β-Apopicropodophyllin functions as a radiosensitizer targeting ER stress in non-small cell lung cancer
•β-Apopicropodophyllin is a candidate drug for treatment of non-small cell lung cancer.•Novel function of β-Apopicropodophyllin as a radiosensitizer was confirmed in vitro and in vivo.•Radiosensiting effect of β-Apopicropodophyllin is exerted by ER stress-mediated apoptosis via JNK activation. In th...
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Published in | Biomedicine & pharmacotherapy Vol. 113; p. 108769 |
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Main Authors | , , , , , , , |
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Abstract | •β-Apopicropodophyllin is a candidate drug for treatment of non-small cell lung cancer.•Novel function of β-Apopicropodophyllin as a radiosensitizer was confirmed in vitro and in vivo.•Radiosensiting effect of β-Apopicropodophyllin is exerted by ER stress-mediated apoptosis via JNK activation.
In this study, we examined whether β-apopicropodophyllin (APP) could act as a radiosensitizer in non-small cell lung cancer (NSCLC) cells.
The in vitro radiosensitizing activity of APP was demonstrated with clonogenic assay, immunoblotting, Annexin V-Propidium iodide (PI) assay, BrdU incorporation, detection of mitochondrial ROS/intracellular of H2O2, mitochondrial membrane potential detection, and performing of isolation of mitochondrial and cytosolic fractions. The in vivo radiosensitizing activity of APP was determined in xenografted mice with co-treatment of APP and IR based on measurement of tumor volumes and apoptotic cell death.
The results of a clonogenic assay indicated that a combination of APP and γ-ionizing radiation (IR) inhibits cell growth and increases cell death in NSCLC cells. Several signal transduction pathways were examined for their potential involvement in the apparent radiosensitization effect of APP, as assessed by immunoblotting analyses and mitochondrial potential determination in vitro. Treatment of NCI-H460 cells with 15 nM APP and NCI-H1299 cells with 10 nM APP yielded dose-enhancement ratios of 1.44 and 1.24, respectively. Enhanced ER stress, disrupted mitochondrial membrane potential, and increased reactive oxygen species (ROS) were observed in cells co-treated with APP and IR, and this was followed by the cytosolic release of cytochrome c and consequent activation of caspase-3 and -9. Notably, inhibition of JNK, which prevents caspase activation, blocked the APP/IR-induced activations of ER stress and apoptotic cell death. In NCI-H460 or NCI-H1299 cell-xenografted mice, APP/IR treatment delayed the time it took tumors to reach a threshold size by 22.38 and 16.83 days, respectively, compared with controls, to yield enhancement factors of 1.53 and 1.38, respectively.
APP has a radiosensitizing function derived from its ability to induce apoptotic cell death via activation of ER stress, disruption of mitochondrial membrane potential, and induction of the caspase pathway. |
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AbstractList | AIMSIn this study, we examined whether β-apopicropodophyllin (APP) could act as a radiosensitizer in non-small cell lung cancer (NSCLC) cells.MAIN METHODSThe in vitro radiosensitizing activity of APP was demonstrated with clonogenic assay, immunoblotting, Annexin V-Propidium iodide (PI) assay, BrdU incorporation, detection of mitochondrial ROS/intracellular of H2O2, mitochondrial membrane potential detection, and performing of isolation of mitochondrial and cytosolic fractions. The in vivo radiosensitizing activity of APP was determined in xenografted mice with co-treatment of APP and IR based on measurement of tumor volumes and apoptotic cell death.KEY FINDINGSThe results of a clonogenic assay indicated that a combination of APP and γ-ionizing radiation (IR) inhibits cell growth and increases cell death in NSCLC cells. Several signal transduction pathways were examined for their potential involvement in the apparent radiosensitization effect of APP, as assessed by immunoblotting analyses and mitochondrial potential determination in vitro. Treatment of NCI-H460 cells with 15 nM APP and NCI-H1299 cells with 10 nM APP yielded dose-enhancement ratios of 1.44 and 1.24, respectively. Enhanced ER stress, disrupted mitochondrial membrane potential, and increased reactive oxygen species (ROS) were observed in cells co-treated with APP and IR, and this was followed by the cytosolic release of cytochrome c and consequent activation of caspase-3 and -9. Notably, inhibition of JNK, which prevents caspase activation, blocked the APP/IR-induced activations of ER stress and apoptotic cell death. In NCI-H460 or NCI-H1299 cell-xenografted mice, APP/IR treatment delayed the time it took tumors to reach a threshold size by 22.38 and 16.83 days, respectively, compared with controls, to yield enhancement factors of 1.53 and 1.38, respectively.SIGNIFICANCEAPP has a radiosensitizing function derived from its ability to induce apoptotic cell death via activation of ER stress, disruption of mitochondrial membrane potential, and induction of the caspase pathway. •β-Apopicropodophyllin is a candidate drug for treatment of non-small cell lung cancer.