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IGHG1 通过调节 AKT 和 VEGF 信号通路促进乳腺癌细胞的恶性进展。

IGHG1 promotes malignant progression in breast cancer cells through the regulation of AKT and VEGF signaling.

机构信息

Department of Surgery, Guang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, China.

Department of Oncology, Beijing Puxiang Traditional Chinese Medicine Cancer Hospital, Beijing, China.

出版信息

Biomol Biomed. 2023 Jul 3;23(4):616-623. doi: 10.17305/bb.2022.8508.

DOI:10.17305/bb.2022.8508
PMID:36883223
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10351095/
Abstract

Immunoglobulin heavy constant chain gamma 1 (IGHG1) is highly expressed in a variety of cancers and is considered an emerging prognostic marker. Overexpression of IGHG1 in breast cancer tissues has also been demonstrated, but an in-depth analysis of its role in disease progression has not been explored. In this study, we used a range of molecular and cell-based assays to show that increased expression of IGHG1 in breast cancer cells activates AKT and vascular endothelial growth factor (VEGF) signaling, leading to enhanced cell proliferation, invasion, and angiogenesis. We further showed that IGHG1-silencing can suppress the neoplastic characteristics of breast cancer cells in vitro and suppresses tumor growth in nude mice. These data reveal a key role of IGHG1 in the malignant progression of breast cancer cells and highlight its potential as a prognostic marker and therapeutic target to control metastasis and angiogenesis in malignant breast tissue.

摘要

免疫球蛋白重链恒定区γ1(IGHG1)在多种癌症中高度表达,被认为是一种新兴的预后标志物。已经证明乳腺癌组织中IGHG1 的过表达,但对其在疾病进展中的作用的深入分析尚未探讨。在这项研究中,我们使用一系列分子和基于细胞的测定法表明,乳腺癌细胞中IGHG1 的表达增加会激活 AKT 和血管内皮生长因子 (VEGF) 信号通路,导致细胞增殖、侵袭和血管生成增强。我们进一步表明,IGHG1 沉默可以抑制体外乳腺癌细胞的肿瘤特征,并抑制裸鼠肿瘤生长。这些数据揭示了 IGHG1 在乳腺癌细胞恶性进展中的关键作用,并强调了其作为预后标志物和治疗靶点的潜力,以控制恶性乳腺组织中的转移和血管生成。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/76d9/10351095/91223528870d/bb-2023-8508f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/76d9/10351095/b878f312d69e/bb-2023-8508f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/76d9/10351095/b0f7aa3c0f3d/bb-2023-8508f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/76d9/10351095/774323c37031/bb-2023-8508f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/76d9/10351095/5b23dee87779/bb-2023-8508f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/76d9/10351095/91223528870d/bb-2023-8508f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/76d9/10351095/b878f312d69e/bb-2023-8508f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/76d9/10351095/b0f7aa3c0f3d/bb-2023-8508f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/76d9/10351095/774323c37031/bb-2023-8508f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/76d9/10351095/5b23dee87779/bb-2023-8508f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/76d9/10351095/91223528870d/bb-2023-8508f5.jpg

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本文引用的文献

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2
Down-regulation of IGHG1 enhances Protoporphyrin IX accumulation and inhibits hemin biosynthesis in colorectal cancer by suppressing the MEK-FECH axis.IGHG1的下调通过抑制MEK-FECH轴增强了原卟啉IX的积累并抑制了结直肠癌中的血红素生物合成。
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IGHG1 upregulation promoted gastric cancer malignancy via AKT/GSK-3β/β-Catenin pathway.
单细胞 RNA 测序揭示了人下咽鳞癌及其淋巴转移中的肿瘤免疫微环境。
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IGHG1 induces EMT in gastric cancer cells by regulating TGF-β/SMAD3 signaling pathway.IGHG1通过调节TGF-β/SMAD3信号通路诱导胃癌细胞发生上皮-间质转化。
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