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Stimulation of Notch Signaling in Mouse Osteoclast Precursors
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Notch signals modulate lgl mediated tumorigenesis by the activation of JNK signaling

Maimuna Sali Paul1, Ankita Singh1, Debdeep Dutta1

  • 1Department of Molecular and Human Genetics, Banaras Hindu University, Varanasi, 221 005, India.

BMC Research Notes
|April 18, 2018
PubMed
Abstract

Insights

Activated Notch signaling combined with loss of the lethal giant larvae (lgl) gene drives tumor overgrowth in Drosophila. This synergy activates JNK signaling and leads to cancer hallmarks like MMP1 upregulation and epithelial disruption.

Area of Science:

  • Developmental Biology
  • Cancer Biology
  • Genetics

Background:

  • Notch signaling is crucial for cell proliferation and cooperates with mutations in cell polarity genes to promote neoplastic overgrowth.
  • Oncogenic Ras and Notch signaling pathways are known to cooperate with the loss of cell polarity genes (scrib, lgl, discs large) in inducing tumor formation and invasion.

Purpose of the Study:

  • To investigate the synergistic effect of activated Notch (Nact) and loss of function of the lethal giant larvae (lgl) gene on tumor overgrowth.
  • To elucidate the mechanism of JNK signaling activation in the context of Nact/lgl-IR induced tumors.

Main Methods:

  • Utilized Drosophila melanogaster as an in vivo model system.
  • Coexpressed activated Notch (Nact) and lgl loss-of-function (lgl-IR) to induce tumor formation.
  • Analyzed tumor progression, MMP1 upregulation, epithelial integrity, JNK signaling activation, and Grindelwald receptor expression.

Main Results:

  • Coexpression of Nact and lgl-IR resulted in massive tumor overgrowth with cancer hallmarks, including MMP1 upregulation and loss of epithelial integrity.
  • Activated JNK signaling and upregulation of its receptor, Grindelwald, were observed in Nact/lgl-IR tumors.
  • Unlike Nact/scrib-/- tumors, Nact/lgl-IR tumors exhibited both massive overgrowth and the presence of dying cells.

Conclusions:

  • Activated Notch signaling synergizes with the loss of lgl function to drive significant tumor overgrowth in Drosophila.
  • The Nact/lgl-IR interaction leads to the activation of JNK signaling and the induction of key cancer-related processes.
  • The presence of dying cells in Nact/lgl-IR tumors suggests a distinct tumor progression mechanism compared to Nact/scrib-/- tumors.
Keywords:
Cell deathDrosophilaJNK signalingNotchTumor overgrowthlgl

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