•Novel function of β-Apopicropodophyllin as a radiosensitizer was confirmed in vitro and in vivo.•Radiosensiting effect of β-Apopicropodophyllin is exerted by ER stress-mediated apoptosis via JNK activation. In this study, we examined whether β-apopicropodophyllin (APP) could act as a radiosensitizer in non-small cell lung cancer (NSCLC) cells. The in vitro radiosensitizing activity of APP was demonstrated with clonogenic assay, immunoblotting, Annexin V-Propidium iodide (PI) assay, BrdU incorporation, detection of mitochondrial ROS/intracellular of H2O2, mitochondrial membrane potential detection, and performing of isolation of mitochondrial and cytosolic fractions. The in vivo radiosensitizing activity of APP was determined in xenografted mice with co-treatment of APP and IR based on measurement of tumor volumes and apoptotic cell death. The results of a clonogenic assay indicated that a combination of APP and γ-ionizing radiation (IR) inhibits cell growth and increases cell death in NSCLC cells. Several signal transduction pathways were examined for their potential involvement in the apparent radiosensitization effect of APP, as assessed by immunoblotting analyses and mitochondrial potential determination in vitro. Treatment of NCI-H460 cells with 15 nM APP and NCI-H1299 cells with 10 nM APP yielded dose-enhancement ratios of 1.44 and 1.24, respectively. Enhanced ER stress, disrupted mitochondrial membrane potential, and increased reactive oxygen species (ROS) were observed in cells co-treated with APP and IR, and this was followed by the cytosolic release of cytochrome c and consequent activation of caspase-3 and -9. Notably, inhibition of JNK, which prevents caspase activation, blocked the APP/IR-induced activations of ER stress and apoptotic cell death. In NCI-H460 or NCI-H1299 cell-xenografted mice, APP/IR treatment delayed the time it took tumors to reach a threshold size by 22.38 and 16.83 days, respectively, compared with controls, to yield enhancement factors of 1.53 and 1.38, respectively. APP has a radiosensitizing function derived from its ability to induce apoptotic cell death via activation of ER stress, disruption of mitochondrial membrane potential, and induction of the caspase pathway. In this study, we examined whether β-apopicropodophyllin (APP) could act as a radiosensitizer in non-small cell lung cancer (NSCLC) cells. The in vitro radiosensitizing activity of APP was demonstrated with clonogenic assay, immunoblotting, Annexin V-Propidium iodide (PI) assay, BrdU incorporation, detection of mitochondrial ROS/intracellular of H O , mitochondrial membrane potential detection, and performing of isolation of mitochondrial and cytosolic fractions. The in vivo radiosensitizing activity of APP was determined in xenografted mice with co-treatment of APP and IR based on measurement of tumor volumes and apoptotic cell death. The results of a clonogenic assay indicated that a combination of APP and γ-ionizing radiation (IR) inhibits cell growth and increases cell death in NSCLC cells. Several signal transduction pathways were examined for their potential involvement in the apparent radiosensitization effect of APP, as assessed by immunoblotting analyses and mitochondrial potential determination in vitro. Treatment of NCI-H460 cells with 15 nM APP and NCI-H1299 cells with 10 nM APP yielded dose-enhancement ratios of 1.44 and 1.24, respectively. Enhanced ER stress, disrupted mitochondrial membrane potential, and increased reactive oxygen species (ROS) were observed in cells co-treated with APP and IR, and this was followed by the cytosolic release of cytochrome c and consequent activation of caspase-3 and -9. Notably, inhibition of JNK, which prevents caspase activation, blocked the APP/IR-induced activations of ER stress and apoptotic cell death. In NCI-H460 or NCI-H1299 cell-xenografted mice, APP/IR treatment delayed the time it took tumors to reach a threshold size by 22.38 and 16.83 days, respectively, compared with controls, to yield enhancement factors of 1.53 and 1.38, respectively. APP has a radiosensitizing function derived from its ability to induce apoptotic cell death via activation of ER stress, disruption of mitochondrial membrane potential, and induction of the caspase pathway. Aims: In this study, we examined whether β-apopicropodophyllin (APP) could act as a radiosensitizer in non-small cell lung cancer (NSCLC) cells. Main methods: The in vitro radiosensitizing activity of APP was demonstrated with clonogenic assay, immunoblotting, Annexin V-Propidium iodide (PI) assay, BrdU incorporation, detection of mitochondrial ROS/intracellular