乳腺癌趋化因子CXCR4和CXCR7受体的溶瘤腺病毒载体CXCL12重靶向研究

Samia M O'Bryan, J Michael Mathis
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引用次数: 2

摘要

乳腺癌是60岁以下女性中最常见的癌症,也是60岁以上女性中第二常见的癌症。虽然在开发针对乳腺癌的靶向疗法方面取得了重大进展,但晚期乳腺癌的死亡率仍然很高,5年生存率很低。因此,目前的治疗方法不足以治疗晚期乳腺癌;迫切需要新的治疗方法来解决晚期乳腺癌的复杂性。溶瘤病毒疗法作为一种能够全身给药,靶向癌细胞,并保留正常组织的治疗方法已被探索。特别是,溶瘤腺病毒由于其易于操作、生产和临床安全性而被用作病毒载体。在这项研究中,我们设计了一种溶瘤腺病毒来靶向趋化因子受体CXCR4和CXCR7。CXCR4和CXCR7的过表达与乳腺癌的发生、生存、发展和转移有关。这两种受体都与配体CXCL12 (SDF-1)结合,该配体已被确定在乳腺癌细胞转移中起关键作用。本研究将与CXCL12融合的T4纤维蛋白纳入腺病毒纤维的尾部结构域,将载体重新靶向到CXCR4和CXCR7趋化因子受体。我们发现,与野生型对照载体相比,修饰后的病毒更有效地靶向和感染过表达CXCR4-和cxcr7的乳腺癌细胞。此外,用修饰的嵌合纤维替代野生型纤维和旋叶不影响溶瘤能力。总之,本研究的结果证明了将腺病毒载体重靶向趋化因子受体阳性肿瘤的可行性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
CXCL12 Retargeting of an Oncolytic Adenovirus Vector to the Chemokine CXCR4 and CXCR7 Receptors in Breast Cancer.

Breast cancer is the most frequently diagnosed cancer in women under 60, and the second most diagnosed cancer in women over 60. While significant progress has been made in developing targeted therapies for breast cancer, advanced breast cancer continues to have high mortality, with poor 5-year survival rates. Thus, current therapies are insufficient in treating advanced stages of breast cancer; new treatments are sorely needed to address the complexity of advanced-stage breast cancer. Oncolytic virotherapy has been explored as a therapeutic approach capable of systemic administration, targeting cancer cells, and sparing normal tissue. In particular, oncolytic adenoviruses have been exploited as viral vectors due to their ease of manipulation, production, and demonstrated clinical safety profile. In this study, we engineered an oncolytic adenovirus to target the chemokine receptors CXCR4 and CXCR7. The overexpression of CXCR4 and CXCR7 is implicated in the initiation, survival, progress, and metastasis of breast cancer. Both receptors bind to the ligand, CXCL12 (SDF-1), which has been identified to play a crucial role in the metastasis of breast cancer cells. This study incorporated a T4 fibritin protein fused to CXCL12 into the tail domain of an adenovirus fiber to retarget the vector to the CXCR4 and CXCR7 chemokine receptors. We showed that the modified virus targets and infects CXCR4- and CXCR7-overexpressing breast cancer cells more efficiently than a wild-type control vector. In addition, the substitution of the wild-type fiber and knob with the modified chimeric fiber did not interfere with oncolytic capability. Overall, the results of this study demonstrate the feasibility of retargeting adenovirus vectors to chemokine receptor-positive tumors.

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