(Credit: Image courtesy of Lund University)
耐激素治療和耐放療或化療的前列腺癌需要新的治療方法。近日,，隆德大學的研究人員開發(fā)出一種新的治療手段——攻擊前列腺癌中具有干細胞樣特征的細胞,。
斯科訥大學馬爾默醫(yī)院醫(yī)學院部的泌尿科癌癥研究教授Rebecka Hellsten高級研究員和Anders Bjartell教授,，隆德大學學院有機化學部的助理教授Martin Johansson領(lǐng)導了兩個研究小組合作開展了這項跨學科研究項目，最新研究成果刊登在PLoS ONE雜志上,。
Anders Bjartell說：“前列腺腫瘤組織中只包含約0.1％的腫瘤干細胞,，但如果不能成功地消除這些干細胞，腫瘤發(fā)展過程中細胞生長仍會有失控的危險,。腫瘤干細胞通常對激素治療和化療反應遲鈍（不敏感）,，所以有必要開發(fā)出一種可以對所有類型的腫瘤細胞都有作用的治療方法。”
研究小組通過研究前列腺癌腫瘤細胞的生物學行為發(fā)現(xiàn),，蛋白STAT3對干細胞樣前列腺癌細胞的生物學功能發(fā)揮重要作用,。研究小組以往的研究已經(jīng)證明，一種天然化合物——Galiellalactone能影響STAT3,，抑制前列腺癌細胞的生長,。
研究人員希望用Galiellalactone當作工具藥，開發(fā)出新的特異性的STAT3抑制劑,，能針對性地攻擊前列腺癌中干細胞樣的腫瘤細胞,，進而抑制腫瘤的生長和擴散。(生物谷 Bioon.com)
doi:10.1371/journal.pone.0022118
PMC:
PMID:
Galiellalactone Inhibits Stem Cell-Like ALDH-Positive Prostate Cancer Cells
Rebecka Hellsten, Martin Johansson, Anna Dahlman, Olov Sterner, Anders Bjartell
Transcriptional coregulators control the activity of many transcription factors and are thought to have wide-ranging effects on gene expression patterns. We show here that muscle-specific loss of nuclear receptor corepressor 1 (NCoR1) in mice leads to enhanced exercise endurance due to an increase of both muscle mass and of mitochondrial number and activity. The activation of selected transcription factors that control muscle function, such as MEF2, PPARβ/, and ERRs, underpins these phenotypic alterations. NCoR1 levels are decreased in conditions that require fat oxidation, resetting transcriptional programs to boost oxidative metabolism. Knockdown of gei-8, the sole C. elegans NCoR homolog, also robustly increased muscle mitochondria and respiration, suggesting conservation of NCoR1 function. Collectively, our data suggest that NCoR1 plays an adaptive role in muscle physiology and that interference with NCoR1 action could be used to improve muscle function.