of H2O2, mitochondrial membrane potential detection, and performing of isolation of mitochondrial and cytosolic fractions. The in vivo radiosensitizing activity of APP was determined in xenografted mice with co-treatment of APP and IR based on measurement of tumor volumes and apoptotic cell death. Key findings: The results of a clonogenic assay indicated that a combination of APP and γ-ionizing radiation (IR) inhibits cell growth and increases cell death in NSCLC cells. Several signal transduction pathways were examined for their potential involvement in the apparent radiosensitization effect of APP, as assessed by immunoblotting analyses and mitochondrial potential determination in vitro. Treatment of NCI-H460 cells with 15 nM APP and NCI-H1299 cells with 10 nM APP yielded dose-enhancement ratios of 1.44 and 1.24, respectively. Enhanced ER stress, disrupted mitochondrial membrane potential, and increased reactive oxygen species (ROS) were observed in cells co-treated with APP and IR, and this was followed by the cytosolic release of cytochrome c and consequent activation of caspase-3 and -9. Notably, inhibition of JNK, which prevents caspase activation, blocked the APP/IR-induced activations of ER stress and apoptotic cell death. In NCI-H460 or NCI-H1299 cell-xenografted mice, APP/IR treatment delayed the time it took tumors to reach a threshold size by 22.38 and 16.83 days, respectively, compared with controls, to yield enhancement factors of 1.53 and 1.38, respectively. Significance: APP has a radiosensitizing function derived from its ability to induce apoptotic cell death via activation of ER stress, disruption of mitochondrial membrane potential, and induction of the caspase pathway. |
ArticleNumber | 108769 |
Author | Park, Jong Kuk Cho, Jeong Hyun Um, Hong-Duck Song, Jie-Young Shin, Hyun-Jin Kim, Ju Yeon Kim, Eun Mi Hwang, Sang-Gu |
Author_xml | – sequence: 1 givenname: Ju Yeon surname: Kim fullname: Kim, Ju Yeon – sequence: 2 givenname: Jeong Hyun surname: Cho fullname: Cho, Jeong Hyun – sequence: 3 givenname: Eun Mi surname: Kim fullname: Kim, Eun Mi – sequence: 4 givenname: Hyun-Jin surname: Shin fullname: Shin, Hyun-Jin – sequence: 5 givenname: Sang-Gu surname: Hwang fullname: Hwang, Sang-Gu – sequence: 6 givenname: Jie-Young surname: Song fullname: Song, Jie-Young – sequence: 7 givenname: Hong-Duck surname: Um fullname: Um, Hong-Duck – sequence: 8 givenname: Jong Kuk surname: Park fullname: Park, Jong Kuk email: jkpark@kirams.re.kri |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/30870718$$D View this record in MEDLINE/PubMed |
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CitedBy_id | crossref_primary_10_3390_molecules27207008 crossref_primary_10_1080_09553002_2020_1683643 crossref_primary_10_3390_f14102002 crossref_primary_10_3390_ijms222413514 crossref_primary_10_1016_j_ajps_2024_100903 crossref_primary_10_1111_1759_7714_13358 |
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Keywords | TFs APP MKK4 JNK ROS/RNS BiP Radiosensitizer SD Gy TUNEL PO1 PDI PPT UPR eIF2 NSCLC ASK1 ER stress IR MAPK ER SAPK DER β-Apopicropodophylli ROS Non-small cell lung cancer PI ATF4 ERK Apoptosis |
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Snippet | •β-Apopicropodophyllin is a candidate drug for treatment of non-small cell lung cancer.•Novel function of β-Apopicropodophyllin as a radiosensitizer was... In this study, we examined whether β-apopicropodophyllin (APP) could act as a radiosensitizer in non-small cell lung cancer (NSCLC) cells. The in vitro... AIMSIn this study, we examined whether β-apopicropodophyllin (APP) could act as a radiosensitizer in non-small cell lung cancer (NSCLC) cells.MAIN METHODSThe... Aims: In this study, we examined whether β-apopicropodophyllin (APP) could act as a radiosensitizer in non-small cell lung cancer (NSCLC) cells. Main methods:... |
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SubjectTerms | Animals Apoptosis Apoptosis - drug effects Apoptosis - radiation effects Carcinoma, Non-Small-Cell Lung - pathology Carcinoma, Non-Small-Cell Lung - radiotherapy Cell Line, Tumor Endoplasmic Reticulum Stress - drug effects Endoplasmic Reticulum Stress - radiation effects ER stress Humans Hydrogen Peroxide - metabolism Lung Neoplasms - pathology Lung Neoplasms - radiotherapy Membrane Potential, Mitochondrial Mice Mice, Inbred BALB C Mice, Nude Mitochondria - metabolism Non-small cell lung cancer Podophyllin - administration & dosage Podophyllin - pharmacology Radiation-Sensitizing Agents - administration & dosage Radiation-Sensitizing Agents - pharmacology Radiosensitizer Reactive Oxygen Species - metabolism ROS Xenograft Model Antitumor Assays β-Apopicropodophylli |
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Title | β-Apopicropodophyllin functions as a radiosensitizer targeting ER stress in non-small cell lung cancer |
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