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Cells were seeded in 96 well paltes, and then treated with the indicated concentration of Capecitabine for 48h. Cell survival was measured by a standarad MTT assay.
Rating
Source
Dr. Helen Sadik of Johns Hopkins University. Capecitabine (Xeloda) purchased from Selleck
Method
MTT assay
Cell Lines
MCF7 cells, MCF10A cells
Concentrations
0.001-100 μM
Incubation Time
48 h
Results
Capecitabine potently inhibited the survival of MCF10A cells and MCF7 cells in a dose-dependent manner.
A. MCF10A-Ras overexpressing a vector control or the gene of interest (GeneX), or MCF7 expressing a scramble or a siRNA for the geneX were treated with DMSO or with Carboplatin for 24h. Resistant colonies were allowed to grow for 2 weeks, and are then stained with Crystal Violet. B. Quantification of the results.
Rating
Source
Dr. Helen Sadik of Johns Hopkins University. Carboplatin purchased from Selleck
Method
colony assays
Cell Lines
MCF10A-Ras cell, MCF7 cells
Concentrations
10/50 μM
Incubation Time
24 h/etc
Results
Reduction of cell colony size formation was observed by the treatment with Carboplatin in MCF10A-Ras cell and MCF7 cells.
A. Viability curve for the c-Kit mutant MelMS melanoma cell line treated with increasing concentrations of imatinib for 72h (relative to DMSO-treated controls; mean ±sd; n=3) B. MelMS melanoma cells were treated with 50nM imatinib for 24h. The effects on c-Kit, ERK and AKT activation were determined by immunoblotting.
Rating
Source
Dr. Helen Rizos from the university of Sydney. Imatinib Mesylate purchased from Selleck
Method
Western blot
Cell Lines
MelMS melanoma cells
Concentrations
50 nM
Incubation Time
24/72h
Results
Imatinib Mesylate treatment resulted in a reduction of c-Kit, ERK and AKT phosphorylation.
Cells were seeded in 96 well paltes, and then treated with the indicated concentration of Gemcitabine for 48 h. Cell survival was measured by a standarad MTT assay.
Rating
Source
Dr. Helen Sadik of Johns Hopkins University. Gemcitabine HCl (Gemzar) purchased from Selleck
Method
Cell Survival Assays
Cell Lines
MCF7 cells, MCF10A cells
Concentrations
0.001-100 μM
Incubation Time
48 h
Results
Gemcitabine HCl potently inhibited the survival of MCF10A cells in a dose-dependent manner. The highest level of inhibition was observed with Gemcitabine HCl in concentration of 0.01 μM in MCF7 cells - See more at: http://www.selleckchem.com/products/Gemcitabine-Hydrochloride(Gemzar).html#sthash.M8dRWV6R.dpuf
Cooperative Effects of AR and mTOR Inhibition In Vitro and In Vivo (A) In vitro response of Pten null;Ar+ murine (CaP8) and human (LNCaP) prostate cancer cells to AR knockdown (sh-AR) or pharmacological inhibition of AR (MDV3100, 10 nM) with and without rapamycin (R: 1 nM) treatment (Sc, control sh oligo). (B and D) In vivo response to treatments with castration, MDV3100, rapamycin, or their combinations as measured by cell proliferation (Ki67+cells) and (C and D) tumor burden in Pb-Cre+;-PtenL/L and Pb-Cre+;PtenL/L:ArL/Y mutants. Scale bars represent 2 mm (C), 200 mm (D), and 75 mm (D, inset). Error bars represent mean ±SD.
Rating
Source
Cancer Cell, 2011, 19, 1–13. Rapamycin (Sirolimus) purchased from Selleck
Method
Cell viability Analysis
Cell Lines
Ar+murine (CaP8) and human (LNCaP) prostate cancer cells, Pb-Cre+;PtenL/L mice, Pb-Cre+;PtenL/L;ArL/Y mice
Concentrations
1 nM, 4 mg/kg
Incubation Time
0-4 weeks
Results
These data suggest that CaPs with AR loss have greater reliance upon the PI3K/AKT/mTOR-signaling pathways and that combined AR/androgen blockage in conjunction with PI3K/AKT/mTOR inhibition (by Rapamycin) is more effective for CaPs initiated by PTEN loss or PI3K/AKT activation.
Sunitinib limits the colonial growth of HT-29 by downregulating HIF-1a. (A) The number and size of colonies formed in soft agar. The numbers of small colonies (<50 μm diameter) were not different among conditions of a serial concentration of sunitinib. On the contrary, large colonies (>50 μm diameter) disappeared after incubation with sunitinib. Each point represents the mean and SD from four separate experiments. (B) HIF-1a expression and hypoxia within HT-29 colony. After colonies grew for 4 weeks, HIF-1a and hypoxia were visualized by immunofluoroscence staining. Bar = 20 μm.
Rating
Source
Biochem Bioph Res Co, 2010, 398, 205–211. Sunitinib Malate (Sutent) purchased from Selleck
We checked whether sunitinib affects the mass formation of cancer cells. Interestingly, sunitinib inhibited the growth of colony, whereas it did not block the formation of colony. The number of large colonies (>50 µm diameter) was noticeably reduced in the presence of sunitinib, while the number of small colonies (<50 µm diameter) did not differ (Fig. 1A). Under confocal microscopy, hypoxic areas were detected within colonies and HIF-1a was prominently expressed in there(Fig. B, top), whereas small colonies were not hypoxic and scarcely expressed HIF-1a (Fig. B, middle). We next tried to examine whether sunitinib inhibits HIF-1a in the HT-29 colonies. However, as no large colonies were built in the presence of 5 or 10 µM sunitinib, we chose the colonies treated with 1 µM sunitinib, which showed a partial inhibition of colony growth. Consequently, HIF-1a expression was substantially reduced, but still remained, in the colonies positively stained with hypoxyprobe (Fig. 1B, bottom).
