LOW CONCENTRATION OF BISPHENOL A INDUCES PROLIFERATION OF GASTRIC CANCER CELLS, HGC-27

Authors

  • Noorul Izzati Hanafi Institute of Molecular Medicine and Biotechnology, Faculty of Medicine, Universiti Teknologi MARA, Selangor, Malaysia
  • Siti Hamimah Sheikh Abdul Kadir Institute of Molecular Medicine and Biotechnology, Faculty of Medicine, Universiti Teknologi MARA, Selangor, Malaysia Biochemistry and Molecular Medicine Discipline, Faculty of Medicine, Universiti Teknologi MARA, Selangor, Malaysia
  • Maslinda Musa Department of Biomolecular Sciences, Faculty of Applied Sciences, Universiti Teknologi MARA, Selangor, Malaysia
  • Mohd Hafiz Dzarfan Othman Advanced Membrane Technology Research Centre (AMTEC), Universiti Teknologi Malaysia, Johor, Malaysia
  • Roziana Kamaludin Advanced Membrane Technology Research Centre (AMTEC), Universiti Teknologi Malaysia, Johor, Malaysia
  • Nur Amira Zulkifli Department of Biomolecular Sciences, Faculty of Applied Sciences, Universiti Teknologi MARA, Selangor, Malaysia
  • Normala Abd Latip Atta-ur-Rahman Institute for Natural Products Discovery (AuRIns), Faculty of Pharmacy, Universiti Teknologi MARA, Selangor, Malaysia
  • Zeti Rahayu A Karim Discipline of Surgery, Surgical Cluster, Universiti Teknologi MARA (UiTM), Selangor, Malaysia

DOI:

https://doi.org/10.11113/jt.v81.13670

Keywords:

BPA, cell proliferation, HGC-27, F-actin, Hif-1 alpha video

Abstract

Bisphenol A, an endocrine disrupting compounds that affect human homeostasis. Studies on BPA are focusing on the impact of BPA in reproductive function and brain development. However, the effect of BPA on gut especially gastric cells is not well explored. Gut is directly in contact with ingested BPA; therefore, we aimed to determine the effect of BPA exposure on gastric cells proliferation at safe recommended concentration. Human gastric cancer cells (HGC-27) were treated with BPA at different concentration (low: 10-9M, 10-7M; high10-5M, 10-4M) and time point (24 hr, 48 hr, 72 hr). Cell viability assays were determined using MTS assay. Cells were further stained with Alexa Fluor-635 (F-actin) and Fluorescein (Hif-1α) protein for immunocytofluorescence. Data were analysed using ANOVA (p<0.05, n≥3). Cells treated with 10-9M BPA showed significance increase of cell viability after 48 hr (Mean ±SEM; 146%±0.03, p=0.01) and 72 hr (113%±0.03, p=0.00) compared to 24 hr treatment (77%±0.11, p=0.002). Similarly, cell treated with 10-7M BPA showed a significance increase after 48 hr (141%±0.03, p=0.03) and 72 hr (190%±0.03, p=0.02) compared to 24 hr cells treated with 10-7M (88%±0.05, p=0.01) and untreated (100%±0.07). Lower concentration of BPA increases the condensation of F-actin in all HGC-27 cells. Meanwhile, translocation of Hif-1α protein were observed in all BPA-exposed cells. Findings of this study revealed that BPA induced proliferation and condensation of F-actin structure of gastric cancer cells at low concentration.

References

L. N. Vandenberg, I. Chahoud, J. J. Heindel, V. Padmanabhan, F. J. R. Paumgartten, G. Schoenfelder. 2010. Urinary, Circulating, and Tissue Biomonitoring Studies Indicate Widespread Exposure to Bisphenol A. Environ. Health Perspect. 118: 1055-1070. Doi:10.1289/ehp.0901716.

H. Y. Anteur, M. Bendahmane, N. A. Khan. 2016. Perinatal Exposure to Bisphenol A Affects Body Weight and the Reproductive Function of Wistar Rat. 6: 1-8.

M. S. U. Rahman, J. Cao. 2016. Estrogen Receptors in Gastric Cancer: Advances and Perspectives. World J. Gastroenterol. 22: 2475-2482. Doi:10.3748/wjg.v22.i8.2475.

Z. Wang, H. Liu, S. Liu. (2017. Low-dose Bisphenol a Exposure: A Seemingly Instigating Carcinogenic Effect on Breast Cancer. Adv. Sci. 4. Doi:10.1002/advs.201600248.

