Quercetin as a JAK-STAT inhibitor: a potential role in solid tumors and neurodegenerative diseases

Hamidreza Zalpoor1,2, Mohsen Nabi-Afjadi3, Razieh Forghaniesfidvajani2

  • 1Shiraz Neuroscience Research Center, Shiraz University of Medical Sciences, Shiraz, Iran.

Insights

Quercetin, a plant polyphenol, inhibits the Janus kinase-signal transducer and activator of transcription (JAK-STAT) pathway. This review explores quercetin

Area of Science:

  • Molecular Biology
  • Immunology
  • Pharmacology
  • Oncology
  • Neuroscience

Background:

  • The JAK-STAT pathway regulates critical cellular processes like growth, proliferation, differentiation, apoptosis, and inflammation.
  • Dysregulation of the JAK-STAT pathway is implicated in cancer progression and neurodegenerative diseases.
  • Current JAK-STAT targeted therapies often show limited long-term efficacy due to pathway complexity and crosstalk.

Purpose of the Study:

  • To review the pharmacological effects of quercetin on the JAK-STAT signaling pathway.
  • To explore quercetin's potential in managing solid tumors and neurodegenerative diseases via JAK-STAT inhibition.

Main Methods:

  • Literature review of studies investigating quercetin's interaction with the JAK-STAT pathway.
  • Analysis of research on quercetin's anti-inflammatory, antitumor, and neuroprotective activities.

Main Results:

  • Quercetin demonstrates significant inhibitory effects on the JAK-STAT pathway through various mechanisms.
  • Quercetin exhibits potent anti-inflammatory and antitumor activities.
  • Quercetin shows promise in controlling neurodegenerative conditions.

Conclusions:

  • Quercetin represents a promising natural compound for targeting the JAK-STAT pathway.
  • Its multifaceted pharmacological effects suggest potential therapeutic applications in oncology and neurodegenerative disorders.

Related Concept Videos

Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
4.9K
The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
9.2K
Chemotherapy-Induced Nausea and Vomiting: Neurokinin-1 Receptor Antagonists01:28

Chemotherapy-Induced Nausea and Vomiting: Neurokinin-1 Receptor Antagonists

Neurokinin 1 (NK1) receptors are distributed across the GI tract, vagal afferents, and key CNS regions including the central vomiting center and chemoreceptor trigger zone (CTZ) Chemotherapy agents stimulate enterochromaffin cells in the gastrointestinal (GI) tract to release large amounts of substance P (SP). SP is a neuropeptide released by specific sensory nerves in response to many different stressors, including those in the GI mucosa affected by chemotherapy.  SP binds and activates...
256
PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a...
3.9K
Cognitive Enhancers: Cholinesterase Inhibitors and NMDA Receptor Antagonists01:30

Cognitive Enhancers: Cholinesterase Inhibitors and NMDA Receptor Antagonists

Cognitive enhancers, also known as "smart drugs," are substances used to enhance memory, mental alertness, and concentration. These can be natural or synthetic and improve cognition in conditions like Alzheimer's disease (AD) and other neurodegenerative diseases. Some common examples include caffeine, amphetamines, methylphenidate, modafinil, arecoline, donepezil, vortioxetine, and piracetam. These enhancers work on the principle of synaptic plasticity and altered circuit function.
199
Targeted Cancer Therapies02:57

Targeted Cancer Therapies

The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against...
7.8K