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{"title"=>"Berberine Targets AP-2/hTERT, NF-κB/COX-2, HIF-1α/VEGF and Cytochrome-c/Caspase Signaling to Suppress Human Cancer Cell Growth", "type"=>"journal", "authors"=>[{"first_name"=>"Lingyi", "last_name"=>"Fu", "scopus_author_id"=>"54981852700"}, {"first_name"=>"Wangbing", "last_name"=>"Chen", "scopus_author_id"=>"54981888500"}, {"first_name"=>"Wei", "last_name"=>"Guo", "scopus_author_id"=>"56555589400"}, {"first_name"=>"Jingshu", "last_name"=>"Wang", "scopus_author_id"=>"54979144700"}, {"first_name"=>"Yun", "last_name"=>"Tian", "scopus_author_id"=>"55555157700"}, {"first_name"=>"Dingbo", "last_name"=>"Shi", "scopus_author_id"=>"49461854500"}, {"first_name"=>"Xiaohong", "last_name"=>"Zhang", "scopus_author_id"=>"56034122800"}, {"first_name"=>"Huijuan", "last_name"=>"Qiu", "scopus_author_id"=>"35173367800"}, {"first_name"=>"Xiangsheng", "last_name"=>"Xiao", "scopus_author_id"=>"56424579100"}, {"first_name"=>"Tiebang", "last_name"=>"Kang", "scopus_author_id"=>"7402965550"}, {"first_name"=>"Wenlin", "last_name"=>"Huang", "scopus_author_id"=>"36065549400"}, {"first_name"=>"Shusen", "last_name"=>"Wang", "scopus_author_id"=>"36807318600"}, {"first_name"=>"Wuguo", "last_name"=>"Deng", "scopus_author_id"=>"7202223628"}], "year"=>2013, "source"=>"PLoS ONE", "identifiers"=>{"issn"=>"19326203", "pui"=>"369345733", "doi"=>"10.1371/journal.pone.0069240", "sgr"=>"84880252424", "scopus"=>"2-s2.0-84880252424", "isbn"=>"2011017111007", "pmid"=>"23869238"}, "id"=>"555e21f8-c9a7-3756-936c-85a09166fe38", "abstract"=>"Berberine (BBR), an isoquinoline derivative alkaloid isolated from Chinese herbs, has a long history of uses for the treatment of multiple diseases, including cancers. However, the precise mechanisms of actions of BBR in human lung cancer cells remain unclear. In this study, we investigated the molecular mechanisms by which BBR inhibits cell growth in human non-small-cell lung cancer (NSCLC) cells. Treatment with BBR promoted cell morphology change, inhibited cell migration, proliferation and colony formation, and induced cell apoptosis. Further molecular mechanism study showed that BBR simultaneously targeted multiple cell signaling pathways to inhibit NSCLC cell growth. Treatment with BBR inhibited AP-2α and AP-2β expression and abrogated their binding on hTERT promoters, thereby inhibiting hTERT expression. Knockdown of AP-2α and AP-2β by siRNA considerably augmented the BBR-mediated inhibition of cell growth. BBR also suppressed the nuclear translocation of p50/p65 NF-κB proteins and their binding to COX-2 promoter, causing inhibition of COX-2. BBR also downregulated HIF-1α and VEGF expression and inhibited Akt and ERK phosphorylation. Knockdown of HIF-1α by siRNA considerably augmented the BBR-mediated inhibition of cell growth. Moreover, BBR treatment triggered cytochrome-c release from mitochondrial inter-membrane space into cytosol, promoted cleavage of caspase and PARP, and affected expression of BAX and Bcl-2, thereby activating apoptotic pathway. Taken together, these results demonstrated that BBR inhibited NSCLC cell growth by simultaneously targeting AP-2/hTERT, NF-κB/COX-2, HIF-1α/VEGF, PI3K/AKT, Raf/MEK/ERK and cytochrome-c/caspase signaling pathways. Our findings provide new insights into understanding the anticancer mechanisms of BBR in human lung cancer