Gold(III) porphyrin 1a prolongs the survival of melanoma-bearing mice and inhibits angiogenesis

Ching Tung Lum, Longfei Huo, Raymond Wai Yin Sun, Ming Li, Hsiang Fu Kung, Chi Ming Che, Marie C.M. Lin

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31 Scopus citations


Background. Gold(III) meso-tetraphenylporphyrin (gold-1a) has previously been shown to prolong the survival of hepatocellular carcinoma (HCC)-bearing rats and nasopharyngeal carcinoma (NPC) metastasis-bearing mice. It has also been proved to inhibit the tumor growth of mice bearing NPC, neuroblastoma and colon carcinoma. Mechanistically, gold-1a induces apoptosis, inhibits cell migration and invasion. In this study the efficacies of gold-1a in inhibiting melanoma and angiogenesis were investigated. Material and methods. A mouse melanoma model was used to investigate the efficacy of gold-1a in inhibiting angiogenesis, tumor growth and prolonging the survival of the tumor-bearing animals. The model was established by inoculation of 2 × - 105 B16-F1 mouse melanoma cells into the right back flanks of the mice by subcutaneous inoculation. When the tumors grew to 0.2-0.4 cm in diameters, the mice were treated with gold-1a, solvent control or dacarbazine (DTIC) for comparison. Tumor sizes and animal survivals were monitored throughout the experiment. Tumor tissues were collected and immunohistochemically stained with CD31 antibodies for evaluation of intra-tumoral microvessel density (iMVD). Results and conclusion. Gold-1a significantly prolonged the survivals, reduced angiogenesis and tumor growth rates of melanoma-bearing mice. The compound induced necrosis and apoptosis in the mouse melanoma tissues. Gold-1a also downregulated the expression of genes playing roles in angiogenesis. Gold-1a may potentially be used to treat melanoma in patients.

Original languageEnglish (US)
Pages (from-to)719-726
Number of pages8
JournalActa Oncologica
Issue number5
StatePublished - Jun 2011
Externally publishedYes

Bibliographical note

Funding Information:
This study was supported by grants from the AoE Scheme of UGC (AoE/P-10/01), RGC (HKU7705/ 07M to MCL) of the Hong Kong Special Administrative Region, China. There are no financial disclosures from any authors.


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