葫芦素D通过下调GATA6表达抑制SGC-7901胃癌细胞增殖迁移的作用机制研究

doi:10.3969/j.issn.1006-6233.2020.04.011

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Abstract Objective: To investigate the mechanism of cucurbitacin D inhibits proliferation and migration of SGC-7901 gastric cancer cells by down-regulating GATA6 expression. Methods: SGC-7901 cells were cultured in vitro. The inhibition rate of cucurbitacin D on SGC-7901 cells was detected by MTT method and the intervention dose of cucurbitacin D was determined. The cells were divided into control group, cisplatin group, cucurbitacin D low, medium and high dose groups. The control group was not treated. The cisplatin group was given cisplatin with a final concentration of 10.0 μmoL/L. The low, medium and high dose groups were given cucurbitacin D with the final concentration of 2.0, 4.0, 8.0 μmoL/L, respectively. The migration ability of SGC-7901 cells, the expression level of mi-R143 and GATA6 in SGC-7901 cells and the apoptosis and cell cycle were detected after 48 hours of culture. Results: With the increase of cucurbitacin D dose, the inhibition rate of SGC-7901 cells was significantly increased (P<0.05). When the dose of cucurbitacin was 8.0μmoL/L, the inhibition rate was 53.07%. Therefore, 8.0μmoL/L was chosen as the highest intervention dose, and 2.0μmoL/L and 4.0μmoL/L were set as two doses. Compared with the control group, the migration ability of SGC-7901 cells, the relative expression of GATA6 mRNA, and the proportion of G0 / G1 cells in the cisplatin group were significantly decreased, and the relative expression of miRNA-143 mRNA, the apoptosis rate, and the proportion of S-phase cells significantly increased(P<0.05). After treatment with cucurbitin D, the migration ability of SGC-7901 cells, the relative expression of GATA6 mRNA, and the ratio of G0 / G1 cells were significantly decreased, and the relative expression of miRNA-143 mRNA, the rate of apoptosis, and the proportion of S cells significantly increased with dose-dependent (P<0.05), but the effect was not as good as the cisplatin group(P<0.05). Conclusion: Cucurbitacin D can inhibit the proliferation and migration of SGC-7901 gastric cancer cells, and has certain anti-cancer activity. The mechanism may be related to the down-regulation of GATA6 expression by cucurbitacin D.

Key words： Cucurbitacin D GATA6 SGC-7901 gastric cancer cell Cell proliferation Cell migration

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	FENG Xiaobo
	LI Minhong
	SHANG Jingjuan
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FENG Xiaobo,LI Minhong,SHANG Jingjuan, et al. The Mechanism of Cucurbitacin D inhibits Proliferation and Migration of SGC-7901 Gastric Cancer Cells by Down-regulating GATA6 Expression[J]. HeBei Med, 2020, 26(4): 571-576.

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http://www.hbyxzzs.cn/EN/10.3969/j.issn.1006-6233.2020.04.011 OR http://www.hbyxzzs.cn/EN/Y2020/V26/I4/571

[1] 王鹏亮,徐惠绵.晚期胃癌转化治疗的若干问题[J].中华肿瘤杂志,2019,41(3):163~167.
[2] Oules B, Rognoni E, Hoste E, et al. Mutant Lef1 controls Gata6 in sebaceous gland development and cancer[J]. EMBO, 2019, 38(9): E100526.
[3] Martinelli P, Carrillo-de Santa Pau E, Cox T, et al. GATA6 regulates EMT and tumour dissemination, and is a marker of response to adjuvant chemotherapy in pancreatic cancer[J]. Gut, 2017, 66(9): 1665~1676.
[4] Shen W, Niu N, Lawson B, et al. GATA6: a new predictor for prognosis in ovarian cancer[J]. Hum Pathol, 2019,86:163~169.
[5] Wang F, Liu J, Zou Y, et al. MicroRNA-143-3p, up-regulated in H. pylori-positive gastric cancer, suppresses tumor growth, migration and invasion by directly targeting AKT2[J]. Oncotarget, 2017, 8(17):28711~28724.
[6] 崔译文,全晶晶,宋艳志,等.葫芦素D抗肿瘤作用研究进展[J].中国现代中药,2017,19(9):1350~1354.
[7] Meng Y, Moore R, Tao W, et al. GATA6 phosphorylation by Erk1/2 propels exit from pluripotency and commitment to primitive endoderm[J]. Dev Biol, 2018, 436(1):55~65.
[8] Li N, Chen J, Zhao J, et al. MicroRNA-3188 targets ETS-domain protein 4 and participates in RhoA/ROCK pathway to regulate the development of atherosclerosis[J]. Die Pharmazie, 2017, 72(11):687~693.
[9] Savova R, De Franco E, Shaw-Smith C, et al. Marked intrafamilial variability of exocrine and endocrine pancreatic phenotypes due to a splice site mutation in GATA6[J]. Biotechnol Biotec Eq, 2017,32(1):124~129.
[10] Ahmed MS, El-Senduny F, Taylor J, et al. Biological screening of cucurbitacin inspired estrone analogs targeting mitogen-activated protein kinase (MAPK) pathway[J]. Chem Biol Drug Des, 2017, 90(3):478~484.
[11] 王文雪,牟艳玲,姚庆强.葫芦素类化合物的抑瘤作用及其作用机制和联合用药研究进展[J].中国药房,2017,28(19):2712~2717.
[12] Xu B, Liu J, Xiang X, et al. Expression of miRNA-143 in pancreatic cancer and its clinical significance[J]. Cancer Biother Radiopharm, 2018, 33(9):373~379.
[13] Song SH, Jeon MS, Nam JW, et al. Aberrant GATA2 epigenetic dysregulation induces a GATA2/GATA6 switch in human gastric cancer[J]. Oncogene, 2018,37(8):993~1004.