Yang Jiawen, Lim James T, Victor Paul, Corona Marcelo G, Chen Chen, Khawaja Hunain, Pan Qiong, Paine-Murrieta Gillian D, Schnellmann Rick G, Roe Denise J, Gokhale Prafulla C, DeCaprio James A, Padi Megha
University of Arizona Cancer Center, Tucson, Arizona, USA.
Department of Molecular and Cellular Biology, University of Arizona, Tucson, Arizona, USA.
bioRxiv. 2024 Dec 20:2023.11.01.565218. doi: 10.1101/2023.11.01.565218.
Merkel Cell Carcinoma (MCC) is an aggressive neuroendocrine cutaneous malignancy arising from either ultraviolet-induced mutagenesis or Merkel cell polyomavirus (MCPyV) integration. Despite extensive research, our understanding of the molecular mechanisms driving the transition from normal cells to MCC remains limited. To address this knowledge gap, we assessed the impact of inducible MCPyV T antigens on normal human fibroblasts by performing RNA sequencing. Our data uncovered changes in expression and regulation of Wnt signaling pathway members. Building on this observation, we bioinformatically evaluated various Wnt pathway perturbagens for their ability to reverse the MCC gene expression signature and identified pyrvinium pamoate, an FDA-approved anthelminthic drug known for its anti-tumor activity in other cancers. Leveraging transcriptomic, network, and molecular analyses, we found that pyrvinium targets multiple MCC vulnerabilities. Pyrvinium not only reverses the neuroendocrine features of MCC by modulating canonical and non-canonical Wnt signaling but also inhibits cancer cell growth by activating p53-mediated apoptosis, disrupting mitochondrial function, and inducing endoplasmic reticulum stress. Finally, we demonstrated that pyrvinium reduces tumor growth in an MCC mouse xenograft model. These findings offer a new understanding of the role of Wnt signaling in MCC and highlight the utility of pyrvinium as a potential treatment for MCC.
默克尔细胞癌(MCC)是一种侵袭性神经内分泌皮肤恶性肿瘤,其起因是紫外线诱导的诱变或默克尔细胞多瘤病毒(MCPyV)整合。尽管进行了广泛研究,但我们对驱动正常细胞转变为MCC的分子机制的理解仍然有限。为了填补这一知识空白,我们通过RNA测序评估了可诱导的MCPyV T抗原对正常人成纤维细胞的影响。我们的数据揭示了Wnt信号通路成员在表达和调控方面的变化。基于这一观察结果,我们通过生物信息学方法评估了各种Wnt通路干扰剂逆转MCC基因表达特征的能力,并确定了帕莫酸吡维铵,一种FDA批准的驱虫药,因其在其他癌症中的抗肿瘤活性而闻名。利用转录组学、网络和分子分析,我们发现吡维铵靶向多个MCC的脆弱点。吡维铵不仅通过调节经典和非经典Wnt信号通路来逆转MCC的神经内分泌特征,还通过激活p53介导的凋亡、破坏线粒体功能和诱导内质网应激来抑制癌细胞生长。最后,我们证明了吡维铵在MCC小鼠异种移植模型中可减少肿瘤生长。这些发现为Wnt信号通路在MCC中的作用提供了新的理解,并突出了吡维铵作为MCC潜在治疗方法的效用。