O'Donnell Brooke L, Johnston Danielle, Bhatt Ayushi, Kardan Zahra, Stefan Dan, Bysice Andrew, Sayedyahossein Samar, Dagnino Lina, Cecchini Matthew, Loganathan Sampath Kumar, Roth Kathryn, Penuela Silvia
Department of Anatomy and Cell Biology, Schulich School of Medicine and Dentistry, University of Western Ontario, London, Ontario, Canada.
Faculty of Medicine, Schulich School of Medicine and Dentistry, University of Western Ontario, London, Ontario, Canada.
J Physiol. 2025 Aug;603(15):4409-4432. doi: 10.1113/JP286172. Epub 2024 Nov 19.
Pannexin (PANX) channels are present in skin and facilitate the movement of signalling molecules during cellular communication. PANX1 and PANX3 function in skin homeostasis and keratinocyte differentiation but were previously reduced in a small cohort of human cutaneous squamous cell carcinoma (cSCC) tumours compared to normal epidermis. In our study we used SCC-13 cells, limited publicly available RNA-seq data and a larger cohort of cSCC patient-matched samples to analyse PANX1 and PANX3 expression and determine the association between their dysregulation and the malignant properties of cSCC. In a bioinformatics analysis, PANX1 transcripts were increased in cSCC and head and neck SCC tumours compared to normal tissues, but PANX3 mRNA showed no differences. However, in our own cohort PANX3 transcripts were decreased in cSCC compared to patient-matched aged skin, whereas PANX1 protein was upregulated in cSCC. PANX1 localized to all regions within the cSCC tumour microenvironment, and increased levels were associated with larger tumour dimensions. To investigate PANX1 function in SCC-13 cells, we deleted PANX1 via CRISPR/Cas9 and treated with PANX1 inhibitors, which markedly reduced cell growth and migration. To assess PANX3 function in cutaneous carcinogenesis, we employed the 7,12-dimethylbenz(a)anthracene/12-otetradecanoylphorbol-13-acetate (DMBA/TPA) model using our global Panx3 knockout (KO) mice, where 60% of wild-type and 100% of KO mice formed precancerous papillomas. Average papilloma volumes at endpoint were significantly increased in KO mice and showed moderate evidence of increases in KO mice over time. Collectively, these findings suggest PANX1 and PANX3 dysregulation may have potential tumour-promoting and tumour-suppressive effects for keratinocyte transformation, respectively. KEY POINTS: Pannexin 1 (PANX1) and pannexin 3 (PANX3) are channel-forming proteins which are critical in the normal maintenance and function of keratinocytes in the skin but may become altered in cutaneous squamous cell carcinoma (cSCC) tumours. In this study we used a combination of culture models, mouse models and patient-derived tissues. We found PANX1 levels are increased in cSCC tumours and present in all tumour regions, functioning to promote cSCC cell growth and migration. Conversely, PANX3 levels are decreased in cSCC tumours, and this protein reduces the incidence and growth of precancerous lesions. Taken together our data indicate that in cSCC these pannexin family members seem to have opposite effects, in either promoting or restricting cancer cell properties. These results help us to better understand the mechanisms of malignant transformation of keratinocytes and offer a new potential therapeutic target for the treatment of advanced cSCC.
泛连接蛋白(PANX)通道存在于皮肤中,并在细胞通讯过程中促进信号分子的移动。PANX1和PANX3在皮肤稳态和角质形成细胞分化中发挥作用,但与正常表皮相比,先前在一小群人皮肤鳞状细胞癌(cSCC)肿瘤中表达降低。在我们的研究中,我们使用了SCC-13细胞、有限的公开可用RNA测序数据以及一大群cSCC患者匹配样本,来分析PANX1和PANX3的表达,并确定它们的失调与cSCC恶性特性之间的关联。在生物信息学分析中,与正常组织相比,cSCC以及头颈部SCC肿瘤中PANX1转录本增加,但PANX3 mRNA没有差异。然而,在我们自己的队列中,与患者匹配的老年皮肤相比,cSCC中PANX3转录本减少,而PANX1蛋白在cSCC中上调。PANX1定位于cSCC肿瘤微环境内的所有区域,其水平升高与更大的肿瘤尺寸相关。为了研究PANX1在SCC-13细胞中的功能,我们通过CRISPR/Cas9删除了PANX1并用PANX1抑制剂处理,这显著降低了细胞生长和迁移。为了评估PANX3在皮肤癌发生中的功能,我们使用我们的全身性Panx3基因敲除(KO)小鼠采用7,12-二甲基苯并(a)蒽/12-十四烷酰佛波醇-13-乙酸酯(DMBA/TPA)模型,其中60%的野生型和100%的KO小鼠形成癌前乳头瘤。终点时KO小鼠的平均乳头瘤体积显著增加,并且随着时间的推移显示出KO小鼠有适度增加的证据。总体而言,这些发现表明PANX1和PANX3失调可能分别对角质形成细胞转化具有潜在的促肿瘤和抑肿瘤作用。要点:泛连接蛋白1(PANX1)和泛连接蛋白3(PANX3)是形成通道的蛋白,对皮肤中角质形成细胞的正常维持和功能至关重要,但在皮肤鳞状细胞癌(cSCC)肿瘤中可能会发生改变。在本研究中,我们结合使用了培养模型、小鼠模型和患者来源的组织。我们发现cSCC肿瘤中PANX1水平升高且存在于所有肿瘤区域,其功能是促进cSCC细胞生长和迁移。相反,cSCC肿瘤中PANX3水平降低,并且这种蛋白可降低癌前病变的发生率和生长。综合我们的数据表明,在cSCC中,这些泛连接蛋白家族成员似乎具有相反的作用,即促进或限制癌细胞特性。这些结果有助于我们更好地理解角质形成细胞恶性转化的机制,并为晚期cSCC的治疗提供新的潜在治疗靶点。