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Related Concept Videos

Catenins01:23

Catenins

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Catenins are characterized by multiple binding domains and dynamic structures that allow them to function as linker proteins in cell junction complexes. All catenins, except α-catenin, contain a characteristic protein sequence called the armadillo repeat and are therefore also called armadillo proteins.
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The gene encoding the main signaling molecules of the Wnt signaling pathways (the Wnt proteins) was discovered almost four decades ago by Nüsslein-Volhard and Wieschaus. They identified and originally named the gene "wingless" (wg) after a phenotype discovered during their landmark genetic screen in Drosophila for body pattern defects. At around the same time, another researcher named Harold Varmus found that a murine tumor virus activates the mammalian wg homolog, Int-1, which...
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Invadosome is a broad category of cell surface structures with proteolytic activity that  degrades the extracellular matrix (ECM). Invadosomes are present in normal cell types, including macrophages, endothelial cells, and neurons, as well as tumor cells. Although the macrophage podosomes and tumor cell invadopodia are classified as invadosomes, they have different structures, molecular pathways, and functions. Podosomes are short structures that last for a few minutes. However,...
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Wnt is a zygotic effect gene that is expressed during very early embryonic development. It regulates various processes in animals starting from early development through the adult stage, such as organogenesis in the embryo and maintenance of neuronal and blood stem cells. Wnt proteins can induce a wide variety of intracellular pathways depending upon the specific abilities of different Wnt ligands to form a complex with shared and cognate receptors in the presence of different co-receptors. The...
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Metastasis02:30

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Metastasis is the spread of cancer cells from the original site to distant locations in the body. Cancer cells can spread via blood vessels (hematogenous) as well as lymph vessels in the body.
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The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
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  1. Home
  3. Β-catenin Mediated Tam Phenotype Promotes Pancreatic Cancer Metastasis Via The Osm/stat3/loxl2 Axis.
  1. Home
  3. Β-catenin Mediated Tam Phenotype Promotes Pancreatic Cancer Metastasis Via The Osm/stat3/loxl2 Axis.

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The Soft Agar Colony Formation Assay
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β-Catenin mediated TAM phenotype promotes pancreatic cancer metastasis via the OSM/STAT3/LOXL2 axis.

Yijia Zhang1, Xinya Zhu2, Liyuan Chen2

  • 1Department of Pharmacology, Shenyang Pharmaceutical University, Shenyang, Liaoning 110016, PR China; Department of Pharmacology, Taizhou University, Taizhou, Zhejiang 318000, PR China.

Neoplasia (New York, N.Y.)
|December 31, 2024

View abstract on PubMed

Summary
This summary is machine-generated.

Tumor-associated macrophages (TAMs) drive pancreatic cancer (PDAC) progression via a novel β-catenin/OSM-STAT3/LOXL2 pathway. This axis regulates TAMs and promotes PDAC cell invasion and metastasis, offering new therapeutic targets.

Keywords:
Epithelial-mesenchymal transitionOncostatin MPancreatic ductal adenocarcinomaTumor-associated macrophagesβ-catenin

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Skeletal Phenotype Analysis of a Conditional Stat3 Deletion Mouse Model
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Related Experiment Videos

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Skeletal Phenotype Analysis of a Conditional Stat3 Deletion Mouse Model
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Skeletal Phenotype Analysis of a Conditional Stat3 Deletion Mouse Model

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Area of Science:

  • Oncology
  • Immunology
  • Molecular Biology

Background:

  • Pancreatic ductal adenocarcinoma (PDAC) has a poor prognosis due to its complex tumor microenvironment.
  • Tumor-associated macrophages (TAMs) are key players in PDAC progression, but the mechanisms are not fully understood.
  • The role of β-catenin signaling in regulating TAM phenotype and function in PDAC requires further investigation.

Purpose of the Study:

  • To elucidate the molecular mechanisms by which TAMs promote PDAC progression, focusing on β-catenin signaling.
  • To investigate the expression patterns of OSM and LOXL2 in PDAC and their correlation with patient survival.
  • To identify novel signaling pathways involved in TAM-mediated PDAC progression.

Main Methods:

  • Analysis of RNA-seq and single-cell RNA-seq (scRNA-seq) datasets.
  • In vitro studies using THP-1-derived macrophages and PDAC cell co-cultures.
  • In vivo studies using a Panc02 lung metastasis model.
  • Pharmacological and genetic inhibition of β-catenin, OSM, and STAT3 signaling.

    • Main Results:

    • Elevated OSM and LOXL2 expression in PDAC correlated with poor patient survival.
    • β-catenin signaling was uniquely activated in TAMs, regulating their polarization and OSM expression.
    • TAM-derived OSM promoted PDAC cell migration, invasion, and lung metastasis, enhancing mesenchymal transition and stemness.
    • A novel β-catenin/OSM-STAT3/LOXL2 signaling axis was identified, mediating TAM-induced PDAC progression.

    Conclusions:

    • β-catenin signaling in TAMs drives PDAC progression through OSM and LOXL2.
    • The identified signaling axis represents a potential therapeutic target for PDAC.
    • Understanding this pathway offers new insights into the interplay between TAMs and PDAC cells.