Related Experiment Video

Updated: May 7, 2026

Network Pharmacology Prediction and Experimental Validation of Trichosanthes-Fritillaria thunbergii Action Mechanism Against Lung Adenocarcinoma
13:18

Network Pharmacology Prediction and Experimental Validation of Trichosanthes-Fritillaria thunbergii Action Mechanism Against Lung Adenocarcinoma

Published on: March 3, 2023

1.9K

Schisandrin A inhibits head and neck squamous cell carcinoma progression via the PI3K/AKT/GSK3β pathway

Han-Yu Wu1, Wen-Jing Wang1, Qian Lin1

  • 1Department of Otolaryngology-Head and Neck Surgery, Renmin Hospital of Wuhan University, 238 Jie-Fang Road, Wuhan, Hubei, 430060, PR China.

Biochimica Et Biophysica Acta. Molecular Basis of Disease
|May 5, 2026
PubMed
Abstract

Insights

Schisandrin A (SchA) effectively inhibits head and neck squamous cell carcinoma (HNSCC) progression. This natural compound targets the PI3K/AKT/GSK3β pathway, showing promise as a novel HNSCC therapeutic.

Area of Science:

  • Oncology
  • Pharmacology
  • Molecular Biology

Background:

  • Head and neck squamous cell carcinoma (HNSCC) presents a significant public health challenge with limited treatment options.
  • There is a critical need for novel, safe, and effective therapies for this aggressive cancer.
  • Schisandrin A (SchA), a lignan from Schisandra chinensis, has demonstrated preliminary anticancer potential but its efficacy in HNSCC is unknown.

Purpose of the Study:

  • To investigate the antitumor effects of Schisandrin A (SchA) in head and neck squamous cell carcinoma (HNSCC).
  • To elucidate the molecular mechanisms underlying SchA's action in HNSCC, focusing on the PI3K/AKT/GSK3β signaling pathway.

Main Methods:

  • In vitro studies on HNSCC cell lines assessed cell viability, proliferation, migration, and apoptosis after SchA treatment.
  • An in vivo xenograft mouse model was used to evaluate SchA's tumor growth inhibition.
  • Western blotting and immunofluorescence staining analyzed the PI3K/AKT/GSK3β pathway modulation.

Main Results:

  • Schisandrin A (SchA) significantly inhibited HNSCC malignant progression in both cell lines and animal models.
  • SchA treatment led to the downregulation of the PI3K/AKT/GSK3β signaling pathway.
  • Reduced phosphorylation of key proteins in the PI3K/AKT/GSK3β cascade confirmed pathway inhibition.

Conclusions:

  • Schisandrin A (SchA) demonstrates potent antitumor activity against HNSCC.
  • The mechanism involves the inhibition of the PI3K/AKT/GSK3β signaling pathway.
  • SchA represents a promising therapeutic candidate for HNSCC treatment.
Keywords:
Head and neck squamous cell carcinomaPI3K/AKT/GSK3βProtein phosphorylationSchisandrin A

More Related Videos

Quantitative PCR-based Assay to Measure Sonic Hedgehog Signaling in Cellular Model of Ciliogenesis07:26

Quantitative PCR-based Assay to Measure Sonic Hedgehog Signaling in Cellular Model of Ciliogenesis

Published on: January 31, 2025

1.1K
Three-Dimensional 3D Tumor Spheroid Invasion Assay12:19

Three-Dimensional 3D Tumor Spheroid Invasion Assay

Published on: May 1, 2015

60.8K

Related Concept Videos

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...
10.3K
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...
4.8K
Inhibition of CDK Activity02:34

Inhibition of CDK Activity

4.3K
Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
4.0K
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...
829