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Disease Markers
Volume 2016 (2016), Article ID 7040312, 8 pages
Research Article

Survivin as a Novel Biomarker in the Pathogenesis of Acne Vulgaris and Its Correlation to Insulin-Like Growth Factor-I

1Department of Dermatology, Faculty of Medicine, Sohag University, P.O. Box 82524, Sohag, Egypt
2Department of Biochemistry and Molecular Biology, Faculty of Pharmacy, Al-Azhar University, Assiut Branch, P.O. Box 71524, Assiut, Egypt
3Department of Biochemistry and Molecular Biology, Qena Faculty of Medicine, South Valley University, P.O. Box 83523, Qena, Egypt
4Department of Zoology, Faculty of Science, Sohag University, P.O. Box 82524, Sohag, Egypt

Received 14 July 2016; Revised 1 September 2016; Accepted 7 September 2016

Academic Editor: Michele Malaguarnera

Copyright © 2016 Hanan A. Assaf et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Survivin, a member of the inhibitor of apoptosis protein family, has an important role in cell cycle regulation. Insulin-like growth factor-I (IGF-I) is a polypeptide hormone with wide range of biologic effects including stimulation of lipogenesis in sebaceous glands. Their overexpression in some fibrotic disorders suggests a possible implication of both IGF-I and survivin in the pathogenesis of acne and/or acne scars. The current study aimed to assess and correlate serum levels of IGF-I and survivin in patients with active acne vulgaris and postinflammatory acne scars and to evaluate their lesional expressions in comparison to healthy controls. Serum IGF-I and survivin were estimated using commercially available ELISA kits and their tissues expressions were investigated using Western blotting. Our findings suggest that IGF-I and survivin could play potential roles in the pathogenesis of active acne vulgaris and more importantly in postinflammatory acne scars with significant positive correlation coefficient between serum levels of IGF-I and survivin which support IGF-I-/PI3K-/AKT-mediated downregulation of nuclear expression of FoxO transcription factors resulting in enhanced survivin expression.