Carfilzomib inhibits the growth of lung adenocarcinoma via upregulation of Gadd45a expression
Proteasome inhibitors have shown remarkable success in the treatment of hematologic neoplasm. There has been a lot of attention to applying these drugs for solid tumor treatment. Recent preclinical study has signified the effectiveness on cell proliferation inhibition in lung adenocarcinoma treated...
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Published in | Journal of Zhejiang University. B. Science Vol. 21; no. 1; pp. 64 - 76 |
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Main Authors | , , , , , , , , |
Format | Journal Article |
Language | English |
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Hangzhou
Zhejiang University Press
2020
Springer Nature B.V |
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Abstract | Proteasome inhibitors have shown remarkable success in the treatment of hematologic neoplasm. There has been a lot of attention to applying these drugs for solid tumor treatment. Recent preclinical study has signified the effectiveness on cell proliferation inhibition in lung adenocarcinoma treated by carfilzomib (CFZ), a second generation proteasome inhibitor. However, no insight has been gained regarding the mechanism. In this study, we have systematically investigated the CFZ functions in cell proliferation and growth, cell cycle arrest, and apoptosis in lung adenocarcinoma cells. Flow cytometry experiments showed that CFZ significantly induced G2/M cell cycle arrest and apoptosis in lung adenocarcinoma. MTS and colony formation assays revealed that CFZ substantially inhibited survival of lung adenocarcinoma cells. All results were consistently correlated to the upregulation expression of
Gadd45a
, which is an important gene in modulating cell cycle arrest and apoptosis in response to physiologic and environmental stresses. Here, upregulation of Gadd45a expression was observed after CFZ treatment. Knocking down Gadd45a expression suppressed G2/M arrest and apoptosis in CFZ-treated cells, and reduced cytotoxicity of this drug. The protein expression analysis has further identified that the AKT/FOXO3a pathway is involved in Gadd45a upregulation after CFZ treatment. These findings unveil a novel mechanism of proteasome inhibitor in anti-solid tumor activity, and shed light on novel preferable therapeutic strategy for lung adenocarcinoma. We believe that Gadd45a expression can be a highly promising candidate predictor in evaluating the efficacy of proteasome inhibitors in solid tumor therapy. |
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AbstractList | Proteasome inhibitors have shown remarkable success in the treatment of hematologic neoplasm. There has been a lot of attention to applying these drugs for solid tumor treatment. Recent preclinical study has signified the effectiveness on cell proliferation inhibition in lung adenocarcinoma treated by carfilzomib (CFZ), a second generation proteasome inhibitor. However, no insight has been gained regarding the mechanism. In this study, we have systematically investigated the CFZ functions in cell proliferation and growth, cell cycle arrest, and apoptosis in lung adenocarcinoma cells. Flow cytometry experiments showed that CFZ significantly induced G2/M cell cycle arrest and apoptosis in lung adenocarcinoma. MTS and colony formation assays revealed that CFZ substantially inhibited survival of lung adenocarcinoma cells. All results were consistently correlated to the upregulation expression of
Gadd45a
, which is an important gene in modulating cell cycle arrest and apoptosis in response to physiologic and environmental stresses. Here, upregulation of Gadd45a expression was observed after CFZ treatment. Knocking down Gadd45a expression suppressed G2/M arrest and apoptosis in CFZ-treated cells, and reduced cytotoxicity of this drug. The protein expression analysis has further identified that the AKT/FOXO3a pathway is involved in Gadd45a upregulation after CFZ treatment. These findings unveil a novel mechanism of proteasome inhibitor in anti-solid tumor activity, and shed light on novel preferable therapeutic strategy for lung adenocarcinoma. We believe that Gadd45a expression can be a highly promising candidate predictor in evaluating the efficacy of proteasome inhibitors in solid tumor therapy. Proteasome inhibitors have shown remarkable success in the treatment of hematologic neoplasm. There has been a lot of attention to applying these drugs for solid tumor treatment. Recent preclinical study has signified the effectiveness on cell proliferation inhibition in lung adenocarcinoma treated by carfilzomib (CFZ), a second generation proteasome inhibitor. However, no insight has been gained regarding the mechanism. In this study, we have systematically investigated the CFZ functions in cell proliferation and growth, cell cycle