Azin Marjan, Demehri Shadmehr
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.
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.
J Invest Dermatol. 2022 Apr;142(4):1007-1009. doi: 10.1016/j.jid.2021.10.003. Epub 2022 Feb 4.
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.
STK11被认为是上皮癌侵袭和转移中的一种肿瘤抑制因子。在《皮肤病学研究杂志》上发表的一篇新文章中，Dzung等人（2021年）表明，皮肤黑色素瘤细胞中STK11的缺失通过激活信号转导子和转录激活子（STAT）3/5以及粘着斑激酶（FAK）信号通路，导致侵袭性转移表型。这些结果表明，在STK11缺陷的黑色素瘤细胞中抑制STAT3/5和FAK可能成为一种针对转移性黑色素瘤的新型治疗策略。
