Heat shock protein B6 potently increases non-small cell lung cancer growth

The aim of the present study was to address the effects of heat shock protein B6 (HspB6) on tumor growth and metastasis in BALB/c mice. Lewis lung carcinoma (LLC) cells were subcutaneously injected into BALB/c mice followed by intraperitoneal injection of recombinant HspB6 (HspB6 groups) or phosphate‑buffered saline (control groups). Tumor growth and metastasis were assessed by size measurement and weighing of tumors and cervical lymph nodes, respectively. Chemokine expression in tumor masses was quantified quantitative polymerase chain reaction and western blotting. Tumor cell apoptosis was detected by flow cytometric analysis. The proliferation and migration of LLC cells, stimulated with HspB6, were detected using Cell Counting Kit 8 and wound scratch assays in vitro. Tumors grafted into the BALB/c mice and intraperitoneally injected with HspB6 were significantly bigger in size than those grafted into the control mice. From 7 days following the injection, the weight of cervical lymph nodes in HspB6 groups was higher than that in the control mice. We also revealed that the apoptotic cell number in tumor masses in the HspB6 groups was lower than that of the control mice. CD31 expression of vascular endothelial cells was higher in tumors grafted in HspB6 groups than those grafted in the control mice. Concomitantly, the tumor tissue mRNA and protein expression enhancement of vascular endothelial growth factor, basic fibroblast growth factor and intercellular adhesion molecule 1 were greater in HspB6 mice than in the control mice. HspB6 also inhibited cell apoptosis and enhanced the migration and proliferation of LLCs in vitro. In conclusion, HspB6 exhibited tumor promotion through increasing tumor angiogenesis, tumor metastasis and inhibiting tumor cell apoptosis.