AMBRA1和FAK1:串扰改善黑色素瘤靶向治疗。

IF 2.6 Q3 ONCOLOGY Molecular and Cellular Oncology Pub Date : 2021-07-13 eCollection Date: 2021-01-01 DOI:10.1080/23723556.2021.1949955

Luca Di Leo, Daniela De Zio

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引用次数: 1

摘要

通过基因工程小鼠黑色素瘤模型，我们发现自噬/beclin 1调节因子1 (Ambra1)是黑色素瘤中新的肿瘤抑制因子。在这些情况下，Ambra1的缺失与局灶黏附激酶1 (Fak1)信号的过度激活有关，Fak1信号的抑制导致肿瘤生长和侵袭性降低。因此，我们提出FAK1抑制可用于AMBRA1-low肿瘤的当前黑色素瘤治疗。缩写:AKT，丝氨酸/苏氨酸激酶1;AMBRA1，自噬/beclin 1调节因子1;v-raf鼠肉瘤病毒癌基因同源物;BRAFi, BRAF抑制剂;欧洲可检索肿瘤细胞系数据库;FAK1, focal adhesion kinase 1;FAKi, FAK1抑制剂;利兹黑色素瘤队列;MAPK/ERK激酶;PP2A，蛋白磷酸酶2A;PTEN，磷酸酶和紧张素同源物;肿瘤基因组图谱-皮肤黑色素瘤;YAP, yes-associated protein

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AMBRA1 and FAK1: crosstalking for improved targeted therapy in melanoma.

Through genetically engineered mouse models of melanoma, we identified Autophagy/beclin 1 regulator 1 (Ambra1) as novel tumor-suppressor in melanoma. In these settings, loss of Ambra1 associated with the hyperactivation of focal adhesion kinase 1 (Fak1) signaling, the inhibition of which resulted in reduced tumor growth and invasiveness. We therefore propose FAK1 inhibition for current melanoma therapy in AMBRA1-low tumors.

Abbreviations: AKT, serine/threonine kinase 1; AMBRA1, autophagy/beclin 1 regulator 1; BRAF, v-raf murine sarcoma viral oncogene homolog; BRAFi, BRAF inhibitor; CCLE, Cancer Cell Line Encyclopedia;g ESTDAB, European Searchable Tumor Line Database; FAK1, focal adhesion kinase 1; FAKi, FAK1 inhibitor; LMC, Leeds Melanoma Cohort; MEK, MAPK/ERK kinase; PP2A, protein phosphatase 2A; PTEN, phosphatase and tensin homolog; TCGA-SKCM, The Cancer Genome Atlas - Skin Cutaneous Melanoma; YAP, yes-associated protein 1.

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来源期刊

Molecular and Cellular Oncology Biochemistry, Genetics and Molecular Biology-Cancer Research

CiteScore

3.20

自引率

0.00%

发文量

期刊介绍： For a long time, solid neoplasms have been viewed as relatively homogeneous entities composed for the most part of malignant cells. It is now clear that tumors are highly heterogeneous structures that evolve in the context of intimate interactions between cancer cells and endothelial, stromal as well as immune cells. During the past few years, experimental and clinical oncologists have witnessed several conceptual transitions of this type. Molecular and Cellular Oncology (MCO) emerges within this conceptual framework as a high-profile forum for the publication of fundamental, translational and clinical research on cancer. The scope of MCO is broad. Submissions dealing with all aspects of oncogenesis, tumor progression and response to therapy will be welcome, irrespective of whether they focus on solid or hematological neoplasms. MCO has gathered leading scientists with expertise in multiple areas of cancer research and other fields of investigation to constitute a large, interdisciplinary, Editorial Board that will ensure the quality of articles accepted for publication. MCO will publish Original Research Articles, Brief Reports, Reviews, Short Reviews, Commentaries, Author Views (auto-commentaries) and Meeting Reports dealing with all aspects of cancer research.