title: The depletion of interleukin-8 causes cell cycle arrest and increases the efficacy of docetaxel in breast cancer cells.
abstract: IL-8 is a multi-functional pro-inflammatory chemokine, which is highly expressed in cancers, such as ER-negative breast cancer. The present study demonstrates the pervasive role of IL-8 in the malignant progression of ER-negative breast cancer. IL-8 siRNA inhibited proliferation and delayed the G1 to S cell cycle progression in MDA-MB-231 and BT549 cells. IL-8 silencing resulted in the upregulation of the CDK inhibitor p27, the downregulation of cyclin D1, and the reduction of phosphorylated-Akt and NF-κB activities. IL-8 depletion also increased the chemosensitivity to docetaxel. These results indicate a role for IL-8 in promoting tumor cell survival and resistance to docetaxel and highlight the potential therapeutic significance of IL-8 depletion in ER-negative breast cancer patients.
authors: Breast Disease Center, The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, PR China.
authors: Nan
authors: N
authors: Shao
authors: Liu-Hua
authors: LH
authors: Chen
authors: Run-Yi
authors: RY
authors: Ye
authors: Ying
authors: Y
authors: Lin
authors: Shen-Ming
authors: SM
authors: Wang
mesh_terms: D000970:Antineoplastic Agents / Q000627:therapeutic use*; D001943:Breast Neoplasms / Q000188:drug therapy* / Q000473:pathology*; D059447:Cell Cycle Checkpoints / Q000187:drug effects / Q000235:genetics; D045744:Cell Line, Tumor; D049109:Cell Proliferation; D000077143:Docetaxel; D019008:Drug Resistance, Neoplasm / Q000235:genetics*; D005260:Female; D006801:Humans; D039661:Integrin beta3 / Q000235:genetics; D016209:Interleukin-8 / Q000235:genetics / Q000502:physiology*; D008875:Middle Aged; D034622:RNA Interference; D034741:RNA, Small Interfering / Q000235:genetics; D043823:Taxoids / Q000627:therapeutic use*
chemical_list: D000970:Antineoplastic Agents; D039661:Integrin beta3; D016209:Interleukin-8; D034741:RNA, Small Interfering; D043823:Taxoids; D000077143:Docetaxel