Presentation is loading. Please wait.

Presentation is loading. Please wait.

Nicotinamide Phosphoribosyltransferase: A Potent Therapeutic Target in Non-small Cell Lung Cancer with Epidermal Growth Factor Receptor-Gene Mutation 

Published byJeffry Carter Modified over 6 years ago

Similar presentations

Presentation on theme: "Nicotinamide Phosphoribosyltransferase: A Potent Therapeutic Target in Non-small Cell Lung Cancer with Epidermal Growth Factor Receptor-Gene Mutation "— Presentation transcript:

1 Nicotinamide Phosphoribosyltransferase: A Potent Therapeutic Target in Non-small Cell Lung Cancer with Epidermal Growth Factor Receptor-Gene Mutation  Shunsuke Okumura, MD, PhD, Takaaki Sasaki, MD, PhD, Yoshinori Minami, MD, Yoshinobu Ohsaki, MD, PhD  Journal of Thoracic Oncology  Volume 7, Issue 1, Pages (January 2012) DOI: /JTO.0b013e318233d686 Copyright © 2012 International Association for the Study of Lung Cancer Terms and Conditions

2 FIGURE 1 Non-small cell lung cancer (NSCLC) cells overexpress NAMPT-mRNA and NAMPT-specific siRNA suppresses proliferation of NSCLC. A, The expression of NAMPT-mRNA in NSCLCs was measured by real-time reverse-transcriptase polymerase chain reaction (RT-PCR). NAMPT-expression levels were normalized to GAPDH-expression levels. The mean values were determined from three independent experiments. B, Cell proliferation was measured by BrdU assay on day 3 after siRNA transfection. The values were converted to a ratio in which each value in treated cells was compared with those in nontreated cells. The mean values were obtained from four independent experiments. Journal of Thoracic Oncology 2012 7, 49-56DOI: ( /JTO.0b013e318233d686) Copyright © 2012 International Association for the Study of Lung Cancer Terms and Conditions

3 FIGURE 2 FK866 suppresses proliferation of non-small cell lung cancer (NSCLC) cells. Cells were treated with the indicated concentrations of FK866 for 72 hours, and proliferation was measured by BrdU assay. The mean values were calculated from the three independent experiments. Journal of Thoracic Oncology 2012 7, 49-56DOI: ( /JTO.0b013e318233d686) Copyright © 2012 International Association for the Study of Lung Cancer Terms and Conditions

4 FIGURE 3 Intracellular ATP levels decrease in FK866-treated non-small cell lung cancer (NSCLC). H1975 cells were treated with 1 nM or 10 nM FK866. ATP bioluminescence was assayed to measure ATP levels on the indicated times. The values are shown as a ratio (treated/nontreated). Journal of Thoracic Oncology 2012 7, 49-56DOI: ( /JTO.0b013e318233d686) Copyright © 2012 International Association for the Study of Lung Cancer Terms and Conditions

5 FIGURE 4 FK866 suppresses phosphorylation of EGFR-signal proteins in non-small cell lung cancer (NSCLC). A, H1975 cells were treated with or without 50 nM FK866 for the indicated periods. The expressions of p-EGFR and β-actin proteins at the indicated hours were assessed by WB. B, H1975 cells were treated with gefitinib or FK866 for 72 hours. The expression of EGFR-signal proteins was evaluated by WB. C, LC2, H1975, and PC9 cells were treated with the indicated concentrations of gefitinib or FK866. MEK1/2 and p-MEK1/2 expressions were assessed by WB. Journal of Thoracic Oncology 2012 7, 49-56DOI: ( /JTO.0b013e318233d686) Copyright © 2012 International Association for the Study of Lung Cancer Terms and Conditions

6 FIGURE 5 FK866 induces apoptosis of H1975 cells. H1975 cells were treated with 10 μM gefitinib or 50 nM FK866 for 72 hours. Apoptosis was visualized by FACS. A, Apoptosis was measured by PI-labeled cell counts (right), and the early phase of apoptosis was measured by annexin V-FITC signals (left). B, Numbers of apoptotic cells in treated cells. The values were converted to the percentage of apoptotic cells. The mean values were obtained from the three independent experiments. Journal of Thoracic Oncology 2012 7, 49-56DOI: ( /JTO.0b013e318233d686) Copyright © 2012 International Association for the Study of Lung Cancer Terms and Conditions

