AI Article Synopsis
- ARNT is a transcription factor linked to cellular stress responses, but its role in cutaneous squamous cell carcinoma (cSCC) is not well understood.
- The study found that ARNT is downregulated in cSCC and precancerous lesions, and reducing ARNT levels enhanced cell growth and metastasis in laboratory settings.
- Results indicate that ARNT regulates cSCC proliferation and invasiveness through the CXCL3 pathway, suggesting it could be a promising target for cSCC treatment.
Article Abstract
The aryl hydrocarbon receptor nuclear translocator (ARNT) is a transcription factor associated with adaptive responses to cellular stress. Its role in cutaneous squamous cell carcinoma (cSCC) remains poorly understood. The aim of this study was to investigate the role of ARNT in cSCC. Immunohistochemistry revealed downregulation of ARNT in cSCC, precancerous lesions (actinic keratosis), and cells. Knockdown of ARNT in A431 and SCL-1 cells significantly enhanced cell growth and metastasis. Microarray analysis and Ingenuity Pathway Analysis confirmed that loss of ARNT in A431 cells was highly correlated with cell growth and movement and upregulated CXCL3 expression. Cellular and xenograft experiments further confirmed that ARNT regulates cSCC proliferation and invasiveness in a CXCL3-dependent manner. ARNT may regulate CXCL3 expression through ROS-STAT3 pathway. In conclusion, this study demonstrates that ARNT plays a critical role in the development of cSCC and significantly affects the proliferation and metastatic ability of cSCC cells. It has the potential to serve as an ideal treatment target for cSCC.
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| http://dx.doi.org/10.1016/j.cellsig.2024.111432 | DOI Listing |
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