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Kmt2a cooperates with menin to suppress tumorigenesis in mouse pancreatic islets

Wenchu Lin1,2, Joshua M Francis2,3, Hong Li1

  • 1a High Magnetic Field Laboratory, Chinese Academy of Sciences , Hefei , Anhui , P.R. China.

Cancer Biology & Therapy
|November 2, 2016
PubMed

Insights

Inactivating Kmt2a in Men1-deficient mice accelerated pancreatic neuroendocrine tumor (PanNET) development and increased cell proliferation. This new Kmt2a/Men1 double knockout mouse model aids in studying advanced PanNETs.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Pancreatic neuroendocrine tumors (PanNETs) incidence is rising, necessitating deeper molecular pathology understanding.
  • Current therapeutic options for PanNETs are limited, highlighting the need for advanced preclinical models.
  • The Men1 knockout mouse model mimics early PanNET development, serving as a basis for improved models.

Purpose of the Study:

  • To investigate the role of KMT2A in PanNET development in conjunction with MEN1.
  • To develop and characterize a novel mouse model for studying advanced PanNETs.

Main Methods:

  • Generation of a Kmt2a/Men1 double knockout mouse model.
  • Analysis of tumor development, cell proliferation, and lifespan in the mouse model.
  • Investigating the interaction between Menin and KMT2A/KMT2B histone methyltransferases.

Main Results:

  • Inactivation of Kmt2a in Men1-deficient mice accelerated pancreatic islet tumorigenesis.
  • Tumor-bearing mice exhibited shortened average lifespans.
  • Increased cell proliferation was observed in double knockout mouse pancreatic islet tumors.

Conclusions:

  • The Kmt2a/Men1 double knockout mouse is a valuable model for studying advanced PanNETs.
  • This model facilitates preclinical testing and research into PanNET molecular pathology.
  • Understanding the interplay between KMT2A and MEN1 is crucial for PanNET research.
Keywords:
Kmt2aMen1PanNETsmethyltransferasetumorigenesis

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