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  • lapc4  (ATCC)
    95
    ATCC lapc4
    Effects of constitutively active AKT expression in different PCa cells Cells of LNCaP C4-2 (A) CWR22R v1 (B) , and <t>LAPC4</t> (C) , infected with the pHAGE lentivirus expressing AKT-null or AKT-myr, were maintained in c.s.FBS medium for 48 hours. Total cell lysates from each experiment were analyzed by Western blotting for expression of the indicated proteins.
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    Effects of constitutively active AKT expression in different PCa cells Cells of LNCaP C4-2 (A) CWR22R v1 (B) , and LAPC4 (C) , infected with the pHAGE lentivirus expressing AKT-null or AKT-myr, were maintained in c.s.FBS medium for 48 hours. Total cell lysates from each experiment were analyzed by Western blotting for expression of the indicated proteins.

    Journal: Experimental cell research

    Article Title: AKT upregulates B-Raf Ser445 phosphorylation and ERK1/2 activation in prostate cancer cells in response to androgen depletion

    doi: 10.1016/j.yexcr.2013.05.008

    Figure Lengend Snippet: Effects of constitutively active AKT expression in different PCa cells Cells of LNCaP C4-2 (A) CWR22R v1 (B) , and LAPC4 (C) , infected with the pHAGE lentivirus expressing AKT-null or AKT-myr, were maintained in c.s.FBS medium for 48 hours. Total cell lysates from each experiment were analyzed by Western blotting for expression of the indicated proteins.

    Article Snippet: LAPC4 (ATCC) was grown in Iscove's medium with 10% FBS.

    Techniques: Expressing, Infection, Western Blot

    Expression of the AR-regulated gene NKX3.1 is enhanced by p52 in an AR-dependent manner. LNCaP cells were transfected with plasmids expressing p52 (1 μg), or p300 and AR siRNAs in FBS or CS-FBS. A, total RNAs were analyzed by qRT-PCR for NKX3.1 mRNA. p52 induced the expression of NKX3.1 mRNA, which was abolished by downregulation of AR. B, ChIP assays were performed with AR, p52, or IgG antibodies. p52 enhanced the recruitment of AR to NKX3.1 promoter, whereas recruitment of p52 was AR dependent. LAPC-4 cells were transfected with plasmids expressing p52, or p300 or AR siRNAs in FBS or CS-FBS. C, total RNAs were analyzed by qRT-PCR for NKX3.1 mRNA. p52-induced expression of NKX3.1 mRNA was abolished by downregulation of AR. D, ChIP assays were performed with AR, p52, or IgG antibodies. p52 induced the recruitment of AR to NKX3.1 promoter, whereas recruitment of p52 was AR dependent.

    Journal: Cancer research

    Article Title: Aberrant Activation of the Androgen Receptor by NF-?B2/p52 in Prostate Cancer Cells

    doi: 10.1158/0008-5472.CAN-09-3703

    Figure Lengend Snippet: Expression of the AR-regulated gene NKX3.1 is enhanced by p52 in an AR-dependent manner. LNCaP cells were transfected with plasmids expressing p52 (1 μg), or p300 and AR siRNAs in FBS or CS-FBS. A, total RNAs were analyzed by qRT-PCR for NKX3.1 mRNA. p52 induced the expression of NKX3.1 mRNA, which was abolished by downregulation of AR. B, ChIP assays were performed with AR, p52, or IgG antibodies. p52 enhanced the recruitment of AR to NKX3.1 promoter, whereas recruitment of p52 was AR dependent. LAPC-4 cells were transfected with plasmids expressing p52, or p300 or AR siRNAs in FBS or CS-FBS. C, total RNAs were analyzed by qRT-PCR for NKX3.1 mRNA. p52-induced expression of NKX3.1 mRNA was abolished by downregulation of AR. D, ChIP assays were performed with AR, p52, or IgG antibodies. p52 induced the recruitment of AR to NKX3.1 promoter, whereas recruitment of p52 was AR dependent.

    Article Snippet: LAPC-4, LNCaP, C4-2, and PC-3 prostate cancer cells were obtained from the American Type Culture Collection and cultured in RPMI 1640 containing either 10% complete fetal bovine serum (FBS) or 10% charcoal-dextran–stripped FBS (CS-FBS) and penicillin/streptomycin.

    Techniques: Expressing, Transfection, Quantitative RT-PCR, Chromatin Immunoprecipitation

    Inhibition of xenograft tumor growth, blood and tissue levels of arctigenin, and reduced expression of growth factors in SCID mice. Male SCID mice (n=10 per group) were inoculated subcutaneously with 5×10 5 androgen-sensitive LAPC-4 prostate tumor cells. The intervention treatments started either one week after (A, B) or two weeks prior to (C, D) the tumor cell inoculation. Arctigenin was administered daily through oral gavage at dose of 50mg/kg or 100mg/kg bw. Tumor size was measured twice a week using calipers and tumor volume calculated using the formula: length × width × height × 0.5236. Tumor weight was measured at mouse sacrifice. Blood and tumor levels of arctigenin (E) was detected with HPLC coupled with CoulArray electrochemical detector after extraction with ethyl acetate. The concentrations of 8 growth factors in tumor tissues were simultaneously measured using a Human Growth Factor ELISA Strip II kit (F). Data are presented as mean ± SD. Arc: arctigenin. Compared to control, *P

    Journal: Clinical nutrition experimental

    Article Title: Arctigenin inhibits prostate tumor cell growth in vitro and in vivo

    doi: 10.1016/j.yclnex.2017.04.001

    Figure Lengend Snippet: Inhibition of xenograft tumor growth, blood and tissue levels of arctigenin, and reduced expression of growth factors in SCID mice. Male SCID mice (n=10 per group) were inoculated subcutaneously with 5×10 5 androgen-sensitive LAPC-4 prostate tumor cells. The intervention treatments started either one week after (A, B) or two weeks prior to (C, D) the tumor cell inoculation. Arctigenin was administered daily through oral gavage at dose of 50mg/kg or 100mg/kg bw. Tumor size was measured twice a week using calipers and tumor volume calculated using the formula: length × width × height × 0.5236. Tumor weight was measured at mouse sacrifice. Blood and tumor levels of arctigenin (E) was detected with HPLC coupled with CoulArray electrochemical detector after extraction with ethyl acetate. The concentrations of 8 growth factors in tumor tissues were simultaneously measured using a Human Growth Factor ELISA Strip II kit (F). Data are presented as mean ± SD. Arc: arctigenin. Compared to control, *P

    Article Snippet: The androgen-sensitive LNCaP and LAPC-4 human prostate cancer cell lines were purchased from ATCC (Chicago, IL, USA).

    Techniques: Inhibition, Expressing, Mouse Assay, High Performance Liquid Chromatography, Enzyme-linked Immunosorbent Assay, Stripping Membranes