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SERPINB3 induces the aggressive basal-like/squamous subtype and promotes invasion and metastasis in pancreatic cancer

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE223909 | GEO | 2023/10/12

REPOSITORIES: GEO

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SERPINB3 induces the aggressive basal-like/squamous subtype and promotes invasion and metastasis in pancreatic cancer II

Project description:Pancreatic cancer is a heterogenous disease and consists of distinct subtypes. Here, we searched for candidate driver genes of the basal-like/squamous subtype, a more aggressive molecular subtype of pancreatic ductal adenocarcinoma (PDAC). Through an integrated transcriptome analysis, we identified the serine/cysteine protease inhibitor, SERPINB3 (squamous cell carcinoma antigen 1, SCCA1), as being upregulated in the basal-like/squamous PDAC using a discovery and validation approach. SERPINB3 upregulation associated with decreased patient survival and a transcriptome profile indicative of the basal-like/squamous subtype. The goal of this study was aimed to identify SERPINB3 induced molecular signatures in PDAC.

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SERPINB3 induces the aggressive basal-like/squamous subtype and promotes invasion and metastasis in pancreatic cancer III

2023-10-12 | GSE224564 | GEO

SERPINB3 induces the aggressive basal-like/squamous subtype and promotes invasion and metastasis in pancreatic cancer I

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SERPINB3 induces the aggressive basal-like/squamous subtype and promotes invasion and metastasis in pancreatic cancer

Project description:SERPINB3 induces the aggressive basal-like/squamous subtype and promotes invasion and metastasis in pancreatic cancer

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SERPINB3 induces the aggressive basal-like/squamous subtype and promotes invasion and metastasis in pancreatic cancer I

Project description:SERPINB3 induces the aggressive basal-like/squamous subtype and promotes invasion and metastasis in pancreatic cancer I

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SERPINB3 induces the aggressive basal-like/squamous subtype and promotes invasion and metastasis in pancreatic cancer II

Project description:SERPINB3 induces the aggressive basal-like/squamous subtype and promotes invasion and metastasis in pancreatic cancer II

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SERPINB3 induces the aggressive basal-like/squamous subtype and promotes invasion and metastasis in pancreatic cancer III

Project description:SERPINB3 induces the aggressive basal-like/squamous subtype and promotes invasion and metastasis in pancreatic cancer III

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SERPINB3-MYC axis induces the basal-like/squamous subtype and enhances disease progression in pancreatic cancer.

Project description:Pancreatic ductal adenocarcinoma (PDAC) exhibits distinct molecular subtypes: classical/progenitor and basal-like/squamous. Our study aimed to identify genes contributing to the development of the basal-like/squamous subtype, known for its aggressiveness. Transcriptome analyses revealed consistent upregulation of SERPINB3 in basal-like/squamous PDAC, correlating with reduced patient survival. SERPINB3 transgene expression in PDAC cells enhanced in vitro invasion and promoted lung metastasis in a mouse PDAC xenograft model. Metabolome analyses unveiled a metabolic signature linked to both SERPINB3 and the basal-like/squamous subtype, characterized by heightened carnitine/acylcarnitine and amino acid metabolism, associated with poor prognosis in patients with PDAC and elevated cellular invasiveness. Further analysis uncovered that SERPINB3 inhibited the cysteine protease calpain, a key enzyme in the MYC degradation pathway, and drove basal-like/squamous subtype and associated metabolic reprogramming through MYC activation. Our findings indicate that the SERPINB3-MYC axis induces the basal-like/squamous subtype, proposing SERPINB3 as a potential diagnostic and therapeutic target for this variant.

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Tumor microbiome contributes to an aggressive phenotype in the basal-like subtype of pancreatic cancer.

Project description:Despite the uniform mortality in pancreatic adenocarcinoma (PDAC), clinical disease heterogeneity exists with limited genomic differences. A highly aggressive tumor subtype termed 'basal-like' was identified to show worse outcomes and higher inflammatory responses. Here, we focus on the microbial effect in PDAC progression and present a comprehensive analysis of the tumor microbiome in different PDAC subtypes with resectable tumors using metagenomic sequencing. We found distinctive microbial communities in basal-like tumors and identified an increasing abundance of Acinetobacter, Pseudomonas and Sphingopyxis to be highly associated with carcinogenesis. Functional characterization of microbial genes suggested the potential to induce pathogen-related inflammation. Host-microbiota interplay analysis provided new insights into the tumorigenic role of specific microbiome compositions and demonstrated the influence of host genetics in shaping the tumor microbiome. Taken together, these findings indicated that the tumor microbiome is closely related to PDAC oncogenesis and the induction of inflammation. Additionally, our data revealed the microbial basis of PDAC heterogeneity and proved the predictive value of the microbiome, which will contribute to the intervention and treatment of disease.

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Project description:Pancreatic cancer is an aggressive disease with dismal prognosis. It is of paramount importance to understand the underlying etiological mechanisms and identify novel, consistent, and easy-to-apply prognostic factors for precision therapy. TUSC3 (tumor suppressor candidate 3) was identified as a potential tumor suppressor gene and previous study showed TUSC3 is decreased in pancreatic cancer at mRNA level, but its putative tumor suppressor function remains to be verified. In this study, TUSC3 expression was found to be suppressed both at mRNA and protein levels in cell line models as well as in clinical samples; decreased TUSC3 expression was associated with higher pathological TNM staging and poorer outcome. In three pairs of cell lines with different NF-?B activity, TUSC3 expression was found to be reversely correlated with NF-?B activity. TUSC3-silenced pancreatic cancer cell line exhibited enhanced potential of proliferation, migration and invasion. In an orthotopic implanted mice model, TUSC3 silenced cells exhibited more aggressive phenotype with more liver metastasis. In conclusion, the current study shows that decreased immunological TUSC3 staining is a factor prognostic of poor survival in pancreatic cancer patients and decreased TUSC3 promotes pancreatic cancer cell proliferation, invasion and metastasis. The reverse correlation between NF-?B activity and TUSC3 expression may suggest a novel regulation pattern for this molecule.

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