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Related Concept Videos

Canonical Wnt Signaling Pathway02:54

Canonical Wnt Signaling Pathway

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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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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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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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Role Of Notch Signalling In Intestinal Stem Cell Renewal01:12

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Notch signaling was first discovered in Drosophila melanogaster, where it is involved in cell lineage differentiation. Notch signaling regulates the maintenance and differentiation of intestinal stem cells or ISCs by controlling the expression of atonal homolog 1 or Atoh1. Atoh1 directs cells to differentiate into secretory cells.
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Cadherins in Tissue Organization01:19

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The cadherins are a superfamily of cell adhesion molecules comprising over 180 variants, with specific tissues expressing a particular combination of cadherin types. Cadherins generally exhibit homophilic binding; i.e., cadherins on one cell bind to cadherins of the same or closely related type on another cell. Thus, cells of the same type have a specific affinity to bind to each other and sort themselves into clusters to form tissues.
Cell Sorting During Development
Cell sorting plays an...
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Erythropoietin-producing hepatocellular carcinoma receptor (Eph) and its ligand, Eph receptor-interacting protein (Ephrin) were first discovered in the human carcinoma cell line, hence the name. Ephrin-Eph interaction guides cells to reach their appropriate location in adult tissues. They also play an essential role in the immune system by helping in immune cell migration, adhesion, and activation. Based on their structure and function, Eph is divided into two classes — EphA and EphB.
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The Soft Agar Colony Formation Assay
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An SETD1A/Wnt/β-catenin feedback loop promotes NSCLC development.

Rui Wang1, Jian Liu1,2, Kai Li1

  • 1Department of Thoracic Surgery, the First Affiliated Hospital of Xi'an Jiaotong University, 277 Yanta West Road, Xi'an, Shaanxi, 710061, P.R. China.

Journal of Experimental & Clinical Cancer Research : CR
|October 14, 2021
PubMed
Summary

SETD1A promotes non-small cell lung cancer (NSCLC) progression by enhancing cancer stem cell properties and reducing cisplatin sensitivity. This occurs through a positive feedback loop involving the Wnt/β-catenin pathway, NEAT1, and EZH2.

Keywords:
EZH2NEAT1NSCLCSETD1Aβ-Catenin

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Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • SETD1A, a H3K4 methyltransferase, is implicated in various cancers.
  • Its specific role in non-small cell lung cancer (NSCLC) pathogenesis is not well understood.

Purpose of the Study:

  • To elucidate the biological function and molecular mechanism of SETD1A in NSCLC.
  • To investigate the relationship between SETD1A and the Wnt/β-catenin pathway in NSCLC.

Main Methods:

  • Quantitative real-time PCR, immunohistochemistry, and western blotting to assess gene and protein expression.
  • Chromatin immunoprecipitation, co-immunoprecipitation, and luciferase reporter assays to determine regulatory mechanisms.
  • Sphere formation, CCK-8, colony formation, and xenograft models to evaluate cellular functions and tumorigenesis.

Main Results:

  • SETD1A overexpression is significantly increased in NSCLC and correlates with poor patient prognosis.
  • SETD1A promotes cancer stem cell characteristics and decreases cisplatin sensitivity via the Wnt/β-catenin pathway.
  • SETD1A interacts with and stabilizes β-catenin, upregulates NEAT1 and EZH2, and forms a positive feedback loop with the Wnt/β-catenin pathway.

Conclusions:

  • SETD1A and the Wnt/β-catenin pathway form a positive feedback loop that drives NSCLC progression.
  • Targeting SETD1A may offer a therapeutic strategy for NSCLC.