We are analyzing https://link.springer.com/article/10.1186/1476-4598-13-89.

Title:
TFAP2B overexpression contributes to tumor growth and a poor prognosis of human lung adenocarcinoma through modulation of ERK and VEGF/PEDF signaling | Molecular Cancer
Description:
Background TFAP2B is a member of the AP2 transcription factor family, which orchestrates a variety of cell processes. However, the roles of TFAP2B in regulating carcinogenesis remain largely unknown. Here, we investigated the regulatory effects of TFAP2B on lung adenocarcinomas growth and identified the underlying mechanisms of actions in non-small cell lung cancer (NSCLC) cells. Methods We first examined the expression of TFAP2B in lung cancer cell lines and tumor tissues. We also analyzed the prognostic predicting value of TFAP2B in lung adenocarcinomas. Then we investigated the molecular mechanisms by which TFAP2B knockdown or overexpression regulated lung cancer cell growth, angiogenesis and apoptosis, and further confirmed the role of TFAP2B in tumor growth in a lung cancer xenograft mouse model. Results TFAP2B was highly expressed in NSCLC cell lines and tumor tissues. Strong TFAP2B expression showed a positive correlation with the poor prognoses of patients with lung adenocarcinomas (P < 0.001). TFAP2B knockdown by siRNA significantly inhibited cell growth and induced apoptosis in NSCLC cells in vitro and in a lung cancer subcutaneous xenograft model, whereas TFAP2B overexpression promoted cell growth. The observed regulation of cell growth was accompanied by the TFAP2B-mediated modulation of the ERK/p38, caspase/cytochrome-c and VEGF/PEDF-dependent signaling pathways in NSCLC cells. Conclusions These results indicate that TFAP2B plays a critical role in regulating lung adenocarcinomas growth and could serve as a promising therapeutic target for lung cancer treatment.
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Keywords {🔍}

tfapb, lung, cancer, cells, cell, article, tumor, expression, pubmed, google, scholar, cas, figure, growth, sirna, knockdown, vegf, human, apoptosis, analysis, analyzed, signaling, factor, protein, levels, pedf, shrna, proteins, overexpression, transcription, adenocarcinomas, role, factors, vivo, tumors, sitfapb, prognosis, effect, control, staining, transfection, lines, results, patients, treatment, survival, stage, transfected, authors, tissues,

Topics {✒️}

annexin v-fitc/pi-staining kit hrp-labeled anti-rabbit igg vegf/pedf-dependent signaling pathways 5 μl annexin v-fitc caspase-dependent apoptotic pathway erk/p38 signaling pathway cancer-related deaths worldwide[1 caspase-dependent signaling pathways pathologic tumor-node-metastasis stage transcription factor tcfap2c/tfap2c pigment epithelium-derived factor sterilized de-ionized water n1–n2-n3–n4 open access license article download pdf small-cell lung cancer caspase-dependent apoptosis pathway mapk signaling pathways pearson chi-square test central south university growth factor-reduced matrigel gc-rich consensus sequences caspase-dependent apoptosis pathways dc-based tfap2b sirna tube formation assay pathologic tumor-node-metastasis tube formation ability state key laboratory anti-apoptotic protein bcl-2 high-tfap2b group compared tfap2b-weakly positive/negative tumors human tfap2b-specific sirna tfap2b sirna-mediated inhibition tumor suppressor activity apoptosis signaling pathway activator protein-2alpha results signaling pathways remain tfap2b overexpression contributes phosphate-buffered saline caspase-dependent pathways transcription factor ap-2 ap-2 transcription factor cancer-related mortality shared pathway underlying normal cell lines related subjects erk/p38 signaling colony formation rate colony formation ratio privacy choices/manage cookies

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         description:TFAP2B is a member of the AP2 transcription factor family, which orchestrates a variety of cell processes. However, the roles of TFAP2B in regulating carcinogenesis remain largely unknown. Here, we investigated the regulatory effects of TFAP2B on lung adenocarcinomas growth and identified the underlying mechanisms of actions in non-small cell lung cancer (NSCLC) cells. We first examined the expression of TFAP2B in lung cancer cell lines and tumor tissues. We also analyzed the prognostic predicting value of TFAP2B in lung adenocarcinomas. Then we investigated the molecular mechanisms by which TFAP2B knockdown or overexpression regulated lung cancer cell growth, angiogenesis and apoptosis, and further confirmed the role of TFAP2B in tumor growth in a lung cancer xenograft mouse model. TFAP2B was highly expressed in NSCLC cell lines and tumor tissues. Strong TFAP2B expression showed a positive correlation with the poor prognoses of patients with lung adenocarcinomas (P < 0.001). TFAP2B knockdown by siRNA significantly inhibited cell growth and induced apoptosis in NSCLC cells in vitro and in a lung cancer subcutaneous xenograft model, whereas TFAP2B overexpression promoted cell growth. The observed regulation of cell growth was accompanied by the TFAP2B-mediated modulation of the ERK/p38, caspase/cytochrome-c and VEGF/PEDF-dependent signaling pathways in NSCLC cells. These results indicate that TFAP2B plays a critical role in regulating lung adenocarcinomas growth and could serve as a promising therapeutic target for lung cancer treatment.
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               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:State Key Laboratory of Oncology in South China, Colaborative Innovation Center of Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, China
      name:Department of Geratology, Xiangya Hospital, Central South University, Changsha, China
      name:State Key Laboratory of Oncology in South China, Colaborative Innovation Center of Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, China
      name:State Key Laboratory of Oncology in South China, Colaborative Innovation Center of Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, China
      name:State Key Laboratory of Oncology in South China, Colaborative Innovation Center of Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, China
      name:State Key Laboratory of Oncology in South China, Colaborative Innovation Center of Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, China
      name:Institute of Cancer Stem Cell, Dalian Medical University, Dalian, China
      name:Institute of Cancer Stem Cell, Dalian Medical University, Dalian, China
      name:State Key Laboratory of Oncology in South China, Colaborative Innovation Center of Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, China
      name:State Key Laboratory of Oncology in South China, Colaborative Innovation Center of Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, China
      name:State Key Laboratory of Oncology in South China, Colaborative Innovation Center of Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, China
      name:State Key Laboratory of Oncology in South China, Colaborative Innovation Center of Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, China
      name:State Key Laboratory of Targeted Drug for Tumors of Guangdong Province, Guangzhou Double Bioproduct Inc., Guangzhou, China
      name:State Key Laboratory of Oncology in South China, Colaborative Innovation Center of Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, China
      name:Institute of Cancer Stem Cell, Dalian Medical University, Dalian, China
      name:State Key Laboratory of Targeted Drug for Tumors of Guangdong Province, Guangzhou Double Bioproduct Inc., Guangzhou, China

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