Related Experiment Video
Updated: Feb 13, 2026
Imaging Spatial Reorganization of a MAPK Signaling Pathway Using the Tobacco Transient Expression System
Published on: March 20, 2016
A novel polysaccharide derived from algae extract inhibits cancer progression via JNK, not via the p38 MAPK signaling
Peiyu Xie1, Fukuko Horio1, Isao Fujii1
1Laboratory of Clinical Pharmacology and Therapeutics, Faculty of Pharmaceutical Sciences, Sojo University, Kumamoto, Kumamoto 860-0822, Japan.
Abstract:
Cancer has long been one of the most malignant diseases worldwide. Processes in cancer cells are often mediated by Jun N-terminal kinase (JNK), p38 mitogen-activated protein kinase (p38 MAPK) and other signaling pathways. Traditional therapies are often problematic. Recently, a novel polysaccharide derived from algae extract was investigated due to the increasing interest in biological activities of compounds from marine organisms. The effect of this novel polysaccharide on human MKN45 gastric carcinoma cells was determined previously. The current aimed to determine whether the polysaccharide affects other types of cancer, and the deeper mechanisms involved in the process. Human MCF-7 breast cancer cells were used to investigate the novel polysaccharide for its role in the cell growth and migration, and determine the mechanisms affected. MTT assay, nuclear staining and fluorescence activated cell sorting analysis demonstrated that the novel polysaccharide reduced the viability of MCF-7 cells by inducing cell apoptosis and arresting the cells at G2/M phase. Results of western blot analysis demonstrated that phosphorylation of JNK and expression of p53, caspase-9 and caspase-3 were upregulated in the polysaccharide-treated MCF-7 cells. SP600125, an inhibitor of JNK, maintained MCF-7 cell viability, prevented cell apoptosis and cycle arrest, and downregulated the polysaccharide-induced protein phosphorylation/expression. However, a migration assay demonstrated that the novel polysaccharide did not change the migration of MCF-7 cells, as well as the expression of p38 MAPK, and matrix metalloproteinase-9 and -2. Taken together, the current study demonstrated that the novel polysaccharide suppressed cancer cell growth, induced cancer cell apoptosis and cell cycle arrest via JNK signaling, but had no effect on cancer cell migration and p38 MAPK signaling.
Insights
A novel algal polysaccharide inhibits breast cancer cell growth by inducing apoptosis and cell cycle arrest through the JNK signaling pathway. This compound shows potential as a therapeutic agent, though it does not impact cancer cell migration.
Area of Science:
- Marine Biotechnology
- Cancer Biology
- Molecular Signaling
Background:
- Cancer remains a leading global health challenge, with signaling pathways like JNK and p38 MAPK crucial in cancer cell processes.
- Traditional cancer therapies present significant challenges, driving interest in novel therapeutic agents from natural sources.
- Marine-derived compounds, particularly polysaccharides, are gaining attention for their potential biological activities.
Purpose of the Study:
- To investigate the anti-cancer effects of a novel algal polysaccharide on human breast cancer cells (MCF-7).
- To elucidate the underlying molecular mechanisms, including cell apoptosis, cell cycle regulation, and signaling pathway involvement.
- To determine the compound's impact on cancer cell migration and related molecular targets.
Main Methods:
- Cell viability was assessed using MTT assays.
- Apoptosis and cell cycle phase distribution were analyzed via nuclear staining and fluorescence-activated cell sorting (FACS).
- Western blotting was employed to evaluate protein expression and phosphorylation, including JNK, p53, caspases, p38 MAPK, and matrix metalloproteinases. Migration assays were also conducted.
Main Results:
- The algal polysaccharide significantly reduced MCF-7 cell viability by inducing apoptosis and G2/M cell cycle arrest.
- Western blot analysis revealed upregulation of phosphorylated JNK, p53, caspase-9, and caspase-3 following treatment.
- Inhibition of JNK signaling by SP600125 reversed the observed effects on cell viability, apoptosis, and cell cycle arrest. The polysaccharide did not affect cell migration or p38 MAPK signaling.
Conclusions:
- The novel algal polysaccharide exhibits potent anti-cancer properties against breast cancer cells by activating the JNK signaling pathway, leading to apoptosis and cell cycle arrest.
- The findings suggest that this marine-derived polysaccharide could be a promising candidate for further development as a breast cancer therapeutic.
- The compound's lack of effect on cell migration indicates a specific mechanism of action focused on proliferation and survival, distinct from metastatic potential.
Related Concept Videos
03:03mTOR Signaling and Cancer Progression
The mTOR pathway or the...
01:07MAPK Signaling Cascades
03:14Notch Signaling Pathway
The Notch gene came into the limelight in 1914 after the discovery that its mutation in Drosophila melanogaster leads to a serrated (or "notched") wing margin phenotype. It was not...
02:33Hedgehog Signaling Pathway
01:19Interactions Between Signaling Pathways
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...
01:41Non-Canonical Wnt Signaling Pathways