Zinc finger protein 367 promotes metastasis by inhibiting the Hippo pathway in breast cancer

Oncogene ◽  
2020 ◽  
Vol 39 (12) ◽  
pp. 2568-2582 ◽  
Author(s):  
Xianqiu Wu ◽  
Xin Zhang ◽  
Liang Yu ◽  
Chen Zhang ◽  
Liping Ye ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Zinc Finger ◽  
Zinc Finger Protein ◽  
Hippo Pathway ◽  
Finger Protein ◽  
The Hippo Pathway

scholarly journals ZNF213 Facilitates ER Alpha Signaling in Breast Cancer Cells

2021 ◽  
Vol 11 ◽  
Author(s):  
Huijie Yang ◽  
Xulei Lv ◽  
Xin Li ◽  
Lanzhi Mao ◽  
Zhiguo Niu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Protein Stability ◽  
Cancer Cells ◽  
Zinc Finger ◽  
Breast Cancer Cells ◽  
Zinc Finger Protein ◽  
Luciferase Assay ◽  
Finger Protein ◽  
Er Alpha ◽  
Positive Breast Cancer

BackgroundBreast cancer is the most common women malignancy worldwide, while estrogen receptor alpha positive type accounts for two third of all breast cancers. Although ER alpha positive breast cancer could be effectively controlled by endocrine therapy, more than half of the cases could develop endocrine resistance, making it an important clinical issue in breast cancer treatment. Thus, decoding the detailed mechanism, which controls ER alpha signaling activation and ER alpha protein stability, is of great importance for the improvement of breast cancer therapy. Several zinc finger proteins were shown to mediate the ubiquitination process and modulate protein stability. Thus, we further explore the function of Zinc finger protein 213 on ER alpha protein stability and tamoxifen resistance.MethodsCCK8 and Edu assay was used to measure cell proliferation. RNA sequence was performed by Ingenuity pathway analysis. The ER alpha signaling activities were measured with luciferase assay, real-time quantitative PCR, and western blotting. Protein stability assay and ubiquitin assay were used to determine ER alpha protein degradation and ubiquitination. The immuno-precipitation was utilized to determine ER alpha and ZNF213 interaction. The ubiquitin-based immuno-precipitation assay was sued to detect specific ubiquitination manner on ER alpha.ResultsWe identified ZNF213 as a novel zinc finger protein, which modulated ER alpha protein. ZNF213 expression correlated with poor outcome in endocrine treated patients. ZNF213 depletion inhibited ER alpha signaling and proliferation in breast cancer cells. Further mechanistic studies showed ZNF213 located in cytosol and nuclear, which modulated ER alpha stability via inhibiting ER alpha K48-linked ubiquitination.ConclusionsOur study reveals an interesting post-translational mechanism between ER alpha and ZNF213 in breast cancer. Targeting ZNF213 could be an appealing strategy for ER alpha positive breast cancer.

scholarly journals Expression of zinc-finger protein X-linked, ZFX, is associated with enhanced survival in patients with breast cancer.

2020 ◽  
Author(s):  
Shahan Mamoor
Keyword(s):  
Breast Cancer ◽  
Zinc Finger ◽  
Survival Data ◽  
Zinc Finger Protein ◽  
Metastatic Breast ◽  
Stage Iv ◽  
Metastatic Tumor ◽  
Finger Protein ◽  
Tumor Tissues ◽  
Protein X

We mined published tumor transcriptome data with paired survival data to discover genes associated with survival outcomes in breast cancer (1, 2). We found that the zinc-finger protein X-linked ZFX (3, 4) was among the genes most differentially expressed in both primary and metastatic tumor tissues when comparing tumor transcriptomes based on survival at 24 months. ZFX expression was significantly higher in the metastatic tumors of patients surviving greater than 24 months, suggesting that increased ZFX expression confers a survival benefit to patients with stage IV metastatic breast cancer.

scholarly journals Zinc finger protein 143 expression is closely related to tumor malignancy via regulating cell motility in breast cancer

BMB Reports ◽  
2017 ◽  
Vol 50 (12) ◽  
pp. 621-627 ◽  
Author(s):  
A Rome Paek ◽  
Ji Young Mun ◽  
Kyeong-Man Hong ◽  
Jongkeun Lee ◽  
Dong Wan Hong ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Motility ◽  
Zinc Finger ◽  
Zinc Finger Protein ◽  
Finger Protein

scholarly journals The tumor suppressor Zinc finger protein 471 suppresses breast cancer growth and metastasis through inhibiting AKT and Wnt/β-catenin signaling

2020 ◽  
Vol 12 (1) ◽  
Author(s):  
Chunfang Tao ◽  
Juan Luo ◽  
Jun Tang ◽  
Danfeng Zhou ◽  
Shujun Feng ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Tumor Suppressor ◽  
Tumor Cell ◽  
Zinc Finger ◽  
Molecular Mechanisms ◽  
Zinc Finger Protein ◽  
Ectopic Expression ◽  
Surgical Margin ◽  
Mesenchymal Transition ◽  
Finger Protein

Abstract Background Zinc-finger protein 471 (ZNF471) is a member of the Krüppel-associated box domain zinc finger protein (KRAB-ZFP) family. ZNF471 is methylated in squamous cell carcinomas of tongue, stomach and esophageal. However, its role in breast carcinogenesis remains elusive. Here, we studied its expression, functions, and molecular mechanisms in breast cancer. Methods We examined ZNF471 expression by RT-PCR and qPCR. Methylation-specific PCR determined its promoter methylation. Its biological functions and related molecular mechanisms were assessed by CCK-8, clonogenicity, wound healing, Transwell, nude mice tumorigenicity, flow cytometry, BrdU-ELISA, immunohistochemistry and Western blot assays. Results ZNF471 was significantly downregulated in breast cell lines and tissues due to its promoter CpG methylation, compared with normal mammary epithelial cells and paired surgical-margin tissues. Ectopic expression of ZNF471 substantially inhibited breast tumor cell growth in vitro and in vivo, arrested cell cycle at S phase, and promoted cell apoptosis, as well as suppressed metastasis. Further knockdown of ZNF471 verified its tumor-suppressive effects. We also found that ZNF471 exerted its tumor-suppressive functions through suppressing epithelial-mesenchymal transition, tumor cell stemness and AKT and Wnt/β-catenin signaling. Conclusions ZNF471 functions as a tumor suppressor that was epigenetically inactivated in breast cancer. Its inhibition of AKT and Wnt/β-catenin signaling pathways is one of the mechanisms underlying its anti-cancer effects.

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