Affiliation:
1. Department of Pharmaceutical Chemistry, Poona College of Pharmacy, Bharati Vidyapeeth (Deemed to be University),
Erandwane, Pune- 411038, Maharashtra, India
2. Centre of Innovation and Translational Research, Poona College of
Pharmacy, Bharati Vidyapeeth, Pune 411038, India
Abstract
Abstract:
Cancer is a leading cause of death worldwide. The Janus kinase (JAK) signal transducer
and activator of transcription (STAT) signalling pathway are activated abnormally, which promotes
carcinogenesis. Several cytokines are important cancer drivers. These proteins bind to receptors and
use the Janus kinase (JAK) and STAT pathways to communicate their responses. Cancer risks are
linked to genetic differences in the JAK-STAT system. JAK inhibitors have been shown to reduce
STAT initiation, tissue propagation, and cell existence in preclinical investigations involving solid
tumour cell line models. JAK inhibitors, notably ruxolitinib, JAK1 or 2 blockers, make cell lines and
mouse models more susceptible to radiotherapy, biological response modifier therapy, and oncolytic
viral treatment. Numerous JAK antagonists have been or are now being evaluated in cancerous patients
as monotherapy or by combining with other drugs in clinical studies. In preclinical investigations,
certain JAK inhibitors showed promising anticancer effects; however, clinical trials explicitly
evaluating their effectiveness against the JAK/STAT system in solid tumours have yet to be completed.
JAK inhibition is a promising strategy to target the JAK/STAT system in solid tumours, and
it deserves to be tested further in clinical studies. The function of directing Janus kinases (JAKs), an
upstream accelerator of STATs, as a technique for lowering STAT activity in various malignant circumstances
is summarized in this article, which will help scientists to generate more specific drug
molecules in the future.
Publisher
Bentham Science Publishers Ltd.
Subject
Cancer Research,Drug Discovery,Pharmacology,Oncology
Cited by
6 articles.
订阅此论文施引文献
订阅此论文施引文献,注册后可以免费订阅5篇论文的施引文献,订阅后可以查看论文全部施引文献