Karyotype analysis of tumorigenic human bronchial epithelial cells transformed by chrysolite asbestos using chemically induced premature chromosome condensation technique

Our plain-English summary of Karyotype analysis of tumorigenic human bronchial epithelial cells transformed by chrysolite asbestos using chemically induced premature chromosome condensation technique, by M. Suzuki, C.Q. Piao, Y.L. Zhao, et al (International Journal of Molecular Medicine, 2001).

The study

• Authors: M. Suzuki, C.Q. Piao, Y.L. Zhao, T.K. Hei
• Journal: International Journal of Molecular Medicine
• Published: 2001;8(1):43-7
• Cited by: 11 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

We examined karyotypic changes of tumorigenic human bronchial epithelial cell lines transformed by asbestos fibers. Using Calyculin A mediated premature chromosome condensation (PCC) assay and Giemsa-trypsin banding, we showed that the common changes of all tumorigenic cell lines were the loss of one or two copies of chromosome 5, the monosomy of chromosome 19 and the increased trisomy of chromosome 8. The results indicate that the karyotypic change of chromosome 5, 8 and 19 could play an important role in asbestos-induced tumorigenic conversion of human bronchial epithelial cells from an immortalized to tumorigenic state.

In plain English

This laboratory study used cells, not people. The authors examined chromosomes of BEP2D, a human airway (bronchial) cell line immortalized with human papillomavirus. They compared it with five tumor-forming lines derived earlier from BEP2D cells treated with chrysotile fibers for 7 days and grown as tumors in nude mice. Chromosomes were condensed early with the chemical Calyculin A and identified by Giemsa-trypsin banding; 20 cells per line were karyotyped. Modal chromosome numbers were 46 to 49 in parental cells and 43 to 44 in tumor-forming lines. Compared with parental cells, tumor-forming lines commonly showed loss of one copy of chromosome 19 (75-95% of cells). They also showed loss of one or two copies of chromosome 5, with only one copy remaining (monosomy) in 45-60% of cells. Extra copies of chromosome 8 were more frequent (65-85%, against 45% in parental cells). The authors concluded that changes in chromosomes 5, 8 and 19 could play an important role in the cells becoming tumor-forming. They stated they had no information on expression of tumorigenicity-related genes on those chromosomes, or their correlation with tumorigenicity.

We wrote this plain-English summary from the full article with the help of AI, and a second AI model checked each sentence against the article. It is not the authors' wording; the abstract and the article are their own account.

What the study did and found

• Design: Laboratory (in vitro) cytogenetic study comparing chromosome karyotypes of an immortalized human bronchial epithelial cell line and tumorigenic cell lines derived from it, using Calyculin A-induced premature chromosome condensation and Giemsa-trypsin banding
• Who was studied: The human papillomavirus-immortalized human bronchial epithelial cell line BEP2D (passage 60) and 5 tumorigenic cell lines (TB, TB2A, TB2B, TE2A, TE2E) derived from it via tumors in nude mice. At least 100 condensed cells per line were scored for chromosome number, and 20 per line were karyotyped.
• Exposure: The tumorigenic lines were derived in an earlier study by treating BEP2D cells with chrysotile fibers for 7 days, at a dose printed in the scanned text as '4 jig/cm2' (apparently 4 micrograms per square centimeter; the unit is garbled by OCR). Cells from the resulting tumors were re-injected into nude mice to obtain secondary tumor lines.
• Main results:
  • The modal chromosome number of the parental BEP2D cells varied from 46 to 49 (hyperaneuploidy), while that of each tumorigenic line was 43 to 44 (hypoaneuploidy). All lines had up to 10% polyploid cells.
  • In the parental BEP2D cells, the most frequent change was monosomy of chromosome 12 (75%). Trisomies of chromosome 5 (85%) and chromosome 14 (65%) were also seen.
  • Changes common among the tumorigenic lines, but not in the parental line, were monosomy of chromosome 19 (75-95%), loss of one or two copies of chromosome 5 (monosomy, meaning one copy remaining, in 45-60%), and increased trisomy of chromosome 8 (65-85%, compared with 45% in parental cells).
  • The TE2E tumorigenic line differed from the others: it showed increased monosomy of chromosome 3 and no changes in chromosomes 4, 11 and 13 compared with the parental or primary tumor line.
  • In method testing, the condensed-chromosome (G2-PCC) indices were 3-8 times higher than the mitotic indices in BEP2D and TE2A cells at 0.5 h of treatment.
• The authors' conclusion: The authors concluded that changes in chromosomes 5, 8 and 19 could play an important role in the asbestos-induced conversion of immortalized human bronchial epithelial cells to a tumorigenic state. They also suggested that the chromosomal changes may occur in a stepwise manner.
• Limitations the authors state:
  • The authors had no information on the expression of tumorigenicity-related genes located on chromosomes 5, 8 and 19, or on their correlation with tumorigenicity.

Topics

The National Library of Medicine indexes this study under subjects our site covers: Chrysotile.

Related studies

• Differentially expressed genes in asbestos-induced tumorigenic human bronchial epithelial cells: implication for mechanism — Y.L. Zhao, C.Q. Piao, et al. (2000)
• Malignant transformation of immortalized human bronchial epithelial cells by asbestos fibers — T.K. Hei, L.J. Wu, et al. (1997)
• Aberrations of chromosome 19 in asbestos-associated lung cancer and in asbestos-induced micronuclei of bronchial epithelial cells in vitro — S.T. Ruosaari, P.E. Nymark, et al. (2008)
• Chrysotile Causes Human Bronchial Epithelial Cell Apoptosis in Response to the Fas-Mediated Apoptosis Pathway — M. Zhang, J. Chen, et al. (2017)
• An early, nonrandom karyotypic change in immortal Syrian hamster cell lines transformed by asbestos: trisomy of chromosome 11 — M. Oshimura, T.W. Hesterberg, et al. (1986)
• Role of mesothelin in carbon nanotube-induced carcinogenic transformation of human bronchial epithelial cells — X. He, E. Despeaux, et al. (2016)

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