fatostatin and 25-hydroxycholesterol

fatostatin has been researched along with 25-hydroxycholesterol* in 1 studies

Other Studies

1 other study(ies) available for fatostatin and 25-hydroxycholesterol

Article	Year
Inhibition of SREBP increases gefitinib sensitivity in non-small cell lung cancer cells. Oncotarget, 2016, Aug-09, Volume: 7, Issue:32 The clinical success of EGFR inhibitors in patients with lung cancer is limited by the inevitable development of treatment resistance. Here, we show that inhibition of SREBP increase gefitinib sensitivity in vitro and in vivo. Interference of SREBP1 binding partner MARVELD1 potentiate the therapeutic effect of gefitinib as well. Mechanistically, SREBP inhibition decreases the cell membrane fluidity, results in a decreased tyrosine phosphorylation of EGFR. Therefore, targeting lipid metabolism combined with EGFR-TKIs is potentially a novel therapeutic strategies for cancer treatment. Topics: Animals; Antineoplastic Agents; Carcinoma, Non-Small-Cell Lung; Cell Line, Tumor; Cell Proliferation; Drug Resistance, Neoplasm; Drug Synergism; Gefitinib; Humans; Hydroxycholesterols; Lung Neoplasms; Membrane Proteins; Mice; Mice, Nude; Microtubule-Associated Proteins; Protein Kinase Inhibitors; Pyridines; Quinazolines; Signal Transduction; Sterol Regulatory Element Binding Protein 1; Thiazoles; Triterpenes; Xenograft Model Antitumor Assays	2016

Article

Year

Inhibition of SREBP increases gefitinib sensitivity in non-small cell lung cancer cells.

Oncotarget, 2016, Aug-09, Volume: 7, Issue:32

The clinical success of EGFR inhibitors in patients with lung cancer is limited by the inevitable development of treatment resistance. Here, we show that inhibition of SREBP increase gefitinib sensitivity in vitro and in vivo. Interference of SREBP1 binding partner MARVELD1 potentiate the therapeutic effect of gefitinib as well. Mechanistically, SREBP inhibition decreases the cell membrane fluidity, results in a decreased tyrosine phosphorylation of EGFR. Therefore, targeting lipid metabolism combined with EGFR-TKIs is potentially a novel therapeutic strategies for cancer treatment.

Topics: Animals; Antineoplastic Agents; Carcinoma, Non-Small-Cell Lung; Cell Line, Tumor; Cell Proliferation; Drug Resistance, Neoplasm; Drug Synergism; Gefitinib; Humans; Hydroxycholesterols; Lung Neoplasms; Membrane Proteins; Mice; Mice, Nude; Microtubule-Associated Proteins; Protein Kinase Inhibitors; Pyridines; Quinazolines; Signal Transduction; Sterol Regulatory Element Binding Protein 1; Thiazoles; Triterpenes; Xenograft Model Antitumor Assays

2016