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Prostate Cancer, JAK/STAT3 Dysregulation, and Flavonoids: Is There a Possible Link?
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Journal Article
Prostate Cancer, JAK/STAT3 Dysregulation, and Flavonoids: Is There a Possible Link?
2026
Overview
Worldwide, prostate cancer (PC) has a rising incidence and is the sixth leading cause of death globally, especially with increasing cases in developing countries. Risk factors for PC include genetic predisposition, family history, race/ethnicity, and various occupational factors like diet, obesity, smoking, and transmitted diseases. The Janus kinase (JAK)-signal transducer and activator of transcription (STAT) pathway can be activated by hormones, cytokines, and growth factors, and it plays a role in many vital biological processes such as cell growth, differentiation, immune regulation, and apoptosis. Dysregulation of JAK/STAT3 can lead to cancer, inflammation, diabetes, and neurodegenerative disorders. In cancers, including PC, STAT3 promotes cell survival, progression, angiogenesis, and metastasis. Inhibitors targeting JAK and STAT3 tested in vivo have shown potential to inhibit malignant cell growth. Additionally, flavonoids are bioactive plant compounds that are important in preventing inflammation, oxidative stress, and cancer. Research indicates that natural flavonoids can be developed into cancer-preventive and therapeutic agents. Experimental studies have demonstrated that some flavonoids can inhibit PC development. The main goal of this review is to present the incidence and risk factors of PC, the JAK/STAT3 pathway and its inhibitors, and how flavonoids may influence this pathology.
Publisher
MDPI AG,Multidisciplinary Digital Publishing Institute (MDPI)
Subject
/ Animals
/ Cancer
/ Disease
/ Flavonoids - therapeutic use
/ Genes
/ Hormones
/ Humans
/ Kinases
/ Ligands
/ Male
/ Mutation
/ Obesity
/ Prostatic Neoplasms - drug therapy
/ Prostatic Neoplasms - etiology
/ Prostatic Neoplasms - metabolism
/ Prostatic Neoplasms - pathology
/ Proteins
/ Review
/ Signal Transduction - drug effects
/ STAT3 Transcription Factor - genetics
/ STAT3 Transcription Factor - metabolism
/ Tumors
