Serpin peptidase inhibitor, clade E nexin group 1 promotes cellular proliferative capacities and malignant behaviors in glioblastoma through upregulating hairy and enhancer of split-1.
Tao Ma, Kai Qian, Tuoye Xu, Xi Wang, Tengda Qian, Jing Shi, Lixin Li
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引用次数: 0
Abstract
Purpose: Glioblastoma (GBM) remains one of the most fatal malignancy with limited available treatment. Serpin peptidase inhibitor, clade E nexin group 1 (SERPINE1) was found up-regulated in multiple cancers and play crucial roles in facilitating tumor progression and metastasis respectively. However, the role of SERPINE1 in glioblastoma was poorly understood.
Methods: We tested the hypothesis that SERPINE1 mediated malignant behaviors in GBM via regulating hairy and enhancer of split-1 (HES1).
Results: First, SERPINE1 is confirmed to be up-regulated in GBM, while further functional analysis demonstrated that SERPINE1 promoted cell proliferation, migration and invasion in GBM by performing the CCK-8 assay, colony formation assay, wound healing assay and transwell assay. Finally, it was proved that SERPINE1 achieved its pro-tumor functions in GBM via regulating the expression of HES1.
Conclusions: Collectively, our results highlight the critical contribution of SERPINE1 in a series of malignant characteristics of GBM via regulating the expression of HES1, which shed new light on a new direction to develop a more effective therapeutic management of malignant tumors like GBM.
期刊介绍：
JBUON aims at the rapid diffusion of scientific knowledge in Oncology.
Its character is multidisciplinary, therefore all aspects of oncologic activities are welcome including clinical research (medical oncology, radiation oncology, surgical oncology, nursing oncology, psycho-oncology, supportive care), as well as clinically-oriented basic and laboratory research, cancer epidemiology and social and ethical aspects of cancer. Experts of all these disciplines are included in the Editorial Board.
With a rapidly increasing body of new discoveries in clinical therapeutics, the molecular mechanisms that contribute to carcinogenesis, advancements in accurate and early diagnosis etc, JBUON offers a free forum for clinicians and basic researchers to make known promptly their achievements around the world.
With this aim JBUON accepts a broad spectrum of articles such as editorials, original articles, reviews, special articles, short communications, commentaries, letters to the editor and correspondence among authors and readers.
JBUON keeps the characteristics of its former paper print edition and appears as a bimonthly e-published journal with continuous volume, issue and page numbers.
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