arrest, and apoptosis in lung adenocarcinoma cells. Flow cytometry experiments showed that CFZ significantly induced G2/M cell cycle arrest and apoptosis in lung adenocarcinoma. MTS and colony formation assays revealed that CFZ substantially inhibited survival of lung adenocarcinoma cells. All results were consistently correlated to the upregulation expression of Gadd45a, which is an important gene in modulating cell cycle arrest and apoptosis in response to physiologic and environmental stresses. Here, upregulation of Gadd45a expression was observed after CFZ treatment. Knocking down Gadd45a expression suppressed G2/M arrest and apoptosis in CFZ-treated cells, and reduced cytotoxicity of this drug. The protein expression analysis has further identified that the AKT/FOXO3a pathway is involved in Gadd45a upregulation after CFZ treatment. These findings unveil a novel mechanism of proteasome inhibitor in anti-solid tumor activity, and shed light on novel preferable therapeutic strategy for lung adenocarcinoma. We believe that Gadd45a expression can be a highly promising candidate predictor in evaluating the efficacy of proteasome inhibitors in solid tumor therapy. |
Author | Chen, Hui Zhu, Jia Ma, Li Liu, Wang-wang Yang, Fang Gan, Yi Huang, Ai-hua Zhou, Fei Zhang, Yan-hua |
AuthorAffiliation | 3 Department of Neurosurgery, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou 310006, China 1 Department of Pathology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou 310006, China 2 Department of Radiology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou 310006, China |
AuthorAffiliation_xml | – name: 3 Department of Neurosurgery, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou 310006, China – name: 1 Department of Pathology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou 310006, China – name: 2 Department of Radiology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou 310006, China |
Author_xml | – sequence: 1 givenname: Fang orcidid: 0000-0003-0688-5690 surname: Yang fullname: Yang, Fang email: xiaoyangpumc@zju.edu.cn organization: Department of Pathology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University – sequence: 2 givenname: Wang-wang surname: Liu fullname: Liu, Wang-wang organization: Department of Pathology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University – sequence: 3 givenname: Hui surname: Chen fullname: Chen, Hui organization: Department of Pathology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University – sequence: 4 givenname: Jia surname: Zhu fullname: Zhu, Jia organization: Department of Pathology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University – sequence: 5 givenname: Ai-hua surname: Huang fullname: Huang, Ai-hua organization: Department of Pathology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University – sequence: 6 givenname: Fei surname: Zhou fullname: Zhou, Fei organization: Department of Radiology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University – sequence: 7 givenname: Yi surname: Gan fullname: Gan, Yi organization: Department of Pathology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University – sequence: 8 givenname: Yan-hua surname: Zhang fullname: Zhang, Yan-hua organization: Department of Pathology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University – sequence: 9 givenname: Li surname: Ma fullname: Ma, Li organization: Department of Neurosurgery, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/31898443$$D View this record in MEDLINE/PubMed |
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CitedBy_id | crossref_primary_10_1016_j_bbrep_2022_101357 crossref_primary_10_1016_j_bcp_2023_115939 crossref_primary_10_1186_s13046_021_02057_8 crossref_primary_10_3724_abbs_2024040 crossref_primary_10_1631_jzus_B2100170 crossref_primary_10_2139_ssrn_4173657 crossref_primary_10_1016_j_biopha_2024_116833 |
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DocumentTitle_FL | Carfilzomib 通过上调 Gadd45a 表达抑制肺腺癌细胞生长 |
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Keywords | R734.2 Carfilzomib Cell cycle arrest 细胞周期阻滞 Gadd45a Lung adenocarcinoma 卡非佐米 (Carfilzomib) 凋亡 Apoptosis 肺腺癌 Carfilzomib; Lung adenocarcinoma; Gadd45a; Cell cycle arrest; Apoptosis |
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SubjectTerms | Adenocarcinoma AKT protein Apoptosis Biomedical and Life Sciences Biomedicine Cell cycle Cell growth Cell proliferation Cytotoxicity Environmental stress Flow cytometry FOXO3 protein Gadd45A protein Gene expression Inhibitors Kinases Lung cancer Lungs Neoplasia Proteasome inhibitors Solid tumors Targeted cancer therapy Toxicity Tumors Up-regulation |
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Title | Carfilzomib inhibits the growth of lung adenocarcinoma via upregulation of Gadd45a expression |
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