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钙三醇和姜黄素抑制人三阴性乳腺癌细胞血管生成拟态的内皮依赖性诱导

Endothelium-Dependent Induction of Vasculogenic Mimicry in Human Triple-Negative Breast Cancer Cells Is Inhibited by Calcitriol and Curcumin.

机构信息

Departamento de Biología de la Reproducción Dr. Carlos Gual Castro, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Vasco de Quiroga No. 15, Belisario Domínguez Sección XVI, Tlalpan, Ciudad de México 14080, Mexico.

Programa de Investigación de Cáncer de Mama, Instituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México, Ciudad de México 04510, Mexico.

出版信息

Int J Mol Sci. 2022 Jul 11;23(14):7659. doi: 10.3390/ijms23147659.

Abstract

In highly aggressive tumors, cancer cells may form channel-like structures through a process known as vasculogenic mimicry (VM). VM is generally associated with metastasis, mesenchymal phenotype, and treatment resistance. VM can be driven by antiangiogenic treatments and/or tumor microenvironment-derived factors, including those from the endothelium. Curcumin, a turmeric product, inhibits VM in some tumors, while calcitriol, the most active vitamin D metabolite, exerts potent antineoplastic effects. However, the effect of these natural products on VM in breast cancer remains unknown. Herein, we studied the effect of both compounds on triple-negative breast cancer (TNBC) VM-capacity in a co-culture model. The process of endothelial cell-induced VM in two human TNBC cell lines was robustly inhibited by calcitriol and partially by curcumin. Calcitriol promoted TNBC cells' morphological change from spindle-like to cobblestone-shape, while curcumin diminished VM 3D-structure. Notably, the treatments dephosphorylated several active kinases, especially those involved in the PI3K/Akt pathway. In summary, calcitriol and curcumin disrupted endothelium-induced VM in TNBC cells partially by PI3K/Akt inactivation and mesenchymal phenotype inhibition. Our results support the possible use of these natural compounds as adjuvants for VM inactivation in patients with malignant tumors inherently capable of forming VM, or those with antiangiogenic therapy, warranting further in vivo studies.

摘要

在高度侵袭性的肿瘤中,癌细胞可能通过一种称为血管生成拟态(VM)的过程形成管状结构。VM 通常与转移、间充质表型和治疗抵抗有关。VM 可被抗血管生成治疗和/或肿瘤微环境来源的因素驱动,包括内皮细胞来源的因素。姜黄素,一种姜黄产品,可抑制一些肿瘤中的 VM,而最活跃的维生素 D 代谢物 1,25-二羟维生素 D3(calcitriol)则发挥强大的抗肿瘤作用。然而,这些天然产物对乳腺癌中 VM 的影响尚不清楚。在此,我们在共培养模型中研究了这两种化合物对三阴性乳腺癌(TNBC)VM 能力的影响。calcitriol 和姜黄素强烈抑制了两种人 TNBC 细胞系中内皮细胞诱导的 VM 形成,calcitriol 部分抑制,姜黄素部分抑制。calcitriol 促进 TNBC 细胞从纺锤形向鹅卵石形的形态变化,而姜黄素则减少了 VM 的 3D 结构。值得注意的是,这些治疗方法使几种活性激酶去磷酸化,特别是那些涉及 PI3K/Akt 途径的激酶。总之,calcitriol 和姜黄素通过 PI3K/Akt 失活和间充质表型抑制部分破坏了 TNBC 细胞中内皮细胞诱导的 VM。我们的结果支持这些天然化合物作为辅助剂用于治疗固有形成 VM 能力的恶性肿瘤或接受抗血管生成治疗的患者中 VM 失活的可能性,值得进一步进行体内研究。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e337/9318499/87aaebdb8daf/ijms-23-07659-g001.jpg

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