1. Gallic acid has an inhibitory effect on skin squamous cell carcinoma and acts on the heat shock protein HSP90AB1.
- Author
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de Jesus SF, de Souza MG, Queiroz LDRP, de Paula DPS, Tabosa ATL, Alves WSM, da Silveira LH, Ferreira ATDS, Martuscelli OJD, Farias LC, de-Paula AMB, Santos SHS, and Guimaraes ALS
- Subjects
- Humans, Heat-Shock Proteins, Gallic Acid pharmacology, Proteomics, Molecular Docking Simulation, HSP90 Heat-Shock Proteins genetics, Carcinoma, Basal Cell metabolism, Carcinoma, Squamous Cell pathology, Skin Neoplasms drug therapy, Skin Neoplasms genetics, Skin Neoplasms metabolism
- Abstract
Differences in the features of aggressiveness of non-melanoma skin cancer (NMSC) subtypes, between basal cell carcinoma (BCC) and squamous cell carcinoma (SCC) are relevant characteristics. Comparing the characteristics between NMSC subtypes might help identify molecules associated with cancer metastasis and invasion. Considering these facts, the current study aimed to identify a molecular target for inhibiting skin cancer metastasis and invasion. Proteomic analysis suggested that heat shock protein 90 kDa, alpha, class B member 1 (HSP90AB1), pentaxin (PTX3), caspase-14 (CASP14), S100, actin-1, and profilin were the primary targets related to metastasis and invasion. However, after a differential expression comparison between BCC and SCC, HSP90AB1 was identified as the best target to repress metastasis and invasion. Based on molecular docking results, gallic acid (GA) was selected to inhibit HSP90AB1. A specific Hsp90ab1 siRNA targeting was designed and compared to GA. Interestingly, GA was more efficient in silencing HSP90AB1 than siRNAhsp90ab1. Hence, our data suggest that HSP90AB1 is a crucial biomarker for identifying invasion and metastasis and that its inhibition may be a viable strategy for treating skin cancer., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2022 Elsevier B.V. All rights reserved.)
- Published
- 2023
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