Sayedyahossein Samar, Huang Kenneth, Zhang Christopher, Karimi Mehdi, Bahmani Mehrnoosh, O'Donnell Brooke L, Wakefield Brent, Li Zhigang, Johnston Danielle, Leighton Stephanie E, Huver Matthew S, Dagnino Lina, Sacks David B, Penuela Silvia
Department of Laboratory Medicine, National Institutes of Health, Bethesda, MD, USA.
Department of Anatomy and Cell Biology, Schulich School of Medicine and Dentistry, The University of Western Ontario, London, Canada.
FEBS J. 2025 Apr;292(7):1633-1653. doi: 10.1111/febs.17396. Epub 2025 Jan 9.
In this study, we explored the intricate relationship between Pannexin 1 (PANX1) and the Hippo signaling pathway effector, Yes-associated protein (YAP). Analysis of The Cancer Genome Atlas (TCGA) data revealed a significant positive correlation between PANX1 mRNA and core Hippo components, Yes-associated protein 1 [YAP], Transcriptional coactivator with PDZ-binding motif [TAZ], and Hippo scaffold, Ras GTPase-activating-like protein IQGAP1 [IQGAP1], in invasive cutaneous melanoma and breast carcinoma. Furthermore, we demonstrated that PANX1 expression is upregulated in invasive melanoma cell lines and is associated with increased YAP protein levels. Notably, our investigations uncovered a previously unrecognized interaction between endogenous PANX1 and the Hippo scaffold protein IQGAP1 in melanoma cells. Moreover, our findings revealed that IQGAP1 exhibits differential expression in melanoma cells and plays a regulatory role in cellular morphology. Functional studies involving PANX1 knockdown provided compelling evidence that PANX1 modulates YAP protein levels and its cotranscriptional activity in melanoma and breast carcinoma cells. Importantly, our study highlights the potential therapeutic significance of targeting PANX1. Pharmacological inhibition of PANX1 using selective FDA-approved inhibitors or PANX1 knockdown reduced YAP levels in melanoma cells. Furthermore, our Clariom™ S analysis unveiled key genes implicated in cell proliferation, such as neuroglin1 (NRG1), β-galactoside binding protein and galectin-3 (LGALS3), that are affected in PANX1-deficient cells. In summary, our investigation delves into the intricate interplay between PANX1 and YAP in the context of invasive melanoma, offering valuable insights into potential therapeutic strategies for effective treatment.
在本研究中,我们探究了泛连接蛋白1(PANX1)与Hippo信号通路效应器Yes相关蛋白(YAP)之间的复杂关系。对癌症基因组图谱(TCGA)数据的分析显示,在侵袭性皮肤黑色素瘤和乳腺癌中,PANX1 mRNA与Hippo核心组分Yes相关蛋白1 [YAP]、含PDZ结合基序的转录共激活因子[TAZ]以及Hippo支架蛋白Ras GTP酶激活样蛋白IQGAP1 [IQGAP1]之间存在显著正相关。此外,我们证明PANX1在侵袭性黑色素瘤细胞系中表达上调,且与YAP蛋白水平升高相关。值得注意的是,我们的研究发现黑色素瘤细胞中内源性PANX1与Hippo支架蛋白IQGAP1之间存在此前未被认识到的相互作用。此外,我们的研究结果显示IQGAP1在黑色素瘤细胞中表现出差异表达,并在细胞形态中发挥调节作用。涉及PANX1敲低的功能研究提供了有力证据,表明PANX1在黑色素瘤和乳腺癌细胞中调节YAP蛋白水平及其共转录活性。重要的是,我们的研究突出了靶向PANX1的潜在治疗意义。使用美国食品药品监督管理局(FDA)批准的选择性抑制剂对PANX1进行药理学抑制或敲低PANX1可降低黑色素瘤细胞中的YAP水平。此外,我们的Clariom™ S分析揭示了与细胞增殖相关的关键基因,如神经调节蛋白1(NRG1)、β-半乳糖苷结合蛋白和半乳糖凝集素-3(LGALS3),这些基因在PANX1缺陷细胞中受到影响。总之,我们的研究深入探究了侵袭性黑色素瘤背景下PANX1与YAP之间的复杂相互作用,为有效治疗的潜在治疗策略提供了有价值的见解。