Bicalutamide Enhances Conventional Chemotherapy in In Vitro and In Vivo Assays Using Human and Canine Inflammatory Mammary Cancer Cell Lines.
Belen CrespoJuan Carlos IlleraGema SilvanPaula Lopez-PlazaMaría Herrera de la MuelaMiriam de la Puente YagüeCristina Díaz Del ArcoPaloma Jimena de AndrésMaria Jose IlleraSara CaceresPublished in: International journal of molecular sciences (2024)
Human inflammatory breast cancer (IBC) and canine inflammatory mammary cancer (IMC) are highly aggressive neoplastic diseases that share numerous characteristics. In IBC and IMC, chemotherapy produces a limited pathological response and anti-androgen therapies have been of interest for breast cancer treatment. Therefore, the aim was to evaluate the effect of a therapy based on bicalutamide, a non-steroidal anti-androgen, with doxorubicin and docetaxel chemotherapy on cell proliferation, migration, tumor growth, and steroid-hormone secretion. An IMC-TN cell line, IPC-366, and an IBC-TN cell line, SUM149, were used. In vitro assays revealed that SUM149 exhibited greater sensitivity, reducing cell viability and migration with all tested drugs. In contrast, IPC-366 exhibited only significant in vitro reductions with docetaxel as a single agent or in different combinations. Decreased estrogen levels reduced in vitro tumor growth in both IMC and IBC. Curiously, doxorubicin resulted in low efficacy, especially in IMC. In addition, all drugs reduced the tumor volume in IBC and IMC by increasing intratumoral testosterone (T) levels, which have been related with reduced tumor progression. In conclusion, the addition of bicalutamide to doxorubicin and docetaxel combinations may represent a potential treatment for IMC and IBC.
Keyphrases
- locally advanced
- endothelial cells
- papillary thyroid
- cell proliferation
- drug delivery
- oxidative stress
- rectal cancer
- high throughput
- cancer therapy
- induced pluripotent stem cells
- squamous cell carcinoma
- radiation therapy
- poor prognosis
- replacement therapy
- cell cycle
- risk assessment
- chemotherapy induced
- drug induced
- human health
- estrogen receptor
- cell therapy