TP53INP1 inhibits hypoxia‐induced vasculogenic mimicry formation via the ROS/snail signalling axis in breast cancer

التفاصيل البيبلوغرافية
العنوان: TP53INP1 inhibits hypoxia‐induced vasculogenic mimicry formation via the ROS/snail signalling axis in breast cancer
المؤلفون: Yanlei Li, Fang Liu, Huizhi Sun, Danfang Zhang, Yanhui Zhang, Dan Fan, Yi Wang, Chunsheng Ni, Shiqi Liu, Xueyi Dong, Zhao Yang, Xiulan Zhao
المصدر: Journal of Cellular and Molecular Medicine
بيانات النشر: John Wiley and Sons Inc., 2018.
سنة النشر: 2018
مصطلحات موضوعية: 0301 basic medicine, Snail, Mice, 0302 clinical medicine, Cell Movement, Nuclear protein, vasculogenic mimicry, Heat-Shock Proteins, medicine.diagnostic_test, biology, Chemistry, Middle Aged, Cadherins, Hedgehog signaling pathway, 030220 oncology & carcinogenesis, Molecular Medicine, Original Article, Female, medicine.symptom, Signal Transduction, TP53INP1, Epithelial-Mesenchymal Transition, Breast Neoplasms, 03 medical and health sciences, Breast cancer, breast cancer, Western blot, Antigens, CD, biology.animal, Cell Line, Tumor, medicine, Animals, Humans, Vasculogenic mimicry, Epithelial–mesenchymal transition, epithelial‐mesenchymal transition, Glycogen Synthase Kinase 3 beta, hypoxia, Cell Biology, Original Articles, Hypoxia (medical), medicine.disease, Hypoxia-Inducible Factor 1, alpha Subunit, Xenograft Model Antitumor Assays, 030104 developmental biology, Cancer research, Tumor Hypoxia, Snail Family Transcription Factors, Carrier Proteins, Reactive Oxygen Species
الوصف: Tumour protein p53‐inducible nuclear protein 1 (TP53INP1) is a tumour suppressor associated with malignant tumour metastasis. Vasculogenic mimicry (VM) is a new tumour vascular supply pattern that significantly influences tumour metastasis and contributes to a poor prognosis. However, the molecular mechanism of the relationship between TP53INP1 and breast cancer VM formation is unknown. Here, we explored the underlying mechanism by which TP53INP1 regulates VM formation in vitro and in vivo. High TP53INP1 expression was not only negatively correlated with a poor prognosis but also had a negative relationship with VE‐cadherin, HIF‐1α and Snail expression. TP53INP1 overexpression inhibited breast cancer invasion, migration, epithelial‐mesenchymal transition (EMT) and VM formation; conversely, TP53INP1 down‐regulation promoted these processes in vitro by functional experiments and Western blot analysis. We established a hypoxia model induced by CoCl2 and assessed the effects of TP53INP1 on hypoxia‐induced EMT and VM formation. In addition, we confirmed that a reactive oxygen species (ROS)‐mediated signalling pathway participated in TP53INP1‐mediated VM formation. Together, our results show that TP53INP1 inhibits hypoxia‐induced EMT and VM formation via the ROS/GSK‐3β/Snail pathway in breast cancer, which offers new insights into breast cancer clinical therapy.
اللغة: English
تدمد: 1582-4934
1582-1838
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::78f07621459b985c95b5113491841103Test
http://europepmc.org/articles/PMC6010892Test
حقوق: OPEN
رقم الانضمام: edsair.doi.dedup.....78f07621459b985c95b5113491841103
قاعدة البيانات: OpenAIRE