therapy.", "link"=>"http://www.mendeley.com/research/berberine-targets-ap2htert-nf%CE%BAbcox2-hif1%CE%B1vegf-cytochromeccaspase-signaling-suppress-human-cancer-cel", "reader_count"=>19, "reader_count_by_academic_status"=>{"Professor > Associate Professor"=>1, "Librarian"=>1, "Researcher"=>4, "Student > Ph. D. Student"=>7, "Student > Postgraduate"=>2, "Other"=>1, "Student > Master"=>2, "Unspecified"=>1}, "reader_count_by_user_role"=>{"Professor > Associate Professor"=>1, "Librarian"=>1, "Researcher"=>4, "Student > Ph. D. Student"=>7, "Student > Postgraduate"=>2, "Other"=>1, "Student > Master"=>2, "Unspecified"=>1}, "reader_count_by_subject_area"=>{"Unspecified"=>4, "Biochemistry, Genetics and Molecular Biology"=>3, "Medicine and Dentistry"=>3, "Agricultural and Biological Sciences"=>6, "Pharmacology, Toxicology and Pharmaceutical Science"=>1, "Physics and Astronomy"=>1, "Immunology and Microbiology"=>1}, "reader_count_by_subdiscipline"=>{"Medicine and Dentistry"=>{"Medicine and Dentistry"=>3}, "Physics and Astronomy"=>{"Physics and Astronomy"=>1}, "Immunology and Microbiology"=>{"Immunology and Microbiology"=>1}, "Agricultural and Biological Sciences"=>{"Agricultural and Biological Sciences"=>6}, "Biochemistry, Genetics and Molecular Biology"=>{"Biochemistry, Genetics and Molecular Biology"=>3}, "Unspecified"=>{"Unspecified"=>4}, "Pharmacology, Toxicology and Pharmaceutical Science"=>{"Pharmacology, Toxicology and Pharmaceutical Science"=>1}}, "reader_count_by_country"=>{"Malaysia"=>1, "India"=>3}, "group_count"=>2}

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• {"files"=>["https://ndownloader.figshare.com/files/1118865"], "description"=>"<p>(<b>A</b>–<b>C</b>) Human NSCLC A549 cells were treated with BBR at the indicated doses. At 48 hours after treatment, the AP-2 and hTERT proteins (<b>A</b>) and mRNA (<b>B</b>) were analyzed by Western blotting and RT-PCR, respectively. GAPDH were used as controls for sample loading. The binding of AP-2 to hTERT promoter probe (<b>C</b>) was analyzed by a streptavidin-agarose pulldown assay. (<b>D</b>) A549 cells were transfected with an AP-2 siRNA or an AP-2-expressing vector for 24 hours, and then treated with BBR (100 µM). At 48 hours after treatment, protein expression and cell viability were determined by Western blot and MTT assay, respectively. The percent cell viability in each treatment group was calculated relative to cells treated with the vehicle control. The data are presented as the mean ± SD of three separate experiments. *, P < 0.05, significant differences between treatment groups and DMSO control groups.</p>", "links"=>[], "tags"=>["inhibited"], "article_id"=>745400, "categories"=>["Biological Sciences"], "users"=>["Lingyi Fu", "Wangbing Chen", "Wei Guo", "Jingshu Wang", "Yun Tian", "Dingbo Shi", "Xiaohong Zhang", "Huijuan Qiu", "Xiangsheng Xiao", "Tiebang Kang", "Wenlin Huang", "Shusen Wang", "Wuguo Deng"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0069240.g003", "stats"=>{"downloads"=>0, "page_views"=>5, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_BBR_inhibited_AP_2_hTERT_signaling_/745400", "title"=>"BBR inhibited AP-2/hTERT signaling.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2013-07-15 01:30:18"}
