Reprogramming tumor-associated macrophages: The role of MEK-STAT3 inhibition in lung cancer

IF 2.9 4区 医学 Q2 PATHOLOGY
Sushama Rawat , Ehssan Moglad , Muhammad Afzal , Ahsas Goyal , R. Roopashree , Pooja Bansal , Shivang Mishra , G.V. Siva Prasad , Atreyi Pramanik , Sami I. Alzarea , Haider Ali , Mohd Imran , Abida
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引用次数: 0

Abstract

Tumor-associated macrophages (TAMs) crucially contribute to lung cancer's advancement and escape from the immune system. TAMs, particularly the M2 phenotype, promote an immunosuppressive microenvironment, facilitating tumor growth and metastasis. The MEK-STAT3 signalling pathway is a critical mediator in this process, driving TAM reprogramming and contributing to lung cancer's resistance to treatment. Inhibiting the MEK and STAT3 pathways disrupts key cancer-promoting mechanisms, including immune evasion, angiogenesis, and metastasis. Preclinical studies have demonstrated the effectiveness of MEK inhibitors, such as trametinib and selumetinib, in synergistic therapies for NSCLC, particularly in modulating the tumor microenvironment. We analyse the present understanding of approaches that can transform TAMs via the inhibition of MEK-STAT3 with either solo or combined treatments in lung cancer therapy.
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来源期刊
CiteScore
5.00
自引率
3.60%
发文量
405
审稿时长
24 days
期刊介绍: Pathology, Research and Practice provides accessible coverage of the most recent developments across the entire field of pathology: Reviews focus on recent progress in pathology, while Comments look at interesting current problems and at hypotheses for future developments in pathology. Original Papers present novel findings on all aspects of general, anatomic and molecular pathology. Rapid Communications inform readers on preliminary findings that may be relevant for further studies and need to be communicated quickly. Teaching Cases look at new aspects or special diagnostic problems of diseases and at case reports relevant for the pathologist''s practice.
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