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

Wu, Xiao; Zhang, Xin; Yu, Liang; Zhang, Chen; Ye, Liping; Ren, Dong; Li, Yue; Sun, Xiao‐Feng; Yu, Lefan; Ouyang, Ying; Chen, Xiangfu; Song, Libing; Liu, Pian; Lin, Xi

doi:10.1038/s41388-020-1166-y

Cited by 34 publications

(28 citation statements)

References 38 publications

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“…The studies of VP in breast cancer mainly focus on TNBC MDA-MB-231 cells, VP (1 μmol/L) inhibits the growth of the paclitaxel-resistant breast cancer cell line MDA-MB-231 [ 28 ], VP (10 μM, 3 h) reduced the expression of YAP in the ZNF367-overexpressing breast cancer MDA-MB-231 and 4 T1 cells, and significantly reduced lung metastases in mouse models [ 33 ], and sensitizes the HER-2 positive breast cancer cell line HCC1569 to lapatinib [ 34 ]. The purpose of this study was to explore the effect of VP on different subtypes of BC and its mechanism by targeting YAP gene under the condition of non-photoactivation.…”

Section: Discussionmentioning

confidence: 99%

Verteporfin inhibits cell proliferation and induces apoptosis in different subtypes of breast cancer cell lines without light activation

Wei

2020

BMC Cancer

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Background Breast cancer (BC) can be divided into five subtypes: Lumina1A, Lumina1B, HER-2 overexpression, Basal-like and Normal breast-like subtype, based on the differently expressed genes in breast cancer tissue. The Hippo signaling pathway plays an indispensable role in BC. The YAP gene is a terminal effector of Hippo pathway, and hyperactivation of YAP mediates tumorigenesis. As an inhibitor of YAP, non-photoactivated verteporfin (VP) can inhibit YAP-mediated tumor proliferation and angiogenesis by eliminating its interaction with TEAD. This study aimed to determine the effect and molecular mechanisms of VP-mediated inhibition of YAP in different subtypes of BC. Methods Luminal A, Luminal B and Basal-like BC cells were cultivated in vitro to study effects of VP on proliferation and apoptosis of these three molecular BC subtypes. Results Our experimental results showed that VP inhibited cell proliferation, YAP-TEAD interaction and expression of its downstream targets. VP also induced tumor cell apoptosis, and promoted the cleavage of Caspase-9 and PARP in the cells of various molecular subtypes of BC. Conclusion These findings provide a basis for the use of VP as a potential anti-tumor therapeutic for BC by targeting the Hippo pathway effector YAP.

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Section: Discussionmentioning

confidence: 99%

Verteporfin inhibits cell proliferation and induces apoptosis in different subtypes of breast cancer cell lines without light activation

Wei

2020

BMC Cancer

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“…They induce EMT through the transcriptional downregulation of E-cadherin (CDH1) while upregulation of mesenchymal-specific genes of Snail Family Transcriptional Repressor 1/2 (SNAI1/ SNA2), Zinc Finger E-Box Binding Homeobox 1/2 (ZEB1/2), Twist basic helix-loop-helix transcription factor 1/2 (TWIST1/2), Forkhead Box C1/2 (FOXC1/2), Transcription factor 3 (TCF3), Goosecoid Homeobox (GSC) [11]. Additional to these transcription factors, a substantial number of recent studies provided evidence in the involvement of other types of proteins including proto-oncogene Cellular Oncogene Fos (c-FOS), Zinc finger protein 367 (ZNF367), ribosomal protein RPL15, RNA-binding protein A-Kinase Anchor Protein (AKAP8) in regulation of breast cancer metastasis [12][13][14][15][16]. However, for understanding the cellular transition mechanisms lying in the heart of breast cancer metastasis, it is very important to shed light over the epigenetic mechanisms besides these regulations.…”

Section: Introductionmentioning

confidence: 99%

A three layered histone epigenetics in breast cancer metastasis

2020

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Thanks to the advancement in science and technology and a significant number of cancer research programs being carried out throughout the world, the prevention, prognosis and treatment of breast cancer are improving with a positive and steady pace. However, a stern thoughtful attention is required for the metastatic breast cancer casesthe deadliest of all types of breast cancer, with a character of relapse even when treated. In an effort to explore the less travelled avenues, we summarize here studies underlying the aspects of histone epigenetics in breast cancer metastasis. Authoritative reviews on breast cancer epigenetics are already available; however, there is an urgent need to focus on the epigenetics involved in metastatic character of this cancer. Here we put forward a comprehensive review on how different layers of histone epigenetics comprising of histone chaperones, histone variants and histone modifications interplay to create breast cancer metastasis landscape. Finally, we propose a hypothesis of integrating histone-epigenetic factors as biomarkers that encompass different breast cancer subtypes and hence could be exploited as a target of larger population.

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“…Interestingly, a recent analysis of TCGA GBM samples [ 31 ] revealed that only 1.5% (3/201) of genes associated with unfavorable prognosis in GBM are ZNF genes, while 18% (12/67) of genes associated with favorable prognosis in GBM are ZNF genes. However, (KRAB-)ZNFs may be double-edged swords since they could act as both tumor suppressors or oncogenes [ 5 , 32 , 33 ]. Even one ZNF can play different roles in different cancer types and upon various stimuli.…”

Section: Discussionmentioning

confidence: 99%

Decreased Expression of ZNF554 in Gliomas is Associated with the Activation of Tumor Pathways and Shorter Patient Survival

Balogh

Reiniger

Hetey

et al. 2020

IJMS

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Zinc finger protein 554 (ZNF554), a member of the Krüppel-associated box domain zinc finger protein subfamily, is predominantly expressed in the brain and placenta in humans. Recently, we unveiled that ZNF554 regulates trophoblast invasion during placentation and its decreased expression leads to the early pathogenesis of preeclampsia. Since ZNF proteins are immensely implicated in the development of several tumors including malignant tumors of the brain, here we explored the pathological role of ZNF554 in gliomas. We examined the expression of ZNF554 at mRNA and protein levels in normal brain and gliomas, and then we searched for genome-wide transcriptomic changes in U87 glioblastoma cells transiently overexpressing ZNF554. Immunohistochemistry of brain tissues in our cohort (n = 62) and analysis of large TCGA RNA-Seq data (n = 687) of control, oligodendroglioma, and astrocytoma tissues both revealed decreased expression of ZNF554 towards higher glioma grades. Furthermore, low ZNF554 expression was associated with shorter survival of grade III and IV astrocytoma patients. Overexpression of ZNF554 in U87 cells resulted in differential expression, mostly downregulation of 899 genes. The “PI3K-Akt signaling pathway”, known to be activated during glioma development, was the most impacted among 116 dysregulated pathways. Most affected pathways were cancer-related and/or immune-related. Congruently, cell proliferation was decreased and cell cycle was arrested in ZNF554-transfected glioma cells. These data collectively suggest that ZNF554 is a potential tumor suppressor and its decreased expression may lead to the loss of oncogene suppression, activation of tumor pathways, and shorter survival of patients with malignant glioma.

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

Cited by 34 publications

References 38 publications

Verteporfin inhibits cell proliferation and induces apoptosis in different subtypes of breast cancer cell lines without light activation

Verteporfin inhibits cell proliferation and induces apoptosis in different subtypes of breast cancer cell lines without light activation

A three layered histone epigenetics in breast cancer metastasis

Decreased Expression of ZNF554 in Gliomas is Associated with the Activation of Tumor Pathways and Shorter Patient Survival

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