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Updated: Feb 25, 2026
Bioluminescence Imaging of an Immunocompetent Animal Model for Glioblastoma
Published on: January 15, 2016
Verteporfin inhibits growth of human glioma in vitro without light activation
Ahmad Al-Moujahed1, Katarzyna Brodowska1, Tomasz P Stryjewski1
1Retina Service, Angiogenesis Laboratory, Massachusetts Eye and Ear Infirmary, Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts, 02114, USA.
Abstract:
Verteporfin (VP), a light-activated drug used in photodynamic therapy for the treatment of choroidal neovascular membranes, has also been shown to be an effective inhibitor of malignant cells. Recently, studies have demonstrated that, even without photo-activation, VP may still inhibit certain tumor cell lines, including ovarian cancer, hepatocarcinoma and retinoblastoma, through the inhibition of the YAP-TEAD complex. In this study, we examined the effects of VP without light activation on human glioma cell lines (LN229 and SNB19). Through western blot analysis, we identified that human glioma cells that were exposed to VP without light activation demonstrated a downregulation of YAP-TEAD-associated downstream signaling molecules, including c-myc, axl, CTGF, cyr61 and survivin and upregulation of the tumor growth inhibitor molecule p38 MAPK. In addition, we observed that expression of VEGFA and the pluripotent marker Oct-4 were also decreased. Verteporfin did not alter the Akt survival pathway or the mTor pathway but there was a modest increase in LC3-IIB, a marker of autophagosome biogenesis. This study suggests that verteporfin should be further explored as an adjuvant therapy for the treatment of glioblastoma.
Insights
Verteporfin (VP) inhibits human glioma cells by downregulating YAP-TEAD signaling without light activation. This suggests VP
Area of Science:
- Oncology
- Molecular Biology
- Cancer Therapeutics
Background:
- Verteporfin (VP) is a light-activated drug used in photodynamic therapy.
- VP has demonstrated efficacy in inhibiting malignant cells, including certain tumor cell lines, via YAP-TEAD complex inhibition, even without photo-activation.
- Glioma remains a challenging cancer with limited treatment options.
Purpose of the Study:
- To investigate the effects of verteporfin (VP) without light activation on human glioma cell lines (LN229 and SNB19).
- To elucidate the molecular mechanisms underlying VP's anti-glioma activity.
- To assess VP's potential as an adjuvant therapy for glioblastoma.
Main Methods:
- Western blot analysis was employed to examine protein expression levels.
- Human glioma cell lines (LN229 and SNB19) were treated with VP without photo-activation.
- Key signaling molecules, cell growth regulators, and autophagosome markers were analyzed.
Main Results:
- VP treatment led to the downregulation of YAP-TEAD downstream signaling molecules (c-myc, axl, CTGF, cyr61, survivin).
- VP upregulated p38 MAPK, a tumor growth inhibitor, and decreased VEGFA and Oct-4 expression.
- VP did not affect the Akt or mTor pathways but induced a modest increase in LC3-IIB, indicating autophagosome biogenesis.
Conclusions:
- Verteporfin exhibits anti-glioma activity independent of light activation by modulating YAP-TEAD signaling.
- VP influences key pathways involved in tumor growth, angiogenesis, and pluripotency.
- Further exploration of verteporfin as an adjuvant therapy for glioblastoma is warranted.
