Heat shock protein 47 (HSP47), also known as SERPINH1, is a product of CBP2 gene located at chromosome 11q13.5, a region frequently amplified in human cancers. HSP47 has been demonstrated to effect on limiting tumor invasion and motility. The previous studies showed that HSP47 is overexpressed in many human cancers, including stomach cancer, lung cancer, pancreatic ductal adenocarcinoma, and ulcerative colitis-associated carcinomas. However, the role of HSP47 in human glioma is still unknown. Here, we examined the expression of HSP47 in a group of glioma tumors and matched non-tumor brain tissues using qRT-PCR. We found that HSP47 is significantly overexpressed in glioma tissues and cell lines and associated with glioma tumor grade. Next, we knockdown the expression of HSP47 in the glioma cells using small interfering RNAs. The result showed that knockdown of HSP47 inhibits glioma cell growth, migration and invasion in vitro. We further investigated the posttranscriptional regulation of HSP47 by microRNAs using bioinformatics analysis and experimental validation. The results suggested that the expression of HSP47 is regulated by miR-29a. Finally, stable knockdown of HSP47 using shRNA inhibits glioma tumor growth and induces apoptosis in mice models in vivo. Therefore, our data suggested that HSP47 regulated by miR-29a to enhance glioma tumor growth and invasion. Taken together, HSP47 plays important role in tumor growth and invasion and thus could be a therapeutic target for treating glioma in the future.
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http://dx.doi.org/10.1007/s11060-014-1412-7 | DOI Listing |
Neurosurg Rev
January 2025
Department of Neurosurgery, Shariati Hospital, Tehran University of Medical Sciences, Tehran, Iran.
The optimal therapeutic intervention for pediatrics with optic pathway glioma (OPG) remained controversial in the literature. Recently, due to substantial adverse events (AEs) of chemotherapy and its impact on children's lives, the efficacy of other options has been investigated. Bevacizumab (BVZ) is an anti-vascular endothelial growth factor (VEGF) agent that alters the lesion microenvironment.
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January 2025
Neurology Unit, Department of Medicine, Faculty of Medicine, Prince of Songkla University, Songkhla, Thailand.
Astrocytoma is a common type of glioma and a frequent cause of brain tumour-related epilepsy. Although the link between glioma and epilepsy is well established, the precise mechanisms underlying epileptogenesis in astrocytoma remain poorly understood. In this study, we performed proteomic analysis of astrocytoma tissue from patients with and without seizures using mass spectrometry-based techniques.
View Article and Find Full Text PDFChem Biol Interact
January 2025
Department of Biological Chemistry, Medical School, National and Kapodistrian University of Athens, 11527 Athens, Greece. Electronic address:
Gliomas constitute the most prevalent primary central nervous system tumors, often characterized by complex metabolic profile, genomic instability, and aggressiveness, leading to frequent relapse and high mortality rates. Traditional treatments are commonly ineffective because of gliomas increased heterogeneity, invasive characteristics and resistance to chemotherapy. Among several pathways affecting cellular homeostasis, cuproptosis has recently emerged as a novel type of programmed cell death, triggered by accumulation of copper ions.
View Article and Find Full Text PDFCancer Lett
January 2025
School of Life Sciences, Peking University Third Hospital Cancer Center, Center for Life Sciences, State Key Laboratory of Membrane Biology, IDG/McGovern Institute for Brain Research, Peking University, Beijing, 100871, China; Peking Union Medical College Hospital, Beijing, 100730, China. Electronic address:
It has become increasingly recognized that neural signals can profoundly influence the prognosis of various cancer types. In the past years, we have witnessed "cancer neuroscience," which primarily focuses on the complex crosstalk between tumors and neural signals, emerging as a new, multidisciplinary direction of biomedical science. This review aims to summarize the current knowledge of this research frontier, with an emphasis on the neuroimmune mechanisms enacted through the reciprocal interactions between tumors and the central or peripheral nervous system.
View Article and Find Full Text PDFNeuron
January 2025
Department of Pathology and Krantz Family Center for Cancer Research, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA; Broad Institute of Harvard and MIT, Cambridge, MA 02142, USA. Electronic address:
Writing in Neuron, Zhang et al. identify a subpopulation of glioblastoma cells from patient tumor samples with progenitor-like features that expresses the potassium ion channel KCND2. In mouse and organoid models, these cells enhance neural activity at the glioma-neural interface.
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