Establishment and characterization of four malignant pleural mesothelioma cell lines from Japanese patients

Usami, Noriyasu; Fukui, Takayuki; Kondo, Masashi; Taniguchi, Tetsuo; Yokoyama, Toshihiko; Mori, Satoshi; Yokoi, Kohei; Horio, Yoshitsugu; Shimokata, Kaoru; Sekido, Yoshitaka; Hida, Toyoaki

doi:10.1111/j.1349-7006.2006.00184.x

Cited by 124 publications

(102 citation statements)

References 26 publications

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“…Homozygous deletion of the p16 INK4A tumor suppressor gene is frequently observed in asbestos-induced mesothelioma in humans. (28)(29)(30) Our data would be helpful for analyzing the pathogenic process associated with homozygous deletions.…”

Section: Discussionmentioning

confidence: 99%

Characteristics and modifying factors of asbestos‐induced oxidative DNA damage

et al. 2008

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Respiratory exposure to asbestos has been linked with mesothelioma in humans. However, its carcinogenic mechanism is still unclear. Here we studied the ability of chrysotile, crocidolite and amosite fibers to induce oxidative DNA damage and the modifying factors using four distinct approaches. Electron spin resonance analyses revealed that crocidolite and amosite containing high amounts of iron, but not chrysotile, catalyzed hydroxyl radical generation in the presence of H 2 O 2 , which was enhanced by an iron chelator, nitrilotriacetic acid, and suppressed by desferal. Natural iron chelators, such as citrate, adenosine 5′-triphosphate and guanosine 5′-triphosphate, did not inhibit this reaction. Second, we used time-lapse video microscopy to evaluate how cells cope with asbestos fibers. RAW264.7 cells, MeT-5 A and HeLa cells engulfed asbestos fibers, which reached not only cytoplasm but also the nucleus. Third, we utilized supercoiled plasmid DNA to evaluate the ability of each asbestos to induce DNA double strand breaks (DSB). Crocidolite and amosite, but not chrysotile, induced DNA DSB in the presence of iron chelators. We cloned the fragments to identify break sites. DSB occurred preferentially within repeat sequences and between two G:C sequences. Finally, i.p. administration of each asbestos to rats induced not only formation of nuclear 8-hydroxy-2′-deoxyguanosine in the mesothelia, spleen, liver and kidney but also significant iron deposits in the spleen. Together with the established carcinogenicity of i.p. chrysotile, our data suggest that asbestos-associated catalytic iron, whether constitutional or induced by other mechanisms, plays an important role in asbestos-induced carcinogenesis and that chemoprevention may be possible through targeting the catalytic iron. (Cancer Sci 2008; 99: 2142-2151) A sbestos fibers have been heavily used in industry from World War II to the present because of their durability, heat-resistance and low cost.(1,2) However, in 1987, the International Agency for Research on Cancer (IARC) designated asbestos fibers as a group I (definite) carcinogen for humans (http:// monographs.iarc.fr/ENG/Classification/crthgr01.php), and asbestos fibers were banned in many European and North American countries in the 1990s.(1,2) In June of 2005, asbestos-associated deaths suddenly attracted social attention in Japan because it was reported that 79 people who worked in factories using asbestos had been killed by an asbestos-associated rare cancer called diffuse malignant mesothelioma (DMM) over the past 26 years. Furthermore, people who lived near those factories also suffered from the same fatal disease.(4) The characteristics of DMM are as follows: (i) it is associated with repeated asbestos exposure; (5,6) (ii) once diagnosed, prognosis is poor; (7) and (iii) it takes 30-40 years after the start of asbestos exposure for DMM to occur.(5,6) It is expected that the incidence of DMM in Japan will peak in 2025 with 100 000 predicted deaths from this neoplasm. (8) There are several hypotheses a...

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Section: Discussionmentioning

confidence: 99%

Characteristics and modifying factors of asbestos‐induced oxidative DNA damage

et al. 2008

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“…A2780 cells were obtained from the NCI Division of Cancer Treatment and Diagnosis (DCTD) Tumor Repository and cultured in RPMI-1640 media and 10% FBS. ACC-MESO-1 and ACC-MESO-4 cells were provided by the RIKEN BioResource Center through the National BioResource Project of the MEXT, Japan, and cultured in RPMI-1640 media and 10% FBS as described previously (35). Companion cell lines to Oncotest PDX models (BXF-1218L, BXF-1352L, PXF-698L, PXF-1118L, and PXF-1752L) were obtained from Oncotest GmbH and cultured in DMEM and 10% FBS.…”

Section: Cell Culturementioning

confidence: 99%

Characterization of LY3023414, a Novel PI3K/mTOR Dual Inhibitor Eliciting Transient Target Modulation to Impede Tumor Growth

Smith

Mader

Cook

et al. 2016

Molecular Cancer Therapeutics

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“…Many studies have been conducted to determine the underlying key genetic and epigenetic events responsible for the development of MPM, some of which may be directly caused by asbestos fibers. New animal models of MM and human MM cell lines are also being established to present more useful tools for detailed analyses of the carcinogenesis of MM and the development of new therapeutic modalities [16,39]. Thus, more in-depth knowledge of key gene alteration, specific expression profiling, and other fundamental abnormalities at the cellular, intercellular, and tissue levels in MM cells will be of great help in developing future strategies for potential molecular targets as well as other therapeutic modalities, such as immunotherapy.…”

Section: Discussionmentioning

confidence: 99%

Molecular biology of malignant mesothelioma

Sekido

2008

Environ Health Prev Med

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Human malignancies develop via a multi-step that involves the accumulation of several key gene alterations with associated genetic and epigenetic events. Although malignant mesothelioma (MM) has been demonstrated to be clearly correlated with asbestos exposure, it remains poorly understood how asbestos fibers confer key gene alterations and induce cellular transformation in normal mesothelial cells, which results in the acquisition of malignant phenotypes, including deregulated cell proliferation and invasion. Malignant mesothelioma presents with the frequent inactivation of tumor suppressor genes of p16 INK4a /p14 ARF on chromosome 9p21 and neurofibromatosis type 2 (NF2) on chromosome 22q12, with the latter being responsible for the NF2 familial cancer syndrome. In contrast, MM shows infrequent mutation of the p53 gene, which is one of the most frequently mutated tumor suppressor genes in human malignancies. Genetic abnormalities of oncogenes have also been studied in MM, but no frequent mutations have been identified, including the epidermal growth factor receptor (EGFR) and K-RAS genes. Recent studies have suggested the activation of other receptor tyrosine kinases, including Met, and the deregulations of mitogen-activated protein kinase (MAPK) and phosphatidylinositol-3-kinase (PI3K)-AKT signaling cascades, although the alterations responsible for their activation are still not clear. Thus, further genome-wide studies of genetic and epigenetic alterations as well as detailed analyses of deregulated signaling cascades in MM are necessary to determine the molecular mechanisms of MM, which would also provide some clues for establishing a new molecular target therapy for MM.

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Establishment and characterization of four malignant pleural mesothelioma cell lines from Japanese patients

Abstract: Malignant pleural mesothelioma (MPM) is an asbestos-related

Cited by 124 publications

References 26 publications

Characteristics and modifying factors of asbestos‐induced oxidative DNA damage

Characteristics and modifying factors of asbestos‐induced oxidative DNA damage

Characterization of LY3023414, a Novel PI3K/mTOR Dual Inhibitor Eliciting Transient Target Modulation to Impede Tumor Growth

Molecular biology of malignant mesothelioma

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