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Peer-reviewedCC BYmicroPublication Biology

CXCR2 knockdown reduces ERK and AKT signaling and migration in PANC-1 pancreatic cancer cells

  • Jacob Krzeminski1
  • Irene K. Guttilla Reed1
  1. 1Biology, University of Saint Joseph
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Abstract

Pancreatic cancer mortality is primarily driven by metastatic disease, and epithelial-mesenchymal transition (EMT) is one mechanism that promotes this process. The chemokine receptor CXCR2 has been implicated in tumor progression, but its role in pancreatic cancer remains unclear. We investigated CXCR2 in HPAF-II (epithelial-like) and PANC-1 (mesenchymal-like) pancreatic cancer cells. siRNA-mediated CXCR2 knockdown reduced ERK and AKT phosphorylation and decreased PI3K subunit expression in PANC-1 cells, but not HPAF-II cells. Furthermore, CXCR2 knockdown significantly reduced wound closure in PANC-1 cells. These findings indicate that CXCR2 may regulate EMT-associated signaling and migration in mesenchymal-like pancreatic cancer cells.

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Cite

BibTeXRIS
BibTeX
@article{krzeminski2026cxcr2,
  title = {{CXCR2 knockdown reduces ERK and AKT signaling and migration in PANC-1 pancreatic cancer cells}},
  author = {Jacob Krzeminski and Irene K. Guttilla Reed},
  journal = {microPublication Biology},
  year = {2026},
  month = sep,
  doi = {10.17912/micropub.biology.002330},
  url = {https://doi.org/10.17912/micropub.biology.002330},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - CXCR2 knockdown reduces ERK and AKT signaling and migration in PANC-1 pancreatic cancer cells
AU  - Jacob Krzeminski
AU  - Irene K. Guttilla Reed
PY  - 2026
DA  - 2026/09/01
JO  - microPublication Biology
DO  - 10.17912/micropub.biology.002330
UR  - https://doi.org/10.17912/micropub.biology.002330
AB  - Pancreatic cancer mortality is primarily driven by metastatic disease, and epithelial-mesenchymal transition (EMT) is one mechanism that promotes this process. The chemokine receptor CXCR2 has been implicated in tumor progression, but its role in pancreatic cancer remains unclear. We investigated CXCR2 in HPAF-II (epithelial-like) and PANC-1 (mesenchymal-like) pancreatic cancer cells. siRNA-mediated CXCR2 knockdown reduced ERK and AKT phosphorylation and decreased PI3K subunit expression in PANC-1 cells, but not HPAF-II cells. Furthermore, CXCR2 knockdown significantly reduced wound closure in PANC-1 cells. These findings indicate that CXCR2 may regulate EMT-associated signaling and migration in mesenchymal-like pancreatic cancer cells.
SN  - 2578-9430
ER  -