JOURNAL OF SHANDONG UNIVERSITY (HEALTH SCIENCES) ›› 2017, Vol. 55 ›› Issue (4): 39-43.doi: 10.6040/j.issn.1671-7554.0.2016.515

Previous Articles     Next Articles

MiR- 498 inhibits A549 cells EMT by targeting FOXM1

TANG Xi1, HU Ya2, XU Yanhua1, WANG Chunlin1, QIU Ping1, WANG Xianghui3   

  1. 1. Cancer Center, Jingzhou Hospital, Tongji Medical College, Huazhong University of Science and Technology, Jingzhou 434020, Hubei, China;
    2. Medical College, Yangtze University, Jingzhou 434023, Hubei, China;
    3. Department of Cardiothoracic Surgey, Jingzhou Hospital, Tongji Medical College, Huazhong University of Science and Technology, Jingzhou 434020, Hubei, China
  • Received:2016-05-09 Online:2017-04-10 Published:2017-04-10

PDF (PC)

254

Abstract: Objective To investigate the effect of miR- 498 on A549 cells epithelial-to-mesenchymal transition(EMT)and its correlated mechanism. Methods After miR- 498 was transfected into A549 cells, the cells were divided into control group, empty vector group and miR- 498 group; Transwell assay was employed to test the migration ability of A549 cells, Western blotting was used to investigate the expressions of E-cadherin, fibronectin, vimentin and FOXM1 in A549 cells. Luciferase assay was used to confirmed whether FOXM1-3'-UTR was the target gene of miR- 498. Then, the cells were divided into miR- 498 group, miR- 498 + FOXM1 group, and miR- 498 + empty plasmid group, and the above biological indicators of A549 cells were detected again. Results Compared with the empty vector group, the expression of E-cadherin was increased(P=0.001), the expression of fibronectin, vimentin and FOXM1were decreased(all P<0.01), and the migration ablitiy of A549 cells was decreased in the miR- 498 group(P=0.001); the Luciferase activity of the FOXM1-3'-UTR plasmid was significantly suppressed by miR- 498(P=0.001); over-expression of FOXM1 could reverse the effect of miR- 498 on A549. Conclusion miR- 498 inhibits A549 cells EMT by down-regulating FOXM1 expression.

Key words: Lung adenocarcinoma, miR- 498, FOXM1, Epithelial-to-mesenchymal transition

CLC Number: 