• {"files"=>["https://ndownloader.figshare.com/files/1118870"], "description"=>"<p>A549 cells were treated with BBR at the indicated doses. At 48 hours after treatment, the expression of HIF-1α, VEGF and PEDF at protein (<b>A</b>) or mRNA levels (<b>B</b>), as well as the total and phosphorylated Akt and ERK1/2 proteins (<b>D</b>), were determined. A549 cells were treated with the HIF-1α-specific siRNA (si-HIF) (<b>C</b>) or the Akt-selective inhibitor LY294002 (LY,30 µM) or the ERK-selective inhibitor U0126 (U, 50 µM) (E) for 24 hours, respectively, and then treated with BBR. At 48 hours after treatment, cell viability was determined by MTT analysis. The percent cell viability in each treatment group was calculated relative to cells treated with the vehicle control. The data are presented as the mean ± SD of three separate experiments. *, P < 0.05, significant differences between treatment groups and DMSO control groups.</p>", "links"=>[], "tags"=>["inhibited", "bbr"], "article_id"=>745405, "categories"=>["Biological Sciences"], "users"=>["Lingyi Fu", "Wangbing Chen", "Wei Guo", "Jingshu Wang", "Yun Tian", "Dingbo Shi", "Xiaohong Zhang", "Huijuan Qiu", "Xiangsheng Xiao", "Tiebang Kang", "Wenlin Huang", "Shusen Wang", "Wuguo Deng"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0069240.g005", "stats"=>{"downloads"=>0, "page_views"=>20, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_BBR_inhibited_BBR_inhibited_HIF_1_945_VEGF_Raf_MEK_ERK_and_PI3K_AKT_signaling_/745405", "title"=>"BBR inhibited BBR inhibited HIF-1α/VEGF Raf/MEK/ERK and PI3K/AKT signaling.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2013-07-15 01:30:18"}
• {"files"=>["https://ndownloader.figshare.com/files/1118863"], "description"=>"<p>(<b>A</b>–<b>C</b>) Human A549 and H1299 cells were treated with BBR at the indicated doses. At 48 hours after treatment, the cell viability was determined by a MTT assay. The IC50 values of BBR for A549 and H1299 cells were calculated (<b>A</b>). The tumor cell A549-induced colony formation was also analyzed (<b>B</b>), and the colony formation rate (<b>C</b>) and colony size (<b>D</b>) were calculated. Cells treated with DMSO were used as the referent group with cell viability set at 100%. The percent cell viability in each treatment group was calculated relative to cells treated with DMSO vehicle control. The data are presented as mean ± SD of three tests. *, P < 0.05, significant differences between treatment groups and DMSO control groups.</p>", "links"=>[], "tags"=>["suppressed", "cancer", "proliferation"], "article_id"=>745398, "categories"=>["Biological Sciences"], "users"=>["Lingyi Fu", "Wangbing Chen", "Wei Guo", "Jingshu Wang", "Yun Tian", "Dingbo Shi", "Xiaohong Zhang", "Huijuan Qiu", "Xiangsheng Xiao", "Tiebang Kang", "Wenlin Huang", "Shusen Wang", "Wuguo Deng"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0069240.g002", "stats"=>{"downloads"=>0, "page_views"=>2, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_BBR_suppressed_lung_cancer_cell_proliferation_and_colony_formation_/745398", "title"=>"BBR suppressed lung cancer cell proliferation and colony formation.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2013-07-15 01:30:18"}
• {"files"=>["https://ndownloader.figshare.com/files/1118871"], "description"=>"<p>A549 and H1299 cells were treated with BBR (20 µM or 100 µM). At 48 hours after treatment, the apoptosis was determined by a FACS analysis (<b>A</b>). The levels of the cleaved caspase-3, 7, 9, cleaved PARP, BAX and Bcl-2 proteins in A549 cells were analyzed by Western blot (<b>B</b>). The release of Cyt-c in A549 cells was analyzed by immunofluorescence imaging analysis to monitor Cyt-c release from the inter-mitochondrial space into the cytosol (<b>C</b>). The apoptosis are represented by relative percentages of apoptotic cells versus that in DMSO-treated cells. *, P<0.05, significant differences between the BBR-treated groups and the DMSO-treated groups.