论著

胰腺癌血清微RNA-486-3p的异常表达及对细胞增殖、凋亡的影响

展开
  • 1.上海交通大学医学院附属第九人民医院老年病科,上海 200011
    2.上海交通大学医学院附属瑞金医院消化科,上海 200025

收稿日期: 2020-12-04

  网络出版日期: 2022-07-26

The serum level of microRNA-486-3p and its effects on proliferation and apoptosis of pancreatic cancer cells

Expand
  • 1. Department of Geratology,Ninth People’s Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200011, China
    2. Department of Gastroenterology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China

Received date: 2020-12-04

  Online published: 2022-07-26

摘要

目的:研究胰腺癌患者血清微RNA(microRNA,miRNA/miR)-486-3p的表达情况及其在体外实验中对人胰腺癌细胞增殖、凋亡的影响。方法:于消化科、胰腺外科及老年科病房收集确诊胰腺癌患者21例为试验组,20名健康成人为对照组,留取外周血并分离血清,实时定量聚合酶链反应(polymerase chain reaction,PCR)检测血清中miR-486-3p的表达水平;体外实验采用细胞计数试剂盒8(cell-counting kit 8,CCK-8)法和流式细胞仪分别检测miR-486-3p对人胰腺癌细胞增殖、细胞凋亡的影响。结果:与健康对照组相比,胰腺癌患者血清中miR-486-3p的表达水平明显升高(50.73±0.82比34.80±0.74,P<0.05); 体外实验中采用干扰小RNA(small interfering RNA,siRNA)瞬时转染的方法增高miR-486-3p的表达,使得人胰腺癌细胞SW1990和PANC-1的增殖能力明显增强(2.77±0.07比2.05±0.06,P<0.05;2.81±0.04比1.89±0.04,P<0.05);抑制miR-486-3p则可明显减少胰腺癌细胞的增殖(1.71±0.03比2.07±0.05,P<0.05;1.61±0.03比2.20±0.07,P<0.05);增高miR-486-3p的表达可明显减少细胞凋亡(24.1%±1.14%比45.9%±1.11%,P<0.05;21.9%±0.25%比42.3%±1.62%,P<0.05)。结论:胰腺癌患者血清中miR-486-3p较健康对照组明显升高,可促进胰腺癌细胞的增殖并抑制细胞凋亡而发挥促癌作用。

本文引用格式

李晓丽, 李为光, 钱爱华, 曹国良 . 胰腺癌血清微RNA-486-3p的异常表达及对细胞增殖、凋亡的影响[J]. 内科理论与实践, 2021 , 16(02) : 121 -125 . DOI: 10.16138/j.1673-6087.2021.02.011

Abstract

Objective To investigate the serum level of microRNA-486-3p (miR-486-3p) and its effects on proliferation and apoptosis of pancreatic cancer cells. Methods Twenty-one patients with pancreatic cancer and twenty healthy controls were enrolled. Real-time polymerase chain reaction(PCR) was used to detect the serum miR-486-3p. The effects of miR-486-3p on pancreatic cancer cells proliferation and apoptosis were respectively examined by cell counting kit 8(CCK8) assay and flow cytometry assay. Results Compared with healthy controls,serum level of miR-486-3p was significantly up-regulated in patients with pancreatic cancer (50.73±0.82 vs 34.80±0.74, P<0.05); The proliferation of pancreatic cancer cells were significantly up-regulated (SW1990: 2.77±0.07 vs 2.05±0.06, P<0.05; PANC-1: 2.81±0.04 vs1.89±0.04, P<0.05) and the apoptosis rates were suppressed by forced expression of miR-486-3p(24.1%±1.14% vs 45.9%±1.11%, P<0.05; 21.9%±0.25% vs 42.3%±1.62%, P<0.05), while inhibition of miR-486-3p significantly down-regulated the proliferation of pancreatic cancer cells(SW1990: 1.71±0.03 vs 2.07±0.05, P<0.05; PANC-1: 1.61±0.03 vs 2.20±0.07, P<0.05). Conclusions The serum miR-486-3p were significantly up-regulated in patients with pancreatic cancer; MiR-486-3p may function as a tumor-promoter by promoting cell proliferation and suppressing apoptosis in pancreatic cancer cells.

