| Literature DB >> 33441062 |
Amir R Afshari1, Ali Motamed-Sanaye2, Hamed Sabri3, Arash Soltani3, Sepideh Karkon-Shayan2, Sarvin Radvar4, Hossein Javid3, Hamid Mollazadeh5, Thozhukat Sathyapalan6, Amirhossein Sahebkar7.
Abstract
The current standard of care in glioblastoma multiforme (GBM), as the most morbid brain tumor, is not adequate, despite substantial progress in cancer therapy. Among patients receiving current standard treatments, including surgery, irradiation, and chemotherapy, the overall survival (OS) period with GBM is less than one year. The high mortality frequency of GBM is due to its aggressive nature, including accelerated growth, deregulated apoptosis, and invasion into surrounding tissues. The understanding of the molecular pathogenesis of GBM is, therefore, crucial for identifying, designing, and repurposing potential agents in future therapeutic approaches. In recent decades, it has been apparent that several neurotransmitters, specifically substance P (SP), an undecapeptide in the family of neuropeptides tachykinins, are found in astrocytes. After binding to the neurokinin-1 receptor (NK-1R), the SP controls cancer cell growth, exerts antiapoptotic impacts, stimulates cell invasion/metastasis, and activates vascularization. Since SP/NK-1R signaling pathway is a growth driver in many cancers, this potential mechanism is proposed as an additional target for treating GBM. Following an evaluation of the function of both SP and its NK-1R inhibitors in neoplastic cells, we recommend a unique and promising approach for the treatment of patients with GBM. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.Entities:
Keywords: GBM; Glioblastoma multiforme; NK1R antagonists.; Neurokinin-1 receptor (NK-1R); apoptosis; substance P
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Year: 2021 PMID: 33441062 DOI: 10.2174/0929867328666210113165805
Source DB: PubMed Journal: Curr Med Chem ISSN: 0929-8673 Impact factor: 4.530