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

Year: 2026

Type: article

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.

Source: PubMed

DOI: 10.17912/micropub.biology.002330

Authors: Jacob Krzeminski, Irene K. Guttilla Reed

Language: English

Topic: Chemokine receptors and signaling

Subfield: Oncology

Field: Medicine

Domain: Health Sciences

SDG: Good health and well-being

Open Access status: green

OpenAlex ID: W7214118383

FWCI:

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