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RAR agonist induced EGCG-elicited cell growth inhibition through 67LR upregulation.

By Ju Hye Lee (364187), Mutsumi Kishikawa (364188), Motofumi Kumazoe (364190), Koji Yamada (210298) and Hirofumi Tachibana (210301)

Abstract

<p><b>A</b>) Cells were treated with or without 0.1 µM ATRA or 0.1 µM TTNPB in DMEM supplemented with 1% FCS for 48 h and were analyzed by Western blot analysis. Levels of 67LR expression were normalized to β-Actin. Band intensities were quantified using NIH Image J software. <b>B</b>) Anti-67 LR antibody conjugated with Alexa Fluor 488 was used at a dilution of 1∶100. Photographs were taken under Keyence BZ-8100 fluorescence microscope. <b>C</b>) Cells were treated with 0.1 µM ATRA or RARα agonist, 0.1 µM TTNPB in DMEM supplemented with 1% FCS for 48 h, then treated with 0.5 µM of EGCG for 48 h. Data shown are means ± S.D. for three samples. Data containing asterisk marks are significantly different from the values in control at **<i>p</i><0.01, ***<i>p</i><0.001. <b>D</b>) B16 cells were treated with 0.1 µM TTNPB in DMEM supplemented with 1% FCS for 48 h, then the cells were treated with either anti-67LR (MLuC5) or control antibody (mouse IgM) for 2 h, and the cells were added 0.5 µM of EGCG for 48 h. Cells proliferation was assessed by the WST-1 reagent. Cell number was measured as 430 nm absorbance and shown as relative of control. Data shown are means ± S.D. for three samples. Data containing asterisk marks are significantly different from the values in control at ***<i>p</i><0.001.</p

Topics: Biochemistry, Medicine, Cancer, agonist, induced, egcg-elicited, inhibition, 67lr
Year: 2013
DOI identifier: 10.1371/journal.pone.0011051.g005
OAI identifier: oai:figshare.com:article/516309
Provided by: FigShare
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