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The Notch signaling pathway is a major intracellular signaling pathway that is highly conserved over a broad spectrum of metazoan species. It stands unique from other intracellular signaling mechanisms in animals because notch protein itself acts as the receptor as well as the primary signaling molecule.
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The Hedgehog gene (Hh) was first discovered due to its control of the growth of disorganized, hair-like bristles phenotype in Drosophila, much like hedgehog spines. Hh plays a crucial role in the development of organs and the maintenance of homeostasis in both invertebrates and vertebrates. However, while Drosophila has only one Hh protein, mammals have multiple functional Hedgehog proteins - Sonic (Shh), Desert (Dhh), and Indian Hedgehog (Ihh). All of these homologous proteins have adapted to...
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Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
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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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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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The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
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Updated: Jan 30, 2026

Mouse Fetal Whole Intestine Culture System for Ex Vivo Manipulation of Signaling Pathways and Three-dimensional Live Imaging of Villus Development
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DHCR7 drives AML development through the IL6/JAK2/STAT3 signalling pathway.

Xu Dai1, Zhaoxing Wu2, Wenjing Zhang3

  • 1Department of Laboratory Medicine, The First Affiliated Hospital of Shihezi University, Shihezi, Xinjiang, China.

British Journal of Haematology
|January 29, 2026
PubMed
Summary

Targeting 7-dehydrocholesterol reductase (DHCR7) inhibits acute myeloid leukaemia (AML) cell growth by disrupting cholesterol metabolism and activating cell death pathways. This finding highlights DHCR7 as a potential therapeutic target for AML treatment.

Keywords:
DHCR77‐DHCAMLIL6/JAK2/STAT3tamoxifen

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Area of Science:

  • Biochemistry
  • Oncology
  • Hematology

Background:

  • Acute myeloid leukaemia (AML) is a complex blood cancer characterized by uncontrolled myeloid cell growth.
  • The role of 7-dehydrocholesterol reductase (DHCR7), an enzyme in cholesterol synthesis, in AML is not fully understood.
  • DHCR7 is implicated as an oncoprotein in various cancers.

Purpose of the Study:

  • To investigate the biological role and therapeutic potential of DHCR7 in acute myeloid leukaemia.
  • To elucidate the mechanisms by which DHCR7 influences AML pathogenesis.

Main Methods:

  • In vitro functional assays involving DHCR7 knockdown and tamoxifen treatment in AML cells.
  • In vivo studies using NSG mouse models of AML.
  • Analysis of intracellular cholesterol levels, 7-dehydrocholesterol (7-DHC) accumulation, endoplasmic reticulum stress, apoptosis, and IL-6/JAK2/STAT3 signaling.

Main Results:

  • DHCR7 inhibition (via knockdown or tamoxifen) suppressed AML cell proliferation, reduced cholesterol, increased 7-DHC, induced endoplasmic reticulum stress, and triggered apoptosis.
  • In vivo, DHCR7 inhibition markedly reduced leukaemia progression in mouse models.
  • DHCR7 promotes leukaemia by activating the IL-6/JAK2/STAT3 signaling pathway.

Conclusions:

  • DHCR7 plays a significant pro-leukaemic role in AML pathogenesis.
  • Targeting DHCR7 offers a promising therapeutic strategy for acute myeloid leukaemia.