4.5 Article

Resistin causes G1 arrest in colon cancer cells through upregulation of SOCS3

Journal

FEBS LETTERS
Volume 591, Issue 10, Pages 1371-1382

Publisher

WILEY
DOI: 10.1002/1873-3468.12655

Keywords

colon cancer; resistin; SOCS3; TLR4

Funding

  1. Central Instrumental Facility
  2. Intramural grant from National Centre for Cell Science (NCCS) - Department of Biotechnology (DBT), Ministry of Science & Technology Government of India

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Resistin, a proinflammatory cytokine, is elevated in a number of pathological disorders, including cancer. The serum resistin level in colon cancer patients is elevated and correlates with tumor grade. However, the implications of increased resistin on colon cancer cells remain unclear. In the present study, we find that resistin binds to TLR4 on colon cancer cell membrane and initiates TLR4-MyD88-dependent activation of ERK. In addition, the upregulation of SOCS3 by ERK downregulates the JAK2/TAT3 pathway and causes the arrest of cells in G1 phase. Interestingly, we observe that resistin-exposed cells survive 5-fluorouracil treatment because of a decrease in drug uptake due to the arrest of cells in G1 phase.

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