Advertisement

The role of MAPK signaling pathway in formation of EMT in oral squamous carcinoma cells induced by TNF-α

  • Xiao-Wei Zhao
  • Jing-Ping Zhou
  • Yu-Lan Bi
  • Jia-Ying Wang
  • Rui Yu
  • Chao Deng
  • Wei-Kang Wang
  • Xian-Zhen Li
  • Rui Huang
  • Jili Zhang
  • De-Tao TaoEmail author
Original Article
  • 43 Downloads

Abstract

To study the role of MAPK signaling pathway in the development of Epithelial-mesenchymal transition in oral squamous cell carcinoma induced by inflammatory factor TNF-α. After the action of TNF-α, the expression of JNK, ERK, P38 in MAPK signaling pathway increased and the expression of E-cadherin, Claudin1 decreased significantly compared to the normal control group. After the addition of corresponding inhibitor, the expression of JNK, ERK, P38 decreased and the expression of E-cadherin, Claudin1 increased compared with TNF-α group. TNF-α regulated the role of EMT in promoting the invasion and metastasis of oral squamous carcinoma cells through MAPK signaling pathway.

Keywords

Oral squamous cell carcinoma TNF-α EMT MAPK 

Notes

Compliance with ethical standards

Conflict of interest

The authors declare that they have no conflict of interest.

Supplementary material

11033_2019_4772_MOESM1_ESM.doc (26 kb)
Supplementary material 1 (DOC 26 kb)

References

  1. 1.
    Tirelli G, Gatto A et al (2018) Prognostic indicators of improved survival and quality of life in surgically treated oral cancer.[J]. Oral Surg Oral Med Oral Pathol Oral Radiol 126:31–40CrossRefGoogle Scholar
  2. 2.
    Gao Z, Yang C et al (2014) Experimental study on TNF-α promoting invasion and metastasis of oral cancer cells by regulating MMPs[J]. Stomatology 34:9–12Google Scholar
  3. 3.
    Glaros EN, Kim WS et al (2010) Mediated. Upregulation of hepatocyte apoA-I synthesis is associated with ERK inhibition[J]. Clin Sci (Lond) 118(12):728–736CrossRefGoogle Scholar
  4. 4.
    Yum HK, Arcaroli J, Kupfner J et al (2001) Involvement of phosphoinositide 3-kinases in neutrophil activation and the development of acute lung injury[J]. J Immunol 167(11):6601–6608CrossRefGoogle Scholar
  5. 5.
    Chen X, Tzekov R et al (2016) Auranofin inhibits retinal pigment epithelium cell survival through reactive oxygen species-dependent epidermal growth factor receptor/mitogen-activated protein kinase signaling pathway[J]. PLoS ONE 11(11):e0166386CrossRefGoogle Scholar
  6. 6.
    Dong L, Zhang X et al (2018) Post-transcription mediated Snail stabilization is involved in radiation exposure induced invasion and migration of hepatocarcinoma cells[J]. Biomed Pharmacother 103:767–772CrossRefGoogle Scholar
  7. 7.
    Xia Z, Dickens M, Raingeaud J et al (1995) Opposing effects of ERK and JNK-p38 MAP kinases on apoptosis.[J]. Science 270(5240):1326–1331CrossRefGoogle Scholar
  8. 8.
    Zou W, Zeng J, Zhuo M et al (2002) Involvement of caspase-3 and p38 mitogen activated protein kinase in cobalt chloride-induced apoptosis in PC12 cells.[J]. J Neurosci Res 67(6):837–843CrossRefGoogle Scholar
  9. 9.
    Jiang K, Lu Q et al (2017) Astragaloside IV inhibits breast cancer cell invasion by suppressing Vav3 mediated Rac1/MAPK signaling[J]. Int Immunopharmacol 42(Complete):195–202CrossRefGoogle Scholar
  10. 10.
    Cicchini M, Buza EL, Sagal KM, Gudiel AA, Durham AC, Feldser DM (2017) Context-dependent effects of amplified mapk signaling during lung adenocarcinoma initiation and progression[J]. Cell Rep 18(8):1958–1969CrossRefGoogle Scholar
  11. 11.
    Zhou JP, Tao DT, Xu Q et al (2015) Expression of E-cadherin and vimentin in oral squamous cell carcinoma. Int J Clin Exp Pathol 8(3):3150–3154Google Scholar
  12. 12.
    Zhou JP, Gao ZL et al (2015) Snail interacts with Id2 in the regulation of TNF-α-induced cancer cell invasion and migration in OSCC. Am J Cancer Res 5(5):1680–1691Google Scholar
  13. 13.
    Fischer MS, Wu VW, Lee JE, O’Malley RC, Glass NL (2018) Regulation of cell-to-cell communication and cell wall integrity by a network of MAP kinase pathways and transcription factors in Neurospora crassa. Genetics 209(2):489–506CrossRefGoogle Scholar

Copyright information

© Springer Nature B.V. 2019

Authors and Affiliations

  1. 1.Oral Diseases Research Centre, Department of Oral Medicine, College of Oral MedicineWannan Medical CollegeWuhuPeople’s Republic of China
  2. 2.Department of StomatologyYijishan Hospital of Wannan Medical CollegeWuhuPeople’s Republic of China

Personalised recommendations