</p>", "links"=>[], "tags"=>["activated", "caspase-dependet", "apoptotic"], "article_id"=>745406, "categories"=>["Biological Sciences"], "users"=>["Lingyi Fu", "Wangbing Chen", "Wei Guo", "Jingshu Wang", "Yun Tian", "Dingbo Shi", "Xiaohong Zhang", "Huijuan Qiu", "Xiangsheng Xiao", "Tiebang Kang", "Wenlin Huang", "Shusen Wang", "Wuguo Deng"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0069240.g006", "stats"=>{"downloads"=>0, "page_views"=>7, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_BBR_activated_caspase_dependet_apoptotic_pathway_/745406", "title"=>"BBR activated caspase-dependet apoptotic pathway.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2013-07-15 01:30:18"}
• {"files"=>["https://ndownloader.figshare.com/files/1118867"], "description"=>"<p>(<b>A</b>) Human A549 cells were treated with BBR at the indicated doses. At 48 hours after treatment, the COX-2 protein was analyzed by Western blotting. GAPDH were used as controls for sample loading. (<b>B</b>) A549 cells were pretreated with the COX-2 selective inhibitor celecoxib (CB, 20 µM) for 24 hours, and then treated with BBR (20 µM). At 48 hours after treatment, cell viability was determined by MTT analysis. The percent cell viability in each treatment group was calculated relative to cells treated with the vehicle control. (<b>C</b>) A549 cells were treated with BBR at the indicated doses. At 48 hours after treatment, the binding of p50 and p65 to COX-2 promoter probe was analyzed by a streptavidin-agarose pulldown assay. (<b>D</b>) A549 cells were treated with BBR (100 nM). At 48 hours after treatment, the effect of BBR on NF-κB p65 and p50 translocation was analyzed by immunofluorescence assay. The data are presented as the mean ± SD of three separate experiments. *, P < 0.05, significant differences between treatment groups and DMSO control groups.</p>", "links"=>[], "tags"=>["inhibited"], "article_id"=>745402, "categories"=>["Biological Sciences"], "users"=>["Lingyi Fu", "Wangbing Chen", "Wei Guo", "Jingshu Wang", "Yun Tian", "Dingbo Shi", "Xiaohong Zhang", "Huijuan Qiu", "Xiangsheng Xiao", "Tiebang Kang", "Wenlin Huang", "Shusen Wang", "Wuguo Deng"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0069240.g004", "stats"=>{"downloads"=>0, "page_views"=>2, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_BBR_inhibited_NF_954_B_COX_2_signaling_/745402", "title"=>"BBR inhibited NF-κB/COX-2 signaling.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2013-07-15 01:30:18"}

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Relative Metric

{"start_date"=>"2013-01-01T00:00:00Z", "end_date"=>"2013-12-31T00:00:00Z", "subject_areas"=>[{"subject_area"=>"/Biology and life sciences", "average_usage"=>[269, 466, 588, 697, 800, 896, 988, 1076, 1165, 1254, 1340, 1417]}, {"subject_area"=>"/Medicine and health sciences/Oncology", "average_usage"=>[249, 468, 599, 718, 820, 920, 1008, 1093, 1181, 1281, 1357, 1444, 1517]}, {"subject_area"=>"/Medicine and health sciences/Pain management", "average_usage"=>[259, 460, 588, 720, 834, 951, 1056, 1139, 1222, 1315, 1391, 1497, 1570]}, {"subject_area"=>"/Medicine and health sciences/Pharmacology", "average_usage"=>[265, 471, 604, 723, 827, 926, 1022, 1113, 1210, 1290, 1377, 1454, 1532]}]}

F1000Prime