STK11 Loss: A Novel Mechanism for Melanoma Metastasis with Therapeutic Implications

Marjan Azin; Shadmehr Demehri

doi:10.1016/j.jid.2021.10.003

STK11 Loss: A Novel Mechanism for Melanoma Metastasis with Therapeutic Implications

J Invest Dermatol. 2022 Apr;142(4):1007-1009. doi: 10.1016/j.jid.2021.10.003. Epub 2022 Feb 4.

Authors

Marjan Azin¹, Shadmehr Demehri²

Affiliations

¹ Center for Cancer Immunology, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, USA; Center for Cancer Research, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, USA; Cutaneous Biology Research Center, Department of Dermatology, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, USA.
² Center for Cancer Immunology, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, USA; Center for Cancer Research, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, USA; Cutaneous Biology Research Center, Department of Dermatology, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, USA. Electronic address: sdemehri1@mgh.harvard.edu.

PMID: 35131083
DOI: 10.1016/j.jid.2021.10.003

Abstract

STK11 is implicated as a tumor suppressor in epithelial cancer invasion and metastasis. In their new article in the Journal of Investigative Dermatology, Dzung et al. (2021) show that loss of STK11 in cutaneous melanoma cells leads to an invasive metastatic phenotype through the activation of the signal transducer and activator of transcription (STAT) 3/5 and FAK signaling pathways. These results suggest that inhibition of STAT3/5 and FAK in STK11-deficient melanoma cells could serve as a novel therapeutic strategy against metastatic melanoma.

MeSH terms

AMP-Activated Protein Kinase Kinases
Cell Line, Tumor
Humans
Melanoma* / drug therapy
Melanoma* / genetics
Melanoma* / metabolism
Neoplasm Metastasis
Protein Serine-Threonine Kinases / genetics
STAT3 Transcription Factor / metabolism
Signal Transduction
Skin Neoplasms* / drug therapy
Skin Neoplasms* / genetics
Skin Neoplasms* / metabolism

Substances

STAT3 Transcription Factor
Protein Serine-Threonine Kinases
STK11 protein, human
AMP-Activated Protein Kinase Kinases