ABSTRACT
Breast cancer is the malignancy with the highest number of new cases worldwide and is the leading cause of cancer-related deaths in women. More than 90% of breast cancer-related deaths are related to its metastasis. Paclitaxel, one of the most commonly used chemotherapeutic agents for the treatment of breast cancer, is an effective means of inhibiting breast cancer metastasis. To overcome the adverse effects of paclitaxel's hydrophobicity and its co-solvent, its nano-drugs have been a hot research topic. Some nanomedicines delivering paclitaxel have been used in clinical practice and have shown satisfactory efficacy and good tolerability. In this review, the research progress on the inhibition of breast cancer metastasis by co-delivered paclitaxel nanomedicines was summarized with the aim of providing a reference for their anti-breast cancer metastasis research.
ABSTRACT
Breast cancer is one of the most common malignant tumors in women, and its incidence has increased year by year, which is one of the most important causes of death among women, especially young women. Studying related cell signal transduction that affects the development and progression of breast cancer can help prevent the occurrence of breast cancer, slow down the cancer progression and improve the prognosis of patients. nitric oxide (NO) is a kind of signaling molecule. Many studies have shown that the production