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Serine Threonine Kinase 17A Maintains the Epithelial State in Colorectal Cancer Cells
Journal article   Open access   Peer reviewed

Serine Threonine Kinase 17A Maintains the Epithelial State in Colorectal Cancer Cells

Sarah P Short, Joshua J Thompson, Anthony J Bilotta, Xi Chen, Frank L Revetta, M Kay Washington and Christopher S Williams
Molecular cancer research, Vol.17(4), pp.882-894
04/01/2019
DOI: 10.1158/1541-7786.MCR-18-0990
PMCID: PMC6941354
PMID: 30655319
url
https://doi.org/10.1158/1541-7786.MCR-18-0990View
Published (Version of record) Open Access

Abstract

Serine threonine kinase 17A (STK17A) is a ubiquitously expressed kinase originally identified as a regulator of apoptosis; however, whether it functionally contributes to colorectal cancer has not been established. Here, we have analyzed STK17A in colorectal cancer and demonstrated decreased expression of STK17A in primary tumors, which is further reduced in metastatic lesions, indicating a potential role in regulating the metastatic cascade. Interestingly, changes in STK17A expression did not modify proliferation, apoptosis, or sensitivity of colorectal cancer cell lines to treatment with the chemotherapeutic 5-fluorouracil. Instead, knockdown induced a robust mesenchymal phenotype consistent with the epithelial-mesenchymal transition, including spindle-like cell morphology, decreased expression of adherens junction proteins, and increased migration and invasion. Additionally, overexpression of decreased cell size and induced widespread membrane blebbing, a phenotype often associated with activation of cell contractility. Indeed, STK17A-overexpressing cells displayed heightened phosphorylation of myosin light chain in a manner dependent on STK17A catalytic activity. Finally, patient-derived tumor organoid cultures were used to more accurately determine STK17A's effect in primary human tumor cells. Loss of STK17A induced morphologic changes, decreased E-cadherin, increased invasion, and augmented organoid attachment on 2D substrates, all together suggesting a more metastatic phenotype. Collectively, these data indicate a novel role for STK17A in the regulation of epithelial phenotypes and indicate its functional contribution to colorectal cancer invasion and metastasis. IMPLICATIONS: Loss of serine threonine kinase 17A occurs in colorectal cancer metastasis, induces mesenchymal morphologies, and contributes to tumor cell invasion and migration in colorectal cancer.
Apoptosis Regulatory Proteins - metabolism Cell Line, Tumor Cell Movement - physiology Colorectal Neoplasms - drug therapy Colorectal Neoplasms - enzymology Colorectal Neoplasms - pathology Epithelial Cells - enzymology Epithelial Cells - pathology Epithelial-Mesenchymal Transition Fluorouracil - pharmacology HCT116 Cells Humans Neoplasm Metastasis Protein-Serine-Threonine Kinases - metabolism

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