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Tumorigenesis promotes Mdm4-S overexpression

Vinod Pant1, Connie A Larsson1, Neeraj Aryal1

  • 1Department of Genetics, M.D. Anderson Cancer Center, Houston, Texas, 77030, USA.

Oncotarget
|May 3, 2017
PubMed

Insights

The splice variant MDM4-S does not cause cancer or worsen tumor progression. MDM4-S overexpression is a result of splicing defects in tumor cells, not a driver of tumor evolution.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Disruption of the p53 tumor suppressor pathway drives tumorigenesis.
  • Overexpression of MDM2 and MDM4, negative regulators of p53, contributes to tumor development.
  • Splice variants of Mdm2 and Mdm4, including MDM4-S, are implicated in tumor progression.

Purpose of the Study:

  • To investigate the role of the MDM4-S splice variant in tumor development.
  • To determine if MDM4-S expression is oncogenic or a consequence of tumorigenesis.
  • To assess the impact of MDM4-S on tumor latency and aggressiveness in a mouse model.

Main Methods:

  • Utilized a transgenic mouse model to study Mdm4-S function.
  • Examined the effect of Mdm4-S on tumor development and progression.
  • Assessed cooperation with other oncogenic factors.

Main Results:

  • Splicing of Mdm4 did not promote tumor development in the mouse model.
  • MDM4-S did not alter tumor latency or aggressiveness when cooperating with other oncogenic insults.
  • MDM4-S overexpression was observed as a consequence of splicing defects.

Conclusions:

  • MDM4-S is not an oncogenic driver of tumor development.
  • Overexpression of MDM4-S is a result of splicing defects, not a cause of tumor evolution.
  • MDM4-S is a consequence, not a cause, of tumorigenesis.
Keywords:
CLLMdm4-S/Mdm4Mdmxsplicingtransgenic mouse

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