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Antineoplastic activity of 2‐methoxyestradiol in human pancreatic and gastric cancer cells with different multidrug‐resistant phenotypes
Author(s) -
Schumacher Guido,
Hoffmann Janine,
Cramer Thorsten,
Spinelli Antonino,
Jacob Dietmar,
Bahra Marcus,
Pratschke Johann,
Pfitzmann Robert,
Schmidt Sven,
Lage Hermann
Publication year - 2007
Publication title -
journal of gastroenterology and hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.214
H-Index - 130
eISSN - 1440-1746
pISSN - 0815-9319
DOI - 10.1111/j.1440-1746.2007.05033.x
Subject(s) - pancreatic cancer , cancer , cancer cell , apoptosis , medicine , multiple drug resistance , cancer research , growth inhibition , 2 methoxyestradiol , phenotype , oncology , endocrinology , immunology , biology , gene , drug resistance , biochemistry , metabolite , microbiology and biotechnology
Background and Aim: Chemoresistance often leads to loss of the last treatment option for cancer. 2‐Methoxyestradiol (2‐ME2) has been shown to inhibit tumor growth. The aim was to examine the efficacy of 2‐ME2 on multidrug‐resistant human cells from pancreatic and gastric cancer. Methods: We investigated the impact of 2‐ME2 on multidrug‐resistant cells derived from human pancreatic and gastric cancer cells that were positive or negative for the MDR1‐gene. Results: In pancreatic cancer cells, growth inhibition was 57% in parental, 72% in MDR1 ‐negative and 87% in MDR1 ‐positive cells after 1 μmol/L 2‐ME2. In gastric cancer cells we found a growth inhibition of 75% in parental, 82% in MDR1 ‐positive and 95% in MDR1 ‐negative cells. Strong induction of apoptosis was induced after a low dose of 2‐ME2. No significant difference in the amount of apoptotic cells was observed between parental and multidrug‐resistant cells of both tumor types. The number of apoptotic cells after 2‐ME2 ranged from 7.5% in parental gastric cancer cells to 20.1% in MDR1 ‐negative gastric cancer cells. Conclusion: 2‐ME2 may therefore have clinical application for chemoresistant cancer.