Ye Yunyao, Yu Shanxun, Guo Ting, Zhang Sihui, Shen Xiaozhou, Han Gaohua
Department of Oncology, Taizhou People's Hospital Affiliated to Nanjing Medical University, Taizhou 225300, China.
Central Lab, Taizhou People's Hospital Affiliated to Nanjing Medical University, Taizhou 225300, China.
Biomolecules. 2024 Nov 28;14(12):1523. doi: 10.3390/biom14121523.
Lung cancer, the leading cause of death worldwide, is associated with the highest morbidity. Non-small cell lung cancer (NSCLC) accounts for 80-85% of lung cancer cases. Advances in the domain of cancer treatment have improved the prognosis and quality of life of patients with metastatic NSCLC. Nevertheless, tumor progression or metastasis owing to treatment failure caused by primary or secondary drug resistance remains the cause of death in the majority of cases. Epithelial-mesenchymal transition (EMT), a vital biological process wherein epithelial cancer cells lose their inherent adhesion and transform into more invasive mesenchymal-like cells, acts as a powerful engine driving tumor metastasis. EMT can also induce immunosuppression in the tumor environment, thereby promoting cancer development and poor prognosis among patients with NSCLC. This review aims to elucidate the effect of EMT on metastasis and the tumor immune microenvironment. Furthermore, it explores the possible roles of EMT inhibition in improving the treatment efficacy of NSCLC. Targeting EMT may be an ideal mechanism to inhibit tumor growth and progression at multiple steps.
肺癌是全球主要的死亡原因,其发病率也最高。非小细胞肺癌(NSCLC)占肺癌病例的80-85%。癌症治疗领域的进展改善了转移性NSCLC患者的预后和生活质量。然而,由于原发性或继发性耐药导致的治疗失败引起的肿瘤进展或转移仍然是大多数病例的死亡原因。上皮-间质转化(EMT)是一个重要的生物学过程,其中上皮癌细胞失去其固有的粘附力并转化为更具侵袭性的间充质样细胞,是驱动肿瘤转移的强大引擎。EMT还可在肿瘤微环境中诱导免疫抑制,从而促进NSCLC患者的癌症发展和不良预后。本综述旨在阐明EMT对转移和肿瘤免疫微环境的影响。此外,还探讨了EMT抑制在提高NSCLC治疗疗效方面的可能作用。靶向EMT可能是在多个步骤抑制肿瘤生长和进展的理想机制。