Please use this identifier to cite or link to this item: https://doi.org/10.1111/j.1600-0625.2007.00627.x
Title: Targeting of Sp1 transcription factor: A novel therapeutic approach for Keloids, an in vitro analysis
Authors: Mukhopadhyay, A.
Khoo, A.
Cheong, H.H.
Chan, S.Y. 
Aalami, O.
Lim, I.J.
Phan, T.T.
Keywords: α-smooth muscle actin
Collagen
Epithelial-mesenhcymal interaction
Fibroblasts
Fibronectin
Keloid
Keloid scar
Keratinocytes
Mitoxanthrone
Sp1
Wp631
Issue Date: Dec-2007
Citation: Mukhopadhyay, A., Khoo, A., Cheong, H.H., Chan, S.Y., Aalami, O., Lim, I.J., Phan, T.T. (2007-12). Targeting of Sp1 transcription factor: A novel therapeutic approach for Keloids, an in vitro analysis. Experimental Dermatology 16 (12) : 1023-1031. ScholarBank@NUS Repository. https://doi.org/10.1111/j.1600-0625.2007.00627.x
Abstract: Keloid scars are fibroproliferative disorders characterized by the accumulation of extracellular matrix (ECM) components resulting in a fibrotic condition. Several ECM promoters are regulated by Sp1. Thus, our aim was to investigate the role of Sp1 in keloid pathogenesis and investigate the antiproliferative and antifibrotic effects of Wp631 and mitoxantrone, potent inhibitors of Sp1-activated transcription. An elevated level of Sp1 was observed in tissue extracts obtained from keloid tissue. Serum stimulation elevated Sp1 levels in keloid fibroblasts (KF). Under coculture conditions Sp1 seemed to be downregulated. Wp631 and mitoxanthrone in serum growth factors resulted in a reduced expression of ECM components in KF. Both Wp631 and mitoxanthrone were also able to inhibit the proliferation of normal and keloid keratinocytes and fibroblasts significantly. As Wp631 seems to be potent in downregulating the ECM components in KF and also inhibiting the proliferation of these cells it could be explored as a possible therapeutic agent in the treatment of keloids. © 2007 The Authors Journal compilation © 2007 Blackwell Munksgaard.
Source Title: Experimental Dermatology
URI: http://scholarbank.nus.edu.sg/handle/10635/106414
ISSN: 09066705
DOI: 10.1111/j.1600-0625.2007.00627.x
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