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Overexpression of IL-8 promotes cell migration via PI3K-Akt signaling pathway and EMT in triple-negative breast cancer.

Abstract
Triple-negative breast cancer (TNBC) is a type of malignant and heterogeneous tumor in premenopausal females with ineffective therapeutic targets. IL-8 is one of the earliest discovered chemotaxis cytokines which expression is closely related to the progress of various cancers. Previous studies show that IL-8 determines the prognosis of TNBC patients, nevertheless how IL-8 influence the progress of TNBC is unclear. In our studies, we discovered that overexpression of IL-8 promotes TNBC cells (TNBCs) migration and tumor growth via the PI3K-Akt and MAPK signaling pathway. Cell-cycle of TNBCs arrest at S phase by overexpression of IL-8, however, there is no significant difference on the cell viability and cell apoptosis of TNBCs. Besides, overexpression of IL-8 result in the downregulation of E-cadherin and the upregulation of Cyclin B1 in MDA-MB-231 cells. Taken together, our results suggest that IL-8 plays a crucial role in the progress of TNBC, and it could be a novel therapeutic target of TNBC.
AuthorsFang Deng, Yaguang Weng, Xian Li, Teng Wang, Mengtian Fan, Qiong Shi
JournalPathology, research and practice (Pathol Res Pract) Vol. 223 Pg. 152824 (Jul 2021) ISSN: 1618-0631 [Electronic] Germany
PMID34000674 (Publication Type: Journal Article)
CopyrightCopyright © 2021. Published by Elsevier GmbH.
Chemical References
  • CXCL8 protein, human
  • Interleukin-8
  • Phosphatidylinositol 3-Kinase
  • Proto-Oncogene Proteins c-akt
Topics
  • Animals
  • Cell Line, Tumor
  • Cell Movement
  • Cell Proliferation
  • Epithelial-Mesenchymal Transition
  • Female
  • Gene Expression Regulation, Neoplastic
  • Humans
  • Interleukin-8 (genetics, metabolism)
  • Mice, Nude
  • Neoplasm Invasiveness
  • Phosphatidylinositol 3-Kinase (metabolism)
  • Proto-Oncogene Proteins c-akt (metabolism)
  • S Phase Cell Cycle Checkpoints
  • Signal Transduction
  • Triple Negative Breast Neoplasms (enzymology, genetics, pathology)
  • Tumor Burden
  • Up-Regulation
  • Mice

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