7 FIGURE 6 FK866 suppresses in vivo growth of H1975 tumors and inactivates ERK1/2 signals in the tumors. A, Nude mice were transplanted with H1975 cells and treated with 12.5 mg/kg gefitinib or 10 mg/kg FK866 on days 14 to 26. The graph shows tumor volumes measured. *p < B, Immunohistochemistry shows the expression of p-ERK1/2 proteins in xenograft tumors (×40). Compared with the control (upper) and gefitinib (lower) groups, FK866 suppressed the expression of p-ERK1/2 in the tumor (middle). Journal of Thoracic Oncology 2012 7, 49-56DOI: ( /JTO.0b013e318233d686) Copyright © 2012 International Association for the Study of Lung Cancer Terms and Conditions

Download ppt "Nicotinamide Phosphoribosyltransferase: A Potent Therapeutic Target in Non-small Cell Lung Cancer with Epidermal Growth Factor Receptor-Gene Mutation "

Similar presentations

Inhibition of autophagy augments 5-fluorouracil chemotherapy in human colon cancer in vitro and in vivo model  Jie Li, Ni Hou, Ahmad Faried, Soichi Tsutsumi,

Inhibition of autophagy augments 5-fluorouracil chemotherapy in human colon cancer in vitro and in vivo model  Jie Li, Ni Hou, Ahmad Faried, Soichi Tsutsumi,
Aldehyde Dehydrogenase 1A1 Possesses Stem-Like Properties and Predicts Lung Cancer Patient Outcome  Xiao Li, MD, Liyan Wan, MD, Jian Geng, MD, Chin-Lee.

Aldehyde Dehydrogenase 1A1 Possesses Stem-Like Properties and Predicts Lung Cancer Patient Outcome  Xiao Li, MD, Liyan Wan, MD, Jian Geng, MD, Chin-Lee.
Overexpression of CRM1: A Characteristic Feature in a Transformed Phenotype of Lung Carcinogenesis and a Molecular Target for Lung Cancer Adjuvant Therapy 

Overexpression of CRM1: A Characteristic Feature in a Transformed Phenotype of Lung Carcinogenesis and a Molecular Target for Lung Cancer Adjuvant Therapy 
INHBA Overexpression Promotes Cell Proliferation and May Be Epigenetically Regulated in Esophageal Adenocarcinoma  Christopher W. Seder, MD, Wibisono.

INHBA Overexpression Promotes Cell Proliferation and May Be Epigenetically Regulated in Esophageal Adenocarcinoma  Christopher W. Seder, MD, Wibisono.
The Autophagy Inhibitor Chloroquine Overcomes the Innate Resistance of Wild-Type EGFR Non-Small-Cell Lung Cancer Cells to Erlotinib  Yiyu Zou, PhD, Yi-He.

The Autophagy Inhibitor Chloroquine Overcomes the Innate Resistance of Wild-Type EGFR Non-Small-Cell Lung Cancer Cells to Erlotinib  Yiyu Zou, PhD, Yi-He.
The Epidermal Growth Factor Receptor-L861Q Mutation Increases Kinase Activity without Leading to Enhanced Sensitivity Toward Epidermal Growth Factor Receptor.

The Epidermal Growth Factor Receptor-L861Q Mutation Increases Kinase Activity without Leading to Enhanced Sensitivity Toward Epidermal Growth Factor Receptor.
PI3K as a Potential Therapeutic Target in Thymic Epithelial Tumors

PI3K as a Potential Therapeutic Target in Thymic Epithelial Tumors
Group IIa secretory phospholipase expression correlates with group IIa secretory phospholipase inhibition–mediated cell death in K-ras mutant lung cancer.

