of PDAC cells both in vitro and in vivo. Furthermore, we showed that TMPRSS4 might promote cell proliferation and inhibit apoptosis through activating ERK1/2 signaling pathway in pancreatic cancer cells. These findings were validated by using ERK1/2 phosphorylation inhibitor SCH772984 both in vitro and in vivo. Taken together, this study suggests that TMPRSS4 is a proto-oncogene, which promotes initiation and progression of PDAC by controlling cell proliferation and apoptosis. Our findings indicate that TMPRSS4 could be a promising prognostic biomarker and a therapeutic target for the treatment of pancreatic cancer.

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TMPRSS4 promotes cell proliferation and inhibits apoptosis in pancreatic ductal adenocarcinoma by activating ERK1/2 signaling pathway

Project description:TMPRSS4 promotes cell proliferation and inhibits apoptosis in pancreatic ductal adenocarcinoma by activating ERK1/2 signaling pathway

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Fibromodulin FMOD promotes oral squamous cell carcinoma via activating EGFR signaling axis

Project description:Fibromodulin FMOD promotes oral squamous cell carcinoma via activating EGFR signaling axis

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EGFR and MEK pathway signature RNA-Seq datasets

Project description:EGFR and MEK pathways were activated alone or in combination in human mammary epithelial cells. We profiled the pathway gene expression signatures using RNA-Seq. mRNA was extracted from human mammary epithelial cells overexpressing EGFR gene, MEK gene, or EGFR and MEK genes in combination (or GFP control) for RNA-Seq analysis. Experiment was performed in six replicates per condition.

2015-03-05 | E-GEOD-59765 | biostudies-arrayexpress

EGFR pathway expression persists in recurrent glioblastoma independent of amplification status

Project description:Background: Glioblastoma mortality is driven by tumour progression or recurrence despite administering a therapeutic arsenal consisting of surgical resection, radiation, and alkylating chemotherapy. The genetic changes underlying tumour progression and chemotherapy resistance are poorly understood. Methods: In this work, we sought to define the relationship between EGFR amplification status, EGFR mRNA expression, and EGFR pathway activity. We compared RNA-sequencing data from matched primary and recurrent tumour samples (N = 40 patients, 20 with EGFR amplification). Results: In the setting of glioblastoma recurrence, the EGFR pathway was overexpressed regardless of EGFR amplification status, suggesting a common genomic endpoint in recurrent glioblastoma, although EGFR amplification did associate with higher EGFR mRNA expression. Three of forty patients in the study cohort had EGFR-amplified tumours and received targeted EGFR therapy. Their molecular subtypes and clinical outcomes did not significantly differ from patients who received conventional chemotherapy. Conclusion: Our findings suggest that while the EGFR amplification may confer a unique molecular profile in primary glioblastoma, pathway analysis reveals upregulation of the EGFR pathway in recurrence, regardless of amplification status. As such, the EGFR pathway may be a key mediator of glioblastoma progression.

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