SP3 is associated with migration, invasion, and Akt/PKB signalling in MDA‐MB‐231 breast cancer cells
Mansour, M. (2020). SP3 is associated with migration, invasion, and Akt/PKB signalling in MDA‐MB‐231 breast cancer cells. Journal of biochemical and molecular toxicology. 35 (3). https://doi.org/10.1002/jbt.22657
© 2020 Wiley Periodicals LLC Specificity proteins (SPs) have pro-oncogenic functions in cancer cells, ranging from cancer cell proliferation, migration, invasion, and angiogenesis. There is strong evidence that several antineoplastic drugs target depletion of SP proteins via different pathways. However, the mode of action of SP3 and the underlying consequences of its depletion are not well understood. Here, we demonstrate that SP3 is overexpressed in invasive breast cancer cells vs normal counterparts. The gene expression analysis from The Cancer Genome Atlas datasets indicated that SP3 is strongly correlated with Akt signalling-related proteins, G protein subunit alpha 13, and RAB33B (RAB33B, member RAS oncogene family). RNA interference of SP3 decreased active phosphorylation of Akt at serine and threonine sites. These findings indicate that SP3 exhibits a pro-oncogenic function, which clearly fits the description of an nononcogene addiction gene. Future analyses are prompted to uncover the SP3 gene regulation function and to reveal downstream targets of SP3 in breast cancer.
|Keywords||Toxicology; Molecular Medicine; Biochemistry; Health, Toxicology and Mutagenesis; Molecular Biology; General Medicine|
|Journal||Journal of biochemical and molecular toxicology|
|Journal citation||35 (3)|
|Digital Object Identifier (DOI)||https://doi.org/10.1002/jbt.22657|
|Online||28 Oct 2020|
|Publication process dates|
|Accepted||09 Oct 2020|
|Deposited||30 Nov 2020|
|Accepted author manuscript|
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This is the peer reviewed version of the following article: SP3 is associated with migration, invasion, and Akt/PKB signalling in MDA‐MB‐231 breast cancer cells, which has been published in final form at https://onlinelibrary.wiley.com/doi/10.1002/jbt.22657. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Use of Self-Archived Versions.
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