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低BOK表达通过Wnt信号通路促进乳腺癌细胞的上皮-间质转化和迁移。

Low BOK Expression Promotes Epithelial-Mesenchymal Transition and Migration via the Wnt Signaling Pathway in Breast Cancer Cells.

作者信息

Liu Ling, He Tiantian, Zhang Zhen, Dai Wenjie, Ding Liyang, Yang Hong, Xu Bo, Shang Yitong, Deng Yu, Fu Xufeng, Du Xing

机构信息

Key Laboratory of Fertility Preservation and Maintenance of Ministry of Education, School of Basic Medical Sciences, Ningxia Medical University, Yinchuan 750004, China.

出版信息

Int J Mol Sci. 2025 Jul 27;26(15):7252. doi: 10.3390/ijms26157252.

DOI:10.3390/ijms26157252
PMID:40806384
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12347190/
Abstract

The B-cell lymphoma 2 (Bcl-2)-related ovarian killer (BOK), a member of the Bcl-2 protein family, shares a similar domain structure and amino acid sequence homology with the pro-apoptotic family members BAX and BAK. Although BOK is involved in the development of various types of cancer, its mechanism of action in breast cancer remains unclear. This study found that BOK was involved in the process of MG132, inhibiting the migration and epithelial-mesenchymal transition (EMT) of breast cancer cells induced by transforming growth factor-β. Furthermore, interfering BOK reversed the inhibition of breast cancer cell migration and the EMT process by MG132. Additional studies revealed that BOK silencing promoted the expression of EMT-related markers in breast cancer cells, while BOK overexpression inhibited EMT and migration. Using RNA-seq sequencing and Western blotting, we confirmed that the Wnt signaling pathway is involved in BOK regulating the EMT process in breast cancer cells. Therefore, we conclude that low BOK expression promotes breast cancer EMT and migration by activating the Wnt signaling pathway. This study enhances our understanding of breast cancer pathogenesis and suggests that BOK may serve as a potential prognostic marker and therapeutic target for breast cancer.

摘要

B细胞淋巴瘤2（Bcl-2）相关卵巢杀手（BOK）是Bcl-2蛋白家族的成员，与促凋亡家族成员BAX和BAK具有相似的结构域结构和氨基酸序列同源性。尽管BOK参与多种类型癌症的发生发展，但其在乳腺癌中的作用机制仍不清楚。本研究发现，BOK参与MG132诱导的过程，抑制转化生长因子-β诱导的乳腺癌细胞迁移和上皮-间质转化（EMT）。此外，干扰BOK可逆转MG132对乳腺癌细胞迁移和EMT过程的抑制作用。进一步研究表明，沉默BOK可促进乳腺癌细胞中EMT相关标志物的表达，而过表达BOK则抑制EMT和迁移。通过RNA测序和蛋白质免疫印迹，我们证实Wnt信号通路参与BOK对乳腺癌细胞EMT过程的调控。因此，我们得出结论，低水平的BOK表达通过激活Wnt信号通路促进乳腺癌EMT和迁移。本研究加深了我们对乳腺癌发病机制的理解，并提示BOK可能作为乳腺癌潜在的预后标志物和治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b7c/12347190/3b021aaea5df/ijms-26-07252-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b7c/12347190/1bd4a3ae09fd/ijms-26-07252-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b7c/12347190/210da3c0e346/ijms-26-07252-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b7c/12347190/047582df1626/ijms-26-07252-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b7c/12347190/3b021aaea5df/ijms-26-07252-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b7c/12347190/1bd4a3ae09fd/ijms-26-07252-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b7c/12347190/210da3c0e346/ijms-26-07252-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b7c/12347190/047582df1626/ijms-26-07252-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b7c/12347190/3b021aaea5df/ijms-26-07252-g007.jpg

相似文献

[1]
Low BOK Expression Promotes Epithelial-Mesenchymal Transition and Migration via the Wnt Signaling Pathway in Breast Cancer Cells.

Int J Mol Sci. 2025-7-27

[2]
SIAH2-AS1 stimulates breast cancer cell proliferation and migration via the Wnt/β-catenin signaling pathway.

Sci Rep. 2025-7-1

[3]
Overexpression of Aquaporin-1 Promotes Epithelial-Mesenchymal Transition and Cancer Stem Cell Properties via Wnt/β-Catenin Signaling Pathway in Advanced Breast Cancer Cells.

Mol Carcinog. 2025-9

[4]
Lysine demethylase 2A promotes the progression of ovarian cancer by regulating the PI3K pathway and reversing epithelial‑mesenchymal transition.

Oncol Rep. 2018-11-27

[5]
PLIN2 promotes colorectal cancer progression through CD36-mediated epithelial-mesenchymal transition.

Cell Death Dis. 2025-7-10

[6]
PLAGL2 as a prognostic biomarker and an EMT-promoting factor in PDAC.

Sci Rep. 2025-7-14

[7]
siRNA treatment targeting integrin α11 overexpressed via EZH2-driven axis inhibits drug-resistant breast cancer progression.

Breast Cancer Res. 2024-4-25

[8]
A New Treatment Strategy for Lung Cancer With HDAC and Wnt/β-Catenin Pathway Inhibitors.

IUBMB Life. 2025-7

[9]
POC1A induces epithelial-mesenchymal transition to promote growth and metastasis through the STAT3 signaling pathway in triple-negative breast cancer.

Mol Med. 2025-8-19

[10]
Inhibitory Impact of the Amino Benzoic Derivative DAB-2-28 on the Process of Epithelial-Mesenchymal Transition in Human Breast Cancer Cells.

Molecules. 2025-8-5

本文引用的文献

[1]
Cancer statistics, 2024.

CA Cancer J Clin. 2024

[2]
Gain-of-Function p53 Mutation Acts as a Genetic Switch for TGFβ Signaling-Induced Epithelial-to-Mesenchymal Transition in Intestinal Tumors.

Cancer Res. 2024-1-2

[3]
Sequential Ubiquitination and Phosphorylation Epigenetics Reshaping by MG132-Loaded Fe-MOF Disarms Treatment Resistance to Repulse Metastatic Colorectal Cancer.

Adv Sci (Weinh). 2023-8

[4]
Bok: real killer or bystander with non-apoptotic roles?

Front Cell Dev Biol. 2023-4-12

[5]
BCL-2 protein family: attractive targets for cancer therapy.

Apoptosis. 2023-2

[6]
EMT mechanism in breast cancer metastasis and drug resistance: Revisiting molecular interactions and biological functions.

Biomed Pharmacother. 2022-11

[7]
BOK controls ER proteostasis and physiological ER stress responses in neurons.

Front Cell Dev Biol. 2022-8-15

[8]
Targeting TGF-β signal transduction for fibrosis and cancer therapy.

Mol Cancer. 2022-4-23

[9]
SARS-CoV-2 membrane protein causes the mitochondrial apoptosis and pulmonary edema via targeting BOK.

Cell Death Differ. 2022-7

[10]
A proteomic analysis of Bcl-2 regulation of cell cycle arrest: insight into the mechanisms.

J Zhejiang Univ Sci B. 2021-10-15

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