The role of interleukin-8 (CXCL8) and CXCR2 in acquired chemoresistance of human colorectal carcinoma cells HCT116.
Daiva DabkevicieneVioleta JonusieneVilmante ZitkuteEgle ZalytePranas GrigaitisVida KirvelieneAusra SasnauskienePublished in: Medical oncology (Northwood, London, England) (2015)
Colorectal cancer is one of the most common malignant diseases and is a leading cause of cancer mortality in the Western world. Primary or acquired resistance to chemotherapeutic drugs is a common phenomenon which causes a failure in cancer treatment. A diverse range of molecular mechanisms has been implicated in drug resistance: DNA damage repair, alterations in drug metabolism, mutation of drug targets, increased rates of drug efflux, and activation of survival signaling pathways. The aim of this study was to investigate the expression of CXCL8-CXCR1/2 pathway, its impact on cell proliferation and cytokine expression in human colorectal carcinoma HCT116 cells, and their chemotherapy-resistant subline. We found that IL-1 alpha stimulates the production of CXCL8 through IL-1 receptor signaling. Our data indicate that CXCL8 is upregulated in chemoresistant subline of colorectal cancer cells HCT116, and modulation of CXCR2 pathway can be a target for proliferation inhibition of chemoresistant colorectal cancer cells.
Keyphrases
- cell cycle arrest
- endothelial cells
- dna damage
- pi k akt
- signaling pathway
- poor prognosis
- cell proliferation
- induced apoptosis
- induced pluripotent stem cells
- cell death
- oxidative stress
- adverse drug
- cell migration
- papillary thyroid
- electronic health record
- cardiovascular disease
- south africa
- cardiovascular events
- cell cycle
- type diabetes
- risk factors
- long non coding rna
- lymph node metastasis
- squamous cell
- squamous cell carcinoma