参考文献

[1] Siegel RL, Miller KD, Jemal A. Cancer statistics, 2017[J]. CA Cancer J Clin, 2017, 67(1): 7-30.
[2] Siegel RL, Miller KD, Jemal A. Cancer statistics, 2018[J]. CA Cancer J Clin, 2018, 68(1), 7-30.
[3] Kuroczycki-Saniutycz S, Grzeszczuk A, Zwierz ZW, et al. Prevention of pancreatic cancer[J]. Contemp Oncol (Pozn), 2017, 21(1): 30-34.
[4] Ryan DP, Hong TS, Bardeesy N. Pancreatic adenocarcinoma[J]. N Engl J Med, 2014, 371(11): 1039-1049.
[5] Anastasiadou E, Jacob LS, Slack FJ. Non-coding RNA networks in cancer[J]. Nat Rev Cancer, 2018, 18(1): 5-18.
[6] Rupaimoole R, Slack FJ. MicroRNA therapeutics: towards a new era for the management of cancer and other diseases[J]. Nat Rev Drug Discov, 2017, 16(3): 203-222.
[7] Li Z, Xu R, Li N. MicroRNAs from plants to animals, do they define a new messenger for communication[J]?. Nutr Metab, 2018, 15: 68.
[8] Hayder H, O’Brien J, Nadeem U, et al. MicroRNAs: crucial regulators of placental development[J]. Reproduction, 2018, 155(6): 259-271.
[9] Chou ST, Peng HY, Mo KC, et al. MicroRNA-486-3p functions as a tumor suppressor in oral cancer by targeting DDR1[J]. J Exp Clin Cancer Res, 2019, 38(1): 281.
[10] Ye HQ, Yu XL, Xia JY, et al. MiR-486-3p targeting ECM1 represses cell proliferation and metastasis in cervical cancer[J]. Biomed Pharmacother, 2016, 80: 109-114.
[11] Li WG, Yuan YZ, Qiao MM, et al. High dose glargine alters the expression profiles of microRNAs in pancreatic cancer cells[J]. World J Gastroenterol, 2012, 18(21): 2630-2639.
[12] Yu J, Li A, Hong SM, et al. MicroRNA alterations of pancreatic intraepithelial neoplasias[J]. Clin Cancer Res, 2012, 18(4): 981-992.
[13] Fest J, Ruiter R, van Rooij FJ, et al. Underestimation of pancreatic cancer in the national cancer registry - reconsidering the incidence and survival rates[J]. Eur J Cancer, 2017, 72: 186-191.
[14] Bouvier AM, Bossard N, Colonna M, et al. Trends in net survival from pancreatic cancer in six European Latin countries: results from the SUDCAN population-based study[J]. Eur J Cancer Prev, 2017, 26: S63-S69.
[15] Zhang S, Ng MK. Gene-microRNA network module ana-lysis for ovarian cancer[J]. BMC Syst Biol, 2016, 10 Suppl 4: 117.
[16] Beheshti A, Vanderburg C, McDonald JT, et al. A circulating microRNA signature predicts age-based development of lymphoma[J]. PLoS One, 2017, 12(1): e0170521.
[17] Shigeyasu K, Toden S, Zumwalt TJ, et al. Emerging role of microRNAs as liquid biopsy biomarkers in gastrointestinal cancers[J]. Clin Cancer Res, 2017, 23(10): 2391-2399.
[18] Youness RA, El-Tayebi HM, Assal RA, et al. MicroRNA-486-5p enhances hepatocellular carcinoma tumor suppression through repression of IGF-1R and its downstream mTOR, STAT3 and c-Myc[J]. Oncol Lett, 2016, 12(4): 2567-2573.
[19] Gu Y, Zhang X, Yang Q, et al. Aberrant placental villus expression of miR-486-3p and miR-3074-5p in recurrent miscarriage patients and uterine expression of these microRNAs during early pregnancy in mice[J]. Gynecol Obstet Invest, 2015. [Epub ahead of print].
[20] Peng X, Wei F, Hu X. Long noncoding RNA DLGAP1-AS1 promotes cell proliferation in hepatocellular carcinoma via sequestering miR-486-5p[J]. J Cell Biochem, 2020, 121(2): 1953-1962.
[21] Jin X, Pang W, Zhang Q, et al. MicroRNA-486-5p improves nonsmall-cell lung cancer chemotherapy sensitivity and inhibits epithelial-mesenchymal transition by targeting twinfilin actin binding protein 1[J]. J Int Med Res, 2019, 47(8): 3745-3756.
[22] Yang S, Sui J, Liu T, et al. Expression of miR-486-5p and its significance in lung squamous cell carcinoma[J]. J Cell Biochem, 2019, 120(8): 13912-13923.
[23] Liu X, Chen X, Zeng K, et al. DNA-methylation-mediated silencing of miR-486-5p promotes colorectal cancer proliferation and migration through activation of PLAGL2/IGF2/β-catenin signal pathways[J]. Cell Death Dis, 2018, 9(10): 1037.
[24] Chen H, Ren C, Han C, et al. Expression and prognostic value of miR-486-5p in patients with gastric adenocarcinoma[J]. PLoS One, 2015, 10(3): e0119384.
[25] Balogh J, Victor D 3rd, Asham EH, Burroughs SG, et al. Hepatocellular carcinoma: a review[J]. J Hepatocell Carcinoma, 2016, 3: 41-53.
[26] Li H, Mou Q, Li P, et al. MiR-486-5p inhibits IL-22-induced epithelial-mesenchymal transition of breast cancer cell by repressing Dock1[J]. J Cancer, 2019, 10(19): 4695-4706.
[27] Yang Y, Ji C, Guo S, et al. The miR-486-5p plays a causative role in prostate cancer through negative regulation of multiple tumor suppressor pathways[J]. Oncotarget, 2017, 8(42): 72835-72846.
[28] Hummel R, Wang T, Watson DI, et al. Chemotherapy-induced modification of microRNA expression in esophageal cancer[J]. Oncol Rep, 2011, 26(4): 1011-1017.
[29] Swierniak M, Wojcicka A, Czetwertynska M, et al. In-depth characterization of the microRNA transcriptome in normal thyroid and papillary thyroid carcinoma[J]. J Clin Endocrinol Metab, 2013, 98(8): E1401-E1409.
[30] Mosakhani N, Sarhadi VK, Borze I, et al. MicroRNA profiling differentiates colorectal cancer according to KRAS status[J]. Genes Chromosomes Cancer, 2012, 51(1): 1-9.
[31] Huang YH, Lin KH, Chen HC, et al. Identification of postoperative prognostic microRNA predictors in hepatocellular carcinoma[J]. PLOS One, 2012, 7(5): e37188.
文章导航

/