Targeting the EphA2 pathway: could it be the way for bone sarcomas?

IF 8.2 2区生物学 Q1 CELL BIOLOGY

Cell Communication and Signaling Pub Date : 2024-09-09 DOI:10.1186/s12964-024-01811-7

Giorgia Giordano, Cristina Tucciarello, Alessandra Merlini, Santina Cutrupi, Ymera Pignochino

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引用次数: 0

Abstract

Bone sarcomas are malignant tumors of mesenchymal origin. Complete surgical resection is the cornerstone of multidisciplinary treatment. However, advanced, unresectable forms remain incurable. A crucial step towards addressing this challenge involves comprehending the molecular mechanisms underpinning tumor progression and metastasis, laying the groundwork for innovative precision medicine-based interventions. We previously showed that tyrosine kinase receptor Ephrin Type-A Receptor 2 (EphA2) is overexpressed in bone sarcomas. EphA2 is a key oncofetal protein implicated in metastasis, self-renewal, and chemoresistance. Molecular, genetic, biochemical, and pharmacological approaches have been developed to target EphA2 and its signaling pathway aiming to interfere with its tumor-promoting effects or as a carrier for drug delivery. This review synthesizes the main functions of EphA2 and their relevance in bone sarcomas, providing strategies devised to leverage this receptor for diagnostic and therapeutic purposes, with a focus on its applicability in the three most common bone sarcoma histotypes: osteosarcoma, chondrosarcoma, and Ewing sarcoma.

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靶向 EphA2 通路：它能否成为治疗骨肉瘤的方法？

骨肉瘤是间质来源的恶性肿瘤。完全手术切除是多学科治疗的基础。然而，晚期无法切除的骨肉瘤仍无法治愈。应对这一挑战的关键一步是了解肿瘤进展和转移的分子机制，为基于精准医疗的创新干预奠定基础。我们之前研究发现，酪氨酸激酶受体Ephrin Type-A Receptor 2（EphA2）在骨肉瘤中过度表达。EphA2 是一种关键的胎盘上蛋白，与转移、自我更新和化疗耐药性有关。目前已开发出针对 EphA2 及其信号通路的分子、遗传、生化和药理学方法，旨在干扰其肿瘤促进效应或将其作为给药载体。这篇综述综述了 EphA2 的主要功能及其在骨肉瘤中的相关性，提供了利用这种受体进行诊断和治疗的策略，重点是其在三种最常见的骨肉瘤组织类型中的适用性：骨肉瘤、软骨肉瘤和尤文肉瘤。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Cell Communication and Signaling CELL BIOLOGY-

CiteScore

11.00

自引率

0.00%

发文量

180

期刊介绍： Cell Communication and Signaling (CCS) is a peer-reviewed, open-access scientific journal that focuses on cellular signaling pathways in both normal and pathological conditions. It publishes original research, reviews, and commentaries, welcoming studies that utilize molecular, morphological, biochemical, structural, and cell biology approaches. CCS also encourages interdisciplinary work and innovative models, including in silico, in vitro, and in vivo approaches, to facilitate investigations of cell signaling pathways, networks, and behavior. Starting from January 2019, CCS is proud to announce its affiliation with the International Cell Death Society. The journal now encourages submissions covering all aspects of cell death, including apoptotic and non-apoptotic mechanisms, cell death in model systems, autophagy, clearance of dying cells, and the immunological and pathological consequences of dying cells in the tissue microenvironment.

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