ArticleThe American journal of pathology2009
Identification of potential therapeutic targets in malignant mesothelioma using cell-cycle gene expression analysis.
Article in The American journal of pathology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 56 citations in OpenAlex.
- A Phase II Trial of Alisertib (MLN8237) in Salvage Malignant Mesothelioma.The oncologist · 2020Trial
- Effects of Autophagy Inhibition by SAR405, a Selective VPS34 Inhibitor, on Pleural Mesothelioma Cells.Thoracic cancer · 2026Article
- FK228 suppress the growth of human malignant pleural mesothelioma tumor independent to epithelioid or non-epithelioid histology.Molecular medicine (Cambridge, Mass.) · 2024Article
- Antagonist of Growth Hormone-Releasing Hormone Potentiates the Antitumor Effect of Pemetrexed and Cisplatin in Pleural Mesothelioma.International journal of molecular sciences · 2022Article
- Integrated genomics point to immune vulnerabilities in pleural mesothelioma.Scientific reports · 2021Observational
- RETRACTED: Identification of Redox-Sensitive Transcription Factors as Markers of Malignant Pleural Mesothelioma.Cancers · 2021Article
- Impact of metallothionein-knockdown on cisplatin resistance in malignant pleural mesothelioma.Scientific reports · 2020Article
- Genomics and Functional Genomics of Malignant Pleural Mesothelioma.International journal of molecular sciences · 2020Review
- Possible reversibility between epithelioid and sarcomatoid types of mesothelioma is independent of ERC/mesothelin expression.Respiratory research · 2020Article
- Antimesothelioma Immunotherapy by CTLA-4 Blockade Depends on Active PD1-Based TWIST1 Vaccination.Molecular therapy oncolytics · 2020Article
- Therapeutic Landscape of Malignant Pleural Mesothelioma: Collateral Vulnerabilities and Evolutionary Dependencies in the Spotlight.Frontiers in oncology · 2020Review
- Suppression of colorectal cancer cell growth by combined treatment of 6-gingerol and γ-tocotrienol via alteration of multiple signalling pathways.Journal of natural medicines · 2019Article
- Transcriptional suppression of the miR-15/16 family by c-Myc in malignant pleural mesothelioma.Oncotarget · 2019Article
- Heterogeneous Contributing Factors in MPM Disease Development and Progression: Biological Advances and Clinical Implications.International journal of molecular sciences · 2018Review
- Overexpressed genes in malignant pleural mesothelioma: implications in clinical management.Journal of thoracic disease · 2018Review
- Article
- Prognostic Significance of Forkhead Box M1 (FOXM1) Expression and Antitumor Effect of FOXM1 Inhibition in Angiosarcoma.Journal of Cancer · 2016Article
- Spontaneous mesotheliomas in F344/N rats are characterized by dysregulation of cellular growth and immune function pathways.Toxicologic pathology · 2014Article
- Abrogating G₂/M checkpoint through WEE1 inhibition in combination with chemotherapy as a promising therapeutic approach for mesothelioma.Cancer biology & therapy · 2014Article
- An RNAi-based screen reveals PLK1, CDK1 and NDC80 as potential therapeutic targets in malignant pleural mesothelioma.British journal of cancer · 2014Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cell-cycle defects are responsible for cancer onset and growth. We studied the expression profile of 60 genes involved in cell cycle in a series of malignant mesotheliomas (MMs), normal pleural tissues, and MM cell cultures using a quantitative polymerase chain reaction-based, low-density array. Nine genes were significantly deregulated in MMs compared with normal controls. Seven genes were overexpressed in MMs, including the following: CDKN2C, cdc6, cyclin H, cyclin B1, CDC2, FoxM1, and Chk1, whereas Ube1L and cyclin D2 were underexpressed. Chk1 is a principal mediator of cell-cycle checkpoints in response to genotoxic stress. We confirmed the overexpression of Chk1 in an independent set of 87 MMs by immunohistochemistry using tissue microarrays. To determine whether Chk1 down-regulation would affect cell-cycle control and cell survival, we transfected either control or Chk1 siRNA into two mesothelioma cell lines and a nontumorigenic (Met5a) cell line. Results showed that Chk1 knockdown increased the apoptotic fraction of MM cells and induced an S phase block in Met5a cells. Furthermore, Chk1 silencing sensitized p53-null MM cells to both an S phase block and apoptosis in the presence of doxorubicin. Our results indicate that cell-cycle gene expression analysis by quantitative polymerase chain reaction can identify potential targets for novel therapies. Chk1 knockdown could provide a novel therapeutic approach to arrest cell-cycle progression in MM cells, thus increasing the rate of cell death.
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