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The Involvement of Splicing Factor hnRNP A1 in UVB-induced Alternative Splicing of hdm2

Jianguo Feng1,2, Li Li1, Lingying Tong2

  • 1Key Laboratory of Biorheological Science and Technology, Ministry of Education, College of Bioengineering, Chongqing University, Chongqing, China.

Photochemistry and Photobiology
|January 13, 2016
PubMed

Insights

Ultraviolet B (UVB) radiation induces human homolog double minute 2 (hdm2) alternative splicing by increasing the expression and binding of heterogeneous nuclear ribonucleoprotein A1 (hnRNP A1) to hdm2 pre-mRNA, impacting tumorigenesis.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • UV Radiation Effects

Background:

  • Human homolog double minute 2 (hdm2) is an oncoprotein that degrades tumor suppressor p53, contributing to tumorigenesis.
  • hdm2 splicing variants are highly expressed in cancers and can be induced by ultraviolet B (UVB) light.
  • The precise mechanisms by which UVB induces hdm2 alternative splicing are not fully understood.

Purpose of the Study:

  • To investigate the roles of splicing factors hnRNP A1 and SRSF1 in UVB-induced hdm2 alternative splicing.
  • To elucidate the molecular mechanisms underlying UVB-mediated hdm2 splicing regulation.

Main Methods:

  • Investigated the expression of hnRNP A1 and SRSF1 after UVB irradiation.
  • Manipulated hnRNP A1 expression (overexpression and downregulation) in HaCaT cells.
  • Performed protein-mRNA binding assays to confirm hnRNP A1 binding to hdm2 pre-mRNA.

Main Results:

  • UVB irradiation induced the expression of both hnRNP A1 and SRSF1.
  • Only hnRNP A1 was found to be involved in UVB-induced hdm2 alternative splicing.
  • hnRNP A1 modulated hdm2-FL and hdm2B levels, and UVB increased hnRNP A1 binding to hdm2 pre-mRNA.

Conclusions:

  • UVB induces hdm2 alternative splicing primarily through hnRNP A1.
  • Increased hnRNP A1 expression and its enhanced binding to hdm2 pre-mRNA are key mechanisms in UVB-induced hdm2 splicing.
  • This finding provides insight into the role of UVB in cancer development via hdm2 regulation.

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