Activation of telomerase in BeWo cells by estrogen and 2,3,7,8-tetrachlorodibenzo-p-dioxin in co-operation with c-Myc

Sarkar P, Poonam Sarkar, Shiizaki K, Kazuhiro Shiizaki, Yonemoto J, Junzo Yonemoto, Sone H, Hideko Sone
International journal of oncology · 2006 · doi:10.3892/ijo.28.1.43 · PMID:16327978
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⚙ AI-generated summary by qwen3.7-flash, 2026-09-06 ⓘ

This study found that TCDD and estrogen increase telomerase activity in BeWo cells via c-Myc, with TCDD counteracting estrogenic effects on cell proliferation, offering insights into dioxin-induced endometriosis mechanisms.

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⚙ AI-generated deep summary by qwen3.7-flash, 2026-09-24 · read from full text ⓘ

This study investigated the molecular mechanisms by which estrogen and the dioxin TCDD influence telomerase activation in human choriocarcinoma BeWo cells. The researchers found that both agents individually increased telomerase activity and c-Myc expression, with TCDD mimicking estrogenic effects through AhR or ER-independent pathways. However, when combined, the treatments did not show an additive effect on telomerase activity, and TCDD partially counteracted estrogen-induced cell proliferation in the S-phase. Relevance to endometriosis: the paper explicitly states that dioxins induce endometriosis and promotes estrogen-dependent tumors, using this context to frame its investigation into telomerase activation mechanisms relevant to such conditions.

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Abstract

Telomerase activation, known to be stimulated by estrogen, is essential for cellular immortalization and trans-formation, both of which play a role in tumorigenesis. Dioxin and dioxin-like compounds have been shown to induce endometriosis and promote estrogen-dependent tumors. In this study, we show that either 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) or a combination of TCDD and 17-beta estradiol (E2) increase telomerase activity and the expression of the human telomerase catalytic subunit (hTERT) in human choriocarcinoma (BeWo) cells. Compared with estrogen or TCDD alone, the combination treatment did not show an additive effect. Likewise, treatment with either E2 or TCDD increased DNA synthesis and the cell population in S-phase, as detected by FACS analysis. However, following treatment with the E2 and TCDD combination, the proportion of cells in S-phase was actually lower than in cells treated with TCDD alone. These results suggest that TCDD alone mimics estrogenic action in telomerase activation and cell proliferation but, in the presence of estrogen, TCDD-induced actions were partially counteracted. E2 and TCDD also induced c-Myc, which is a transcriptional activator of hTERT in Bewo, but neither of these agents induced telomerase activity in HO15.19 c-myc-null cells. In contrast, only TCDD upregulated telomerase in TGR-1 cells, which are c-Myc expressing but lacking ER expression. The findings suggest that TCDD induces telomerase activity mediated through AhR signaling and/or ER-independent c-Myc signaling. The present study provides insight into the mechanism of promoter activity of TCDD in estrogen-related tumors.
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Print ISSN: 1019-6439 Online ISSN: 1791-2423 International Journal of Molecular Medicine is an international journal devoted to molecular mechanisms of human disease. International Journal of Oncology is an international journal devoted to oncology research and cancer treatment. Covers molecular medicine topics such as pharmacology, pathology, genetics, neuroscience, infectious diseases, molecular cardiology, and molecular surgery. Oncology Reports is an international journal devoted to fundamental and applied research in Oncology. Experimental and Therapeutic Medicine is an international journal devoted to laboratory and clinical medicine. Oncology Letters is an international journal devoted to Experimental and Clinical Oncology. Explores a wide range of biological and medical fields, including pharmacology, genetics, microbiology, neuroscience, and molecular cardiology. International journal addressing all aspects of oncology research, from tumorigenesis and oncogenes to chemotherapy and metastasis. Multidisciplinary open-access journal spanning biochemistry, genetics, neuroscience, environmental health, and synthetic biology. Open-access journal combining biochemistry, pharmacology, immunology, and genetics to advance health through functional nutrition. Publishes open-access research on using epigenetics to advance understanding and treatment of human disease. An International Open Access Journal Devoted to General Medicine. Article - Authors: - Pages: 43-51|Published online on: January 1, 2006https://doi.org/10.3892/ijo.28.1.43 - Expand metrics + Telomerase activation, known to be stimulated by estrogen, is essential for cellular immortalization and trans-formation, both of which play a role in tumorigenesis. Dioxin and dioxin-like compounds have been shown to induce endometriosis and promote estrogen-dependent tumors. In this study, we show that either 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) or a combination of TCDD and 17-β estradiol (E2) increase telomerase activity and the expression of the human telomerase catalytic subunit (hTERT) in human choriocarcinoma (BeWo) cells. Compared with estrogen or TCDD alone, the combination treatment did not show an additive effect. Likewise, treatment with either E2 or TCDD increased DNA synthesis and the cell population in S-phase, as detected by FACS analysis. However, following treatment with the E2 and TCDD combination, the proportion of cells in S-phase was actually lower than in cells treated with TCDD alone. These results suggest that TCDD alone mimics estrogenic action in telomerase activation and cell proliferation but, in the presence of estrogen, TCDD-induced actions were partially counteracted. E2 and TCDD also induced c-Myc, which is a transcriptional activator of hTERT in Bewo, but neither of these agents induced telomerase activity in HO15.19 c-myc-null cells. In contrast, only TCDD upregulated telomerase in TGR-1 cells, which are c-Myc expressing but lacking ER expression. The findings suggest that TCDD induces telomerase activity mediated through AhR signaling and/or ER-independent c-Myc signaling. The present study provides insight into the mechanism of promoter activity of TCDD in estrogen-related tumors. Copy and paste a formatted citation Spandidos Publications style Sarkar P, Shiizaki K, Yonemoto J and Sone H: Activation of telomerase in BeWo cells by estrogen and 2,3,7,8-tetrachlorodibenzo-p-dioxin in co-operation with c-Myc. Int J Oncol 28: 43-51, 2006. APA Sarkar, P., Shiizaki, K., Yonemoto, J., & Sone, H. (2006). Activation of telomerase in BeWo cells by estrogen and 2,3,7,8-tetrachlorodibenzo-p-dioxin in co-operation with c-Myc. International Journal of Oncology, 28, 43-51. https://doi.org/10.3892/ijo.28.1.43 MLA Sarkar, P., Shiizaki, K., Yonemoto, J., Sone, H."Activation of telomerase in BeWo cells by estrogen and 2,3,7,8-tetrachlorodibenzo-p-dioxin in co-operation with c-Myc". International Journal of Oncology 28.1 (2006): 43-51. Chicago Sarkar, P., Shiizaki, K., Yonemoto, J., Sone, H."Activation of telomerase in BeWo cells by estrogen and 2,3,7,8-tetrachlorodibenzo-p-dioxin in co-operation with c-Myc". International Journal of Oncology 28, no. 1 (2006): 43-51. https://doi.org/10.3892/ijo.28.1.43

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endometriosis

MeSH descriptors

Choriocarcinoma Choriocarcinoma Estradiol Polychlorinated Dibenzodioxins Telomerase Teratogens Uterine Neoplasms Uterine Neoplasms Choriocarcinoma Choriocarcinoma DNA-Binding Proteins DNA-Binding Proteins Enzyme Activation Estradiol Female Humans Polychlorinated Dibenzodioxins Pregnancy Promoter Regions, Genetic Proto-Oncogene Proteins c-myc

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