In the current review, we cover the state-of-the-art study, development and progress on Cav1 and breast cancer, altogether describing the role of Cav1 in breast cancer progression and application in clinical treatment, in the hope of providing a basis for further research and promoting <i>CAV1</i> gene as a potential target to diagnose and treat aggressive breast cancers.
Therefore, the present study demonstrated that miR‑192 serves an important role as a regulator in breast cancer and the miR‑192/CAV1 axis has a potential as a therapeutic target for treatment of breast cancer.
Here we show that the expression of β3GalT5 significantly correlates with tumor progression and poor survival in patients, and the globo-series GSLs in breast cancer cells form a complex in membrane lipid raft with caveolin-1 (CAV1) and focal adhesion kinase (FAK) which then interact with AKT and receptor-interacting protein kinase (RIP), respectively.
Mechanistically, RNA sequencing and experimental validation results suggested that EEOD might inhibit breast cancer metastasis by attenuating the expression of caveolin-1 (Cav-1) as overexpression of Cav-1 could weaken the anti-metastasis efficacy of EEOD.
Enrichment analysis and experimental validation demonstrated that ADQ might improve breast cancer chemosensitivity <i>via</i> inhibiting caveolin-1, which further triggered expression changes of cell cycle-related proteins p21/cyclinB1 and apoptosis-associated proteins PARP1, BAX and Bcl-2.
Parenchymal expression of Cav-1 is able to promote EGFR signaling in breast cancer, potentially being required for EGFR-mediated initiation of mitosis.
This study was conducted to evaluate the cavolin-2 (cav-2) transcripts expression changes in tumoral and corresponding tissues and in contralateral breast, to investigate their variation associated with the variation of caveolin-1 (cav-1) expression in breast cancer.
The aim of the present study is to describe the biological roles of Cav-1 in breast cancers considering its contrasting dual functions as an oncogene and as a tumor suppressor.
Our results showed that genetic changes of CAV-1 might modify the risk for breast cancer and point out the importance of more studies for variants of this gene in breast cancer.
Besides, it has been reported that the loss of stromal Cav-1 might predict poor prognosis in breast cancer, gastric cancer, pancreas cancer, prostate cancer, oral SCC and esophageal SCC.
This study was designed to investigate the potential of L-CAV to enhance the toxicity of chemotherapeutic drugs in the human breast cancer cell line MCF-7, and determine the most favorable drug combination to exert synergistic interaction in the presence or absence of arginine in the medium.
The aim of this study was to evaluate the coexpression of caveolin-1 (CAV-1), angiotensin II type 1 receptor (AT1-R) and forkhead box Ml (FOXM1) in prostate and breast cancer cell lines, in comparison with normal cell lines.
Finally, new roles of CAV1 in BC both on epithelium and stroma may be useful as prognostic indicators for patient treatment and help clinicians in the selection of the best personalized therapy.
In the present study, caveolin 1 small interfering RNA was used to knock down caveolin 1 expression in order to investigate the association between caveolin 1 and the proliferation and metastatic abilities of human breast cancer BT474 cells.