Kumari Seema, Ponamgi S P D, Chelikani Prashen, Srilatha Mundla, Nagaraju Ganji Purnachandra, Peela Sujatha
Department of Biotechnology, College of Science, Dr. B.R. Ambedkar University, Srikakulam, 532410, AP, India.
Department of Biotechnology, AU College of Science & Technology, Andhra University, Visakhapatnam, 530003, AP, India.
Biochim Biophys Acta Rev Cancer. 2025 Sep;1880(4):189359. doi: 10.1016/j.bbcan.2025.189359. Epub 2025 May 30.
Lung cancer is a significant health concern worldwide. It is caused by smoking and exposure to carcinogens, although other factors like genetics, epigenetics, and transcription factors also play a role. Yin Yang 1 (YY1) is a transcription factor with a multifaceted role in regulating cellular functions in various cancers. It has a vital role in lung cancer progression, but also has tumor-suppressing activity. YY1 regulates epigenetic changes through DNA methylation, histone alteration, and non-coding RNAs. In lung cancer, YY1 is overexpressed and involved in metastatic mechanisms, including epithelial and mesenchymal transition (EMT), invasion, migration, and angiogenesis. These metastatic properties are influenced by various signaling pathways (PI3K-Akt-mTOR, RAF-MEK-ERK, JAK-STAT, and Wnt-β-catenin) through PD-L1 expression, autophagy, and drug insensitivity. The current review recapitulates the recent advances on YY1 research in lung cancer progression and its influence on oncogenic pathways, immune regulation, and clinical significance. Furthermore, this review also discusses using YY1 as a biomarker and targeted molecule in lung cancer.
肺癌是全球范围内一个重大的健康问题。它由吸烟和接触致癌物引起,不过其他因素如遗传学、表观遗传学和转录因子也起作用。阴阳1(YY1)是一种转录因子,在多种癌症中调节细胞功能方面具有多方面作用。它在肺癌进展中起关键作用,但也具有肿瘤抑制活性。YY1通过DNA甲基化、组蛋白改变和非编码RNA调节表观遗传变化。在肺癌中,YY1过度表达并参与转移机制,包括上皮-间质转化(EMT)、侵袭、迁移和血管生成。这些转移特性受各种信号通路(PI3K-Akt-mTOR、RAF-MEK-ERK、JAK-STAT和Wnt-β-连环蛋白)通过程序性死亡受体配体1(PD-L1)表达、自噬和药物不敏感性的影响。本综述概述了YY1在肺癌进展研究方面的最新进展及其对致癌途径、免疫调节和临床意义的影响。此外,本综述还讨论了将YY1用作肺癌的生物标志物和靶向分子。