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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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			Action	DRS
	SRR31488510_1.fastq.gz	Fastqsanger.gz
	SRR31488510_2.fastq.gz	Fastqsanger.gz
	SRR31488511_1.fastq.gz	Fastqsanger.gz
	SRR31488511_2.fastq.gz	Fastqsanger.gz
	SRR31488512_1.fastq.gz	Fastqsanger.gz

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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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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

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Lactate influx promotes immunoevasion in pancreatic cancer by activating autophagy of pancreatic stellate cells

Project description:It has been reported that lactate plays as a bridging signaling molecule to coordinates tumor cell and tumor stroma. As pancreatic stellate cells (PSC) is the most majority and functional cells in tumor microenvironment (TME) of pancreatic cancer (PC), whether the lactate involving the crosstalk between PSC and pancreatic acinar cells (PACs) in tumorigenesis of PC has not been defined. The present study showed that lactate transporter, monocarboxylate transporter 1 (MCT1) was predominantly expressed in pancreatic stellate cells (PSC), and correlates with worse prognosis in PC patients. Moreover, we revealed lactate induced autophagy-mediated activation of PSC, while knockout MCT1 in PSC (PSC-MCT1-/- mice) obviously inhibited the proliferation and metastasis of PC in vivo. Meanwhile, results of single-cell sequence demonstrated that the PD-1 expression in CD8+T cells was dramatically increased. Mechanistically, the MCT1-mediated influx of lactate activated PSC by inducing lactylation of lysine residues K356 and K781 on Vps34, a key regulator for autophagy. Moreover, the PSC-derived CXCL9/CXCL10 upregulated PD-1 expression via activating CXCR3/STAT3 pathway in CD8+ T. Consistently, the growth of pancreatic tumor in situ was significantly inhibited in mice treated with MCT1 inhibitor AZD3965, which was further suppressed by combination with PD-1 antibody. In conclusion, our study implicates lactate functions as TME transducer mediating activation of PSC and formation of immunosuppressive TME, and indicates the synergistic effect of targeting PSC activation in immune checkpoint therapy in PC.

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