English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Reduced expression levels of caveolin‑1 (Cav‑1) in tumor stromal fibroblasts influences the occurrence and progression of tumors, particularly in breast cancer, but the relevant molecular mechanism is unclear. The present study aimed to clarify the potential mechanism underlying the promotion of tumor growth by reduced Cav‑1 expression levels, by investigating Cav‑1‑targeted molecules in fibroblasts and breast cancer cells. The expression of growth factors in the ESF fibroblast cell line transfected with Cav‑1 small interfering RNA (siRNA) was examined. The expression of apoptotic regulators in the BT474 breast cancer cell line that was co‑cultured with the fibroblasts, was also investigated. The transfection of Cav‑1‑targeting siRNA in ESF cells resulted in efficient and specific inhibition of Cav‑1 expression. The downregulation of Cav‑1 increased the expression and secretion of stromal cell‑derived factor‑1 (SDF‑1), epidermal growth factor (EGF) and fibroblast‑specific protein‑1 (FSP‑1) in ESF cells. This resulted in the accelerated proliferation of the breast cancer cells. Tumor protein 53‑induced glycolysis and apoptosis regulator (TIGAR) was upregulated in the BT474 cells under the condition of co‑culture with Cav‑1 siRNA fibroblasts, while levels of reactive oxygen species (ROS) were decreased, resulting in apoptosis inhibition in the breast cancer cells. These results demonstrated that the downregulation of Cav‑1 promoted the growth of breast cancer cells through increasing SDF‑1, EGF and FSP‑1 in tumor stromal fibroblasts, and TIGAR levels in breast cancer cells. To the best of our knowledge, the present study supports the hypothesis that Cav‑1 possesses tumor‑suppressor properties, with the mechanism of Cav‑1‑dependent signaling involving the regulation of SDF‑1, EGF, FSP‑1 and TIGAR.

Downregulation of caveolin-1 upregulates the expression of growth factors and regulators in co-culture of fibroblasts with cancer cells