在乳腺癌中偶联PI3Kα和WNT/β-catenin信号的晚期核内体信号中枢。

IF 2.6 Q3 ONCOLOGY Molecular and Cellular Oncology Pub Date : 2021-09-09 eCollection Date: 2021-01-01 DOI:10.1080/23723556.2021.1954470

Samuel J Rodgers, Sabryn A Hamila, Christina A Mitchell, Lisa M Ooms

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引用次数: 0

摘要

AKT是中心磷酸肌醇激酶(PI3K)信号效应因子，然而，PIK3CA (PI3K α的p110α亚基)突变型雌激素受体阳性(ER+)乳腺癌表现出最小的AKT激活，下游信号传导特征不明显。我们发现，pik3ca突变型ER+乳腺癌的一个亚群表现出肌醇多磷酸4-磷酸酶II型(INPP4B)表达增加，这促进了内核体的晚期形成和糖原合成酶激酶3β (GSK3β)的运输，导致无翼相关整合位点(WNT)/连环蛋白β 1 (β-连环蛋白)的激活增强。

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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A late endosome signaling hub that couples PI3Kα and WNT/β-catenin signaling in breast cancer.

AKT is the central phosphoinositide 3-kinase (PI3K) signaling effector, however, PIK3CA (p110α subunit of PI3Kα)-mutant estrogen receptor-positive (ER⁺) breast cancers exhibit minimal AKT activation and the downstream signaling is poorly characterized. We discovered that a subset of PIK3CA-mutant ER⁺ breast cancers exhibit increased inositol polyphosphate 4-phosphatase type II (INPP4B) expression, which promotes late endosome formation and glycogen synthase kinase 3 beta (GSK3β) trafficking, leading to enhanced Wingless-related integration site (WNT)/catenin beta 1 (β-catenin) activation.

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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%

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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.