  • R734.2
[1] Bao B, Wang Z, Ali S, et al. Over-expression of FoxM1 leads to epithelial-mesenchymal transition and cancer stem cell phenotype in pancreatic cancer cells[J]. J Cell Biochem, 2011, 112(9): 2296-2306.
[2] Chen QY, JIao DM, Wang J, et al. miR-206 regulates cisplatin resistance and EMT in human lung adenocarcinoma cells partly by targeting MET[J]. Oncotarget, 2016, 7(17):24510-24526.
[3] Tang WB, Ling GH, Sun L, et al. Smad anchor for receptor activation regulates high glucose-induced EMT via modulation of Smad2 and Smad3 activities in renal tubular epithelial cells[J]. Nephron, 2015, 130(3): 213-220.
[4] Guo L, Peng W, Tao J, et al. Hydrogen sulfide inhibits transforming growth factor-beta1-induced EMT via wnt/catenin pathway[J]. PLoS One, 2016, 11(1): e0147018. doi: 10.1371/journal.pone.0147018.
[5] Sun Y, Yu X, Bai Q. miR-204 inhibits invasion and epithelial-mesenchymal transition by targeting FOXM1 in esophageal cancer[J]. Int J Clin Exp Pathol, 2015, 8(10): 12775-12783.
[6] Gopalan V, Smith RA, Lam AK. Downregulation of microRNA- 498 in colorectal cancers and its cellular effects[J]. Exp Cell Res, 2015, 330(2): 423-428.
[7] Matamala N, Vargas MT, Gonzalez-Campora R, et al. MicroRNA deregulation in triple negative breast cancer reveals a role of miR- 498 in regulating BRCA1 expression[J]. Oncotarget, 2016, 7(15): 20068-20079.
[8] Liu R, Liu F, Li L, et al. MiR- 498 regulated FOXO3 expression and inhibited the proliferation of human ovarian cancer cells[J]. Biomed Pharmacother, 2015, 72: 52-57.
[9] Wang M, Zhang Q, Wang J, et al. MicroRNA- 498 is downregulated in non-small cell lung cancer and correlates with tumor progression[J]. J Cancer Res Ther, 2015, 11(Suppl 1): C107-C111.
[10] Li Z, Ying X, Chen H, et al. MicroRNA-194 inhibits the epithelial-mesenchymal transition in gastric cancer cells by targeting FoxM1[J]. Dig Dis Sci, 2014, 59(9): 2145-2152.
[11] Ke Y, Zhao W, Xiong J, et al. miR-149 inhibits non-small-cell lung cancer cells EMT by targeting FOXM1[J]. Biochem Res Int, 2013, 2013: 506731. doi:10.1155/2013/506731.
[12] Tang O, Chen XM, Shen S, et al. MiRNA-200b represses transforming growth factor-beta1-induced EMT and fibronectin expression in kidney proximal tubular cells[J]. Am J Physiol Renal Physiol, 2013, 304(10): F1266-F1273.
[13] Li Y, An H, Pang J, et al. MicroRNA profiling identifies miR-129-5p as a regulator of EMT in tubular epithelial cells[J]. Int J Clin Exp Med, 2015, 8(11): 20610-20616.
[14] Li J, Wang Y, Luo J, et al. miR-134 inhibits epithelial to mesenchymal transition by targeting FOXM1 in non-small cell lung cancer cells[J]. FEBS Lett, 2012, 586(20): 3761-3765.
[15] Tan X, Fu Y, Chen L, et al. miR-671-5p inhibits epithelial-to-mesenchymal transition by downregulating FOXM1 expression in breast cancer[J]. Oncotarget, 2016, 7(1): 293-307.
[16] Liu Z, Jin ZY, Liu CH, et al. MicroRNA-21 regulates biological behavior by inducing EMT in human cholangiocarcinoma[J]. Int J Clin Exp Pathol, 2015, 8(5): 4684-4694.
[17] Li S, Qin X, Li Y, et al. MiR-133a suppresses the migration and invasion of esophageal cancer cells by targeting the EMT regulator SOX4[J]. Am J Transl Res,2015, 7(8): 1390-1403.
[18] Sun Y, Wang H, Liu M, et al. Resveratrol abrogates the effects of hypoxia on cell proliferation, invasion and EMT in osteosarcoma cells through downregulation of the HIF-1alpha protein[J]. Mol Med Rep, 2015, 11(3): 1975-1981.
[19] Kogo R, How C, Chaudary N, et al. The microRNA-218~Survivin axis regulates migration, invasion, and lymph node metastasis in cervical cancer[J]. Oncotarget, 2015, 6(2): 1090-1100.
[20] Tu K, Li C, Zheng X, et al. Prognostic significance of miR-218 in human hepatocellular carcinoma and its role in cell growth[J]. Oncol Rep, 2014, 32(4): 1571-1577.
[21] Feng Y, Wang L, Zeng J, et al. FoxM1 is overexpressed in Helicobacter pylori-induced gastric carcinogenesis and is negatively regulated by miR-370[J]. Mol Cancer Res, 2013, 11(8): 834-844.
[22] Song IS, Jeong YJ, Jeong SH, et al. FOXM1-induced PRX3 regulates stemness and survival of colon cancer cells via maintenance of mitochondrial function[J]. Gastroenterology, 2015, 149(4): 1006-1016.
[23] Gu C, Yang Y, Sompallae R, et al. FOXM1 is a therapeutic target for high-risk multiple myeloma[J]. Leukemia, 2016, 30(4): 873-882.
[24] Inoguchi S, Seki N, Chiyomaru T, et al. Tumour-suppressive microRNA-24-1 inhibits cancer cell proliferation through targeting FOXM1 in bladder cancer[J]. FEBS Lett, 2014, 588(17): 3170-3179.
[1] ZHANG Zhihui, WANG Lili, GAO Hua, ZHANG Jian, LI Juan, LI Yuan, WU Chunxiao, LU Zhiming. Role of hypoxia-inducible factor-1α in the regulation of programmed death ligand 1 expression in lung adenocarcinoma [J]. JOURNAL OF SHANDONG UNIVERSITY (HEALTH SCIENCES), 2017, 55(4): 65-70.
[2] QUE Xinxiang, DING Sentai, WU Fei, BI Dongbin, LÜ Jiaju, DING Kejia. Expressions of TGF-β1 and α-SMA in autosomal dominant polycystic kidney disease [J]. JOURNAL OF SHANDONG UNIVERSITY (HEALTH SCIENCES), 2014, 52(7): 78-81.
[3] SUN Jie, MU Xiaoyan, DONG Xueli. Combinational and sequential effect of sunitinib and gemcitabine on K-RAS mutant A549 cells [J]. JOURNAL OF SHANDONG UNIVERSITY (HEALTH SCIENCES), 2014, 52(3): 45-49.
[4] DONG Xue-li, MU Xiao-yan, LIU Qing-liang, SUN Jie. Effects of erlotinib combined with celecoxib on growth and angiogenesis of human lung cancer xenograft model [J]. JOURNAL OF SHANDONG UNIVERSITY (HEALTH SCIENCES), 2013, 51(2): 49-52.
[5] TIAN Tian-tian1, LI Ji-sheng1, WANG Ya-wei1, MA Dao-xin2, WANG Xiu-wen1. Genistein exerts antitumor effects in small cell lung cancer H446 cells via suppressing the activity of FoxM1 pathway [J]. JOURNAL OF SHANDONG UNIVERSITY (HEALTH SCIENCES), 2013, 51(06): 44-48.
[6] FAN Heng-jian, ZHANG Yu-ke, XIAO Wei, ZHANG Yi, LI Hai-jun, WANG De-xiang. Changes of Treg and Th17 cells in the peripheral bloods of patients with
lung adenocarcinoma and their prognostic significance [J]. JOURNAL OF SHANDONG UNIVERSITY (HEALTH SCIENCES), 2012, 50(9): 73-78.
[7] MA Yu-hua1,2, ZHENG Yan3, JIA Yan-fei3, WANG Yun-shan3. GFR and DEC1 protein co-expression promotes lymph node
metastasis in lung adenocarcinoma [J]. JOURNAL OF SHANDONG UNIVERSITY (HEALTH SCIENCES), 2012, 50(3): 24-28.
[8] LI Haijun, XIAO Wei. Increased frequency of Th17 cells in the peripheral blood of patients  with lung adenocarcinoma and its clinical significance [J]. JOURNAL OF SHANDONG UNIVERSITY (HEALTH SCIENCES), 2011, 49(8): 108-112.
[9] L V Yi-jing, REN Min, WANG Bo, GE Ru-qing, ZHANG Ji-dong. Expressions of EZH2 and CTGF Gene in lung adenocarcinoma [J]. JOURNAL OF SHANDONG UNIVERSITY (HEALTH SCIENCES), 2011, 49(5): 94-97.
Viewed
Full text


Abstract

Cited
  Shared   
  Discussed   
No Suggested Reading articles found!
Copyright 2018 © Editorial office of Journal of Shandong University (Health Sciences)
Supported by Beijing Magtech Co.Ltd