Influence of MSA on Proliferation, Migration, Apoptosis, and Cell Cycle of Oral Squamous Cell Carcinoma Tca8113 and KB Cells

doi:10.13701/j.cnki.kqyxyj.2019.06.014

Abstract

Abstract: Objective: To explore the influence of MSA on the proliferation, migration, apoptosis, and cell cycle of oral squamous cell carcinoma Tca8113 and KB cells. Methods: MTS assay was used to detect cell proliferation activity. Wound healing assay was used to detect the capability of cell migration. The cell cycle distribution and apoptotic rate were measured using flow cytometry assay. Results: MSA inhibited the proliferation of Tca8113 and KB cells and reduced the cell migration. MSA suppressed the apoptosis of Tca8113 and KB cells markedly in a dose dependent manner. Cell cycle was blocked at G2 stage and the number of cell at G1 and S stage was reduced when stimulated with MSA. Conclusions: MSA can inhibit the proliferation and migration, induce the apoptosis, and change cell cycle of oral squamous cell carcinoma Tca8113 and KB cells in vitro. MSA is expected to be a new method to prevent and treat the oral cancer.

Key words: MSA, Oral squamous cell carcinoma, Proliferation, Apoptosis, Migration, Cell cycle

ZHOU Tong, ZHANG Tong-fei, ZHANG Ze-bing, QUAN Hai-ying. Influence of MSA on Proliferation, Migration, Apoptosis, and Cell Cycle of Oral Squamous Cell Carcinoma Tca8113 and KB Cells[J]. Journal of Oral Science Research, 2019, 35(6): 568-572.

References

[1] Siegel RL, Miller KD, Jemal A. Cancer statistics, 2015[J]. CA Cancer J Clin, 2015, 65(1): 5-29.
[2] Rayman MP. The importance of selenium to human health [J]. Lancet, 2000, 356(9225):233-241.
[3] Richard V , Sebastian P , Nair MG , et al. Multiple drug resistant, tumorigenic stem-like cells in oral cancer [J]. Cancer Lett, 2013, 338(2):300-316.
[4] 马壮,张胜,朱郁文,等.人舌鳞癌细胞SOCS1基因沉默对细胞增殖和化疗药物敏感性的影响[J].口腔医学研究, 2015, 31(3):283-286.
[5] Rayman MP. Selenium and human health [J]. Lancet, 2012, 379(9822):1256-1268.
[6] Gao F, Yuan Q, Gao L, et al. Cytotoxicity and therapeutic effect of irinotecan combined with selenium nanoparticles [J]. Biomaterials, 2014, 35(31):8854-8866.
[7] Abdel-Aziz AK, Azab SSE, Youssef SS, et al. Modulation of imatinib cytotoxicity by selenite in HCT116 colorectal cancer cells [J]. Basic Clin Pharmacol Toxicol, 2015, 116(1):37-46.
[8] Sundaram S, Yan L . Dietary supplementation with methylseleninic acid inhibits mammary tumorigenesis and metastasis in male MMTV-PyMT mice [J]. Biol Trace Elem Res, 2017, 184(1):186-195.
[9] Tarradocastellarnau M, Cortés R, Zanuy M, et al. Methylseleninic acid promotes antitumour effects via nuclear FOXO3a translocation through Akt inhibition [J]. Pharmacol Res, 2015, 102:218-234.
[10] Wang L, Guo X, Wang J, et al. Methylseleninic acid super-activates p53-senescence cancer progression barrier in prostate lesions of Pten-knockout mouse [J]. Cancer Prev Res, 2016, 9(1):35.
[11] Tan Y, Feng Q, Sun X, et al. Effects of methylseleninic acid on cisplatin-resistant ovarian cancer cells (SKOV3/DDP) and the mechanisms [J]. Zhong Nan Da Xue Xue Bao Yi Xue Ban, 2016, 41(12):1305-1311.
[12] Hu C, Liu M, Zhang W, et al. Upregulation of KLF4 by methylseleninic acid in human esophageal squamous cell carcinoma cells: Modification of histone H3 acetylation through HAT/HDAC interplay [J]. Mol Carcinog, 2015, 54(10):1051-1059.
[13] Zeng H, Wu M. The inhibitory efficacy of methylseleninic acid against colon cancer xenografts in C57BL/6 mice [J]. Nutr Cancer, 2015, 67(5):831-838.
[14] 何荣根,徐秀祺,周晓健,等.人舌鳞状细胞癌Tca8113细胞系的建立及其生物学特性[J].肿瘤,1983,3(3):97-100.
[15] Shigemi Z, Manabe K, Hara N, et al. Methylseleninic acid and sodium selenite induce severe ER stress and subsequent apoptosis through UPR activation in PEL cells [J]. Chem Biol Interact, 2017, 266:28-37.
[16] Zhang Y, Zheng S, Zheng JS, et al. Synergistic induction of apoptosis by methylseleninic acid and cisplatin, the role of ROS-ERK/AKT-p53 pathway [J]. Mol Pharm, 2014, 11(4): 1282-1293.