C. Weinhouse, O. S. Anderson, I. L. Bergin, D. J. Vandenbergh, J. P. Gyekis, M. a. Dingman, J. Yang, D. C. Dolinoy. 2014. Dose-dependent Incidence of Hepatic Tumors in Adult Mice Following Perinatal Exposure to Bisphenol A. Environ. Health Perspect. 122: 485-491. Doi:10.1289/ehp.1307449.

S. J. Kim, S. Y. Yu, H. J. Yoon, S. Y. Lee, J. P. Youn, S. Y. Hwang. 2015. Epigenetic Regulation of miR-22 in a BPA-exposed Human Hepatoma Cell. Biochip J. 9: 76-84. Doi: 10.1007/s13206-014-9110-2.

N. Chevalier, A. Bouskine, P. Fenichel. 2012. Bisphenol A Promotes Testicular Seminoma Cell Proliferation through GPER/GPR30. Int. J. Cancer. 130: 241-242. Doi: 10.1002/ijc.25972.

P. Tarapore, J. Ying, B. Ouyang, B. Burke, B. Bracken, S. M. Ho. 2014. Exposure to Bisphenol a Correlates with Early-onset Prostate Cancer and Promotes Centrosome Amplification and Anchorage-independent Growth in Vitro. PLoS One. 9. Doi: 10.1371/journal.pone.0090332.

X. Gao, H. S. Wang. 2014. Impact of Bisphenol A on the Cardiovascular System - Epidemiological and Experimental Evidence and Molecular Mechanisms. Int. J. Environ. Res. Public Health. 11: 8399-8413. Doi: 10.3390/ijerph110808399.

L. Le Corre, P. Besnard, M.-C. Chagnon, B. P. A. 2015. An Energy Balance Disruptor. Crit. Rev. Food Sci. Nutr. 55: 769-777. Doi:10.1080/10408398.2012.678421.

A. D. Cypher, J. R. Ickes, B. Bagatto. 2015. Bisphenol A Alters the Cardiovascular Response to Hypoxia in Danio Rerio Embryos. Comp. Biochem. Physiol. C. Toxicol. Pharmacol. 174-175: 39-45. Doi: 10.1016/j.cbpc.2015.06.006.

D. P. Provvisiero, C. Pivonello, G. Muscogiuri, M. Negri, C. de Angelis, C. Simeoli, R. Pivonello, A. Colao. 2016. Influence of Bisphenol a on Type 2 Diabetes Mellitus. Int. J. Environ. Res. Public Health. 13. Doi: 10.3390/ijerph13100989.

X.Y. Qin, T. Fukuda, L. Yang, H. Zaha, H. Akanuma, Q. Zeng, J. Yoshinaga, H. Sone. 2012. Effects of Bisphenol A Exposure on the Proliferation and Senescence of Normal Human Mammary Epithelial Cells. Cancer Biol. Ther. 13: 296-306. Doi: 10.4161/cbt.18942.

A. Can, O. Semiz, O. Cinar. 2005. Bisphenol-A Induces Cell Cycle Delay and Alters Centrosome and Spindle Microtubular Organization in Oocytes during Meiosis. Mol. Hum. Reprod. 11: 389-396. Doi: 10.1093/molehr/gah179.

D. D. Seachrist, K. W. Bonk, S. Ho, G. S. Prins, A. M. Soto, R. a Keri, R. a Keri. 2017. A Review of the Carcinogenic Potential of Bisphenol A. Reprod Toxicol. 59: 167-182. Doi: 10.1016/j.reprotox.2015.09.006.A.

X. Wang, Q. Chen, X. Huang, F. Zou, Z. Fu, Y. Chen, Y. Li, Z. Wang, L. Liu. 2017. Effects of 17β-estradiol and Tamoxifen on Gastric Cancer Cell Proliferation and Apoptosis and ER-α36 Expression. Oncol. Lett. 13: 57-62. Doi: 10.3892/ol.2016.5424.

W.-S. Ryu, J.-H. Kim, Y.-J. Jang, S.-S. Park, J.-W. Um, S.-H. Park, S.-J. Kim, Y.-J. Mok, C.-S. Kim. 2012. Expression of Estrogen Receptors in Gastric Cancer and their Clinical Significance. J. Surg. Oncol. 106: 456-461. Doi: 10.1002/jso.23097.

