Role of cyclin D1 in carcinogenesis of human cells induced by quartz.

Ke xia Yan, Bing ci Liu, Xiang lin Shi, Bao rong You, Ming Xu, Ning Kang, Chao ying Zhao

Research output: Contribution to journalArticlepeer-review

3 Scopus citations


OBJECTIVE: To study the role of cyclin D1 in malignant transformation of human embryonic lung diploid fibroblasts (HELF) induced by quartz. METHODS: pXJ41-cyclin D1 expressing sense and antisense cyclin D1 RNA were transinfected into malignant transformed HELF induced by quartz with DNA recombination and gene transduction. The expression of cyclin D1 was detected with hybridization in situ and immunohistochemistry methods to analyze changes in cell growth, double multiplication time, distribution of cell cycles, colony forming ability on soft agar, etc., before and after cyclin D1 transduction. RESULTS: During the process of malignant transformation of HELF induced by quartz, cyclin D1 gene was overexpressed. Antisense pXJ41-cyclin D1 RNA could suppress the growth and proliferation of malignant transformed cells induced by quartz. Growth speed of antisense pXJ41-cyclin D1 transinfected cells decreased by 58.69% on the 8th day in culture, as compared to malignant transformed cells induced by quartz, and its double multiplication time prolonged from 21.0 h to 31.4 h. Antisense cyclin D1 RNA led to cell cycle arrest, resulting in lengthened G1 phase (proportion of cells in phase G1 increased to 52.7% from 45.1% and that of cells in phase S decreased to 33.1% from 40.3%). Colony forming rate reduced significantly and size of colony became smaller. CONCLUSIONS: Abnormal expression of cyclin D1 in cells related to their malignant transformation induced by quartz. Highly expressed cyclin D1 could play an important role in maintaining the transformed phenotype of malignant cells.

Original languageEnglish
Pages (from-to)396-399
Number of pages4
JournalZhonghua yu fang yi xue za zhi [Chinese journal of preventive medicine]
Issue number6
StatePublished - Nov 2004

ASJC Scopus subject areas

  • General Medicine


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