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SHR Neuro Krebs Kardio Lipid Stoffw Microb

Aguiriano-Moser, V; Svejda, B; Li, ZX; Sturm, S; Stuppner, H; Ingolic, E; Höger, H; Siegl, V; Meier-Allard, N; Sadjak, A; Pfragner, R.
Ursolic acid from Trailliaedoxa gracilis induces apoptosis in medullary thyroid carcinoma cells.
Mol Med Rep. 2015; 12(4):5003-5011 Doi: 10.3892/mmr.2015.4053 [OPEN ACCESS]
Web of Science PubMed PUBMED Central FullText FullText_MUG

 

Führende Autor*innen der Med Uni Graz
Aguiriano Moser Victor
Pfragner Roswitha
Co-Autor*innen der Med Uni Graz
Meier-Allard Nathalie
Sadjak Anton
Siegl Veronika
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Abstract:
Medullary thyroid carcinoma (MTC) originates from the C‑cells of the thyroid and is not sensitive to radiation or chemotherapy. Therefore, surgical removal of the tumor tissue in its entirety is the only curative treatment for MTC. The present study aimed to examine the potential mechanisms of action of extracts of Trailliaedoxa gracilis (TG; WW Smith & Forrest), a plant from the province of Sichuan, China, and of ursolic acid (UA), a pentacyclic triterpen present in TG, on the MTC‑SK MTC cell line. A total of 13 TG fractions and UA were examined in vitro for their effects on cell morphology, cell number, proliferation and rates of apoptosis. Reverse transcription‑quantitative polymerase chain reaction of nuclear factor‑κB essential modifier (NEMO) was performed to delineate the role of the apoptotic pathway following treatment with UA. TG and UA were examined in vivo in xenotransplanted MTC‑bearing severe combined immunodeficient mice. The TG fractions exhibited antiproliferative effects, with inhibition of mitochondrial activity in the tumor cells at concentrations, which caused no impairment of the normal control cells. The apoptotic rates of the MTC‑SK cells treated with the TG fractions and UA were determined, in which no marked tumor inhibition was observed in the treated MTC‑mice, and no change in the expression of NEMO was detected in the treated MTC‑SK cells. The observation of early‑onset activation of caspase 8 suggested that the responsible factor was linked to NEMO, an anti‑apoptotic protein. However, no differences in the mRNA transcription levels of NEMO were detected in MTC‑SK cells treated with UA, suggesting that this protein was not associated with the signal transducer and activator of transcription 3 pathway.
Find related publications in this database (using NLM MeSH Indexing)
Animals -
Antineoplastic Agents, Phytogenic - pharmacology
Apoptosis - drug effects
Carcinoma, Neuroendocrine - drug therapy
Carcinoma, Neuroendocrine - genetics
Carcinoma, Neuroendocrine - metabolism
Carcinoma, Neuroendocrine - pathology
Caspase 8 - genetics
Caspase 8 - metabolism
Cell Line -
Cell Line, Tumor -
Cell Proliferation - drug effects
Cell Survival - drug effects
Child, Preschool -
Female -
Fibroblasts - cytology
Fibroblasts - drug effects
Fibroblasts - metabolism
Founder Effect -
Gene Expression - drug effects
Humans -
I-kappa B Kinase - genetics
I-kappa B Kinase - metabolism
Male -
Mice -
Mice, SCID -
Middle Aged -
Plant Extracts - chemistry
Rubiaceae - chemistry
Thyroid Neoplasms - drug therapy
Thyroid Neoplasms - genetics
Thyroid Neoplasms - metabolism
Thyroid Neoplasms - pathology
Triterpenes - pharmacology
Tumor Burden - drug effects
Xenograft Model Antitumor Assays -

Find related publications in this database (Keywords)
neuroendocrine tumors
medullary thyroid carcinoma
Trailliaedoxa gracilis
bioactive agents
ursolic acid
nuclear factor-kappa B essential modulator
apoptosis
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