J. Frederick S. vom Saal, Susan C. Nagel, Benjamin L. Coe, Brittany M. Angle, A. Taylor. 2013. The Estrogenic Endocrine Disrupting Chemical Bisphenol A (BPA) and Obesity. Mol. Cell. Endocrinol. 354: 74-84. Doi: 10.1016/j.mce.2012.01.001.THE.

B. J. M. Alrawi, A. U. Rehman, A. Ahmad, A. Mohammed, S. B. Jamal. 2014. Prediction of Binding Mode of Bisphenol-A (A Carcinogen) in Estrogen and Testosterone Receptors by Applying Computational Docking Approach. 4: 101-105.

H. Song, T. Zhang, P. Yang, M. Li, Y. Yang, Y. Wang, J. Du, K. Pan, K. Zhang. 2015. Low Doses of Bisphenol A Stimulate the Proliferation of Breast Cancer Cells via ERK1/2/ERRgamma Signals. Toxicol. In Vitro. 30: 521-528. Doi: 10.1016/j.tiv.2015.09.009.

S. Wu, X. Wei, J. Jiang, L. Shang, W. Hao. 2012. Effects of Bisphenol A on the Proliferation and Cell Cycle of HBL-100 Cells. Food Chem. Toxicol. 50: 3100-3105. Doi: 10.1016/j.fct.2012.06.029.

Roberto Dominguez and Kenneth C. Holmes. 2011. Actin Structure and Function. Annu Rev Biophys. 40: 169-186.

Doi: 10.1146/annurev-biophys-042910-155359.

I. Nedeva, G. Koripelly, D. Caballero, L. Chieze, B. Guichard, B. Romain, E. Pencreach, J.-M. Lehn, M.-F. Carlier, D. Riveline. 2013. Synthetic Polyamines Promote Rapid Lamellipodial Growth by Regulating Actin Dynamics. Nat. Commun. 42165. Doi: 10.1038/ncomms3165.

T. Akagi, T. Kimoto. 1976. Human Cell Line (HGC 27) Derived from the Metastatic Lymph Node of Gastric Cancer. Acta Med. Okayama. 30: 215-219.

E. Pfeiffer, B. Rosenberg, S. Deuschel, M. Metzler. 1997. Interference with Microtubules and Induction of Micronuclei in Vitro by Various Bisphenols. Mutat. Res. 390 21-31.

Y. Gao, H. Chen, X. Xiao, W.Y. Lui, W.M. Lee, D.D. Mruk, C.Y. Cheng. 2017. Perfluorooctanesulfonate (PFOS)-induced Sertoli Cell Injury through a Disruption of F-actin and Microtubule Organization is Mediated by Akt1/2. Sci. Rep. 7: 1-14. Doi: 10.1038/s41598-017-01016-8.

H. Chen, Y. Gao, D.D. Mruk, X. Xiao, C.M. John, P.J. Turek, W. Lui, W.M. Lee, B. Silvestrini, C.Y. Cheng. 2017. Rescue of PFOS-induced human Sertoli Cell Injury by Overexpressing a p-FAK-Y407E Phosphomimetic Mutant. Sci. Rep. 7: 15810.

Doi: 10.1038/s41598-017-15671-4.

T. Yu, B. Tang, X. Sun. 2017. Development of Inhibitors Targeting Hypoxia-inducible Factor 1 and 2 for Cancer Therapy. Yonsei Med. J. 58: 489-496. Doi: 10.3349/ymj.2017.58.3.489.

N. Urano, Y. Fujiwara, Y. Doki, M. Tsujie, H. Yamamoto, H. Miyata, S. Takiguchi, T. Yasuda, M. Yano, M. Monden. 2006. Overexpression of Hypoxia-inducible Factor-1 Alpha in Gastric Adenocarcinoma. Gastric Cancer. 9: 44-49. Doi: 10.1007/s10120-005-0356-1.

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Published

2019-09-22

Issue

Vol. 81 No. 6: November 2019

Section

Science and Engineering

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Copyright of articles that appear in Jurnal Teknologi belongs exclusively to Penerbit Universiti Teknologi Malaysia (Penerbit UTM Press). This copyright covers the rights to reproduce the article, including reprints, electronic reproductions, or any other reproductions of similar nature.

How to Cite

LOW CONCENTRATION OF BISPHENOL A INDUCES PROLIFERATION OF GASTRIC CANCER CELLS, HGC-27. (2019). Jurnal Teknologi, 81(6). https://doi.org/10.11113/jt.v81.13670