Group IIa secretory phospholipase expression correlates with group IIa secretory phospholipase inhibition–mediated cell death in K-ras mutant lung cancer.
Yunguang Sun, PhD, Luigi Moretti, MD, Nicholas J

Yunguang Sun, PhD, Luigi Moretti, MD, Nicholas J
Upregulation of PD-L1 by EGFR Activation Mediates the Immune Escape in EGFR- Driven NSCLC: Implication for Optional Immune Targeted Therapy for NSCLC Patients.

Upregulation of PD-L1 by EGFR Activation Mediates the Immune Escape in EGFR- Driven NSCLC: Implication for Optional Immune Targeted Therapy for NSCLC Patients.
Integrin αvβ6 Promotes Lung Cancer Proliferation and Metastasis through Upregulation of IL-8–Mediated MAPK/ERK Signaling  Pengwei Yan, Huanfeng Zhu, Li.

Integrin αvβ6 Promotes Lung Cancer Proliferation and Metastasis through Upregulation of IL-8–Mediated MAPK/ERK Signaling  Pengwei Yan, Huanfeng Zhu, Li.
Inactivation of Both FHIT and p53 Cooperate in Deregulating Proliferation-Related Pathways in Lung Cancer  Francesca Andriani, PharmD, Elena Roz, MD,

Inactivation of Both FHIT and p53 Cooperate in Deregulating Proliferation-Related Pathways in Lung Cancer  Francesca Andriani, PharmD, Elena Roz, MD,
Nicotine Induces Resistance to Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitor by α1 Nicotinic Acetylcholine Receptor–Mediated Activation in.

Nicotine Induces Resistance to Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitor by α1 Nicotinic Acetylcholine Receptor–Mediated Activation in.
Knockdown of secretory phospholipase A2 IIa reduces lung cancer growth in vitro and in vivo  Jessica A. Yu, MD, David Mauchley, MD, Howard Li, MD, Xianzhong.

Knockdown of secretory phospholipase A2 IIa reduces lung cancer growth in vitro and in vivo  Jessica A. Yu, MD, David Mauchley, MD, Howard Li, MD, Xianzhong.
INHBA Overexpression Promotes Cell Proliferation and May Be Epigenetically Regulated in Esophageal Adenocarcinoma  Christopher W. Seder, MD, Wibisono.

INHBA Overexpression Promotes Cell Proliferation and May Be Epigenetically Regulated in Esophageal Adenocarcinoma  Christopher W. Seder, MD, Wibisono.
Improved Response to nab-Paclitaxel Compared with Cremophor-Solubilized Paclitaxel is Independent of Secreted Protein Acidic and Rich in Cysteine Expression.

Improved Response to nab-Paclitaxel Compared with Cremophor-Solubilized Paclitaxel is Independent of Secreted Protein Acidic and Rich in Cysteine Expression.
MET Tyrosine Kinase Inhibitor Crizotinib (PF-02341066) Shows Differential Antitumor Effects in Non-small Cell Lung Cancer According to MET Alterations 

MET Tyrosine Kinase Inhibitor Crizotinib (PF ) Shows Differential Antitumor Effects in Non-small Cell Lung Cancer According to MET Alterations 
IFN-γ Induces Gastric Cancer Cell Proliferation and Metastasis Through Upregulation of Integrin β3-Mediated NF-κB Signaling  Yuan-Hua Xu, Zheng-Li Li,

IFN-γ Induces Gastric Cancer Cell Proliferation and Metastasis Through Upregulation of Integrin β3-Mediated NF-κB Signaling  Yuan-Hua Xu, Zheng-Li Li,
EGFR and KRAS Mutations in Triple-Mutated Lung Cancer

EGFR and KRAS Mutations in Triple-Mutated Lung Cancer
The Zinc Ionophore PCI-5002 Radiosensitizes Non-small Cell Lung Cancer Cells by Enhancing Autophagic Cell Death  Kwang Woon Kim, PhD, Christina K. Speirs,

The Zinc Ionophore PCI-5002 Radiosensitizes Non-small Cell Lung Cancer Cells by Enhancing Autophagic Cell Death  Kwang Woon Kim, PhD, Christina K. Speirs,

Similar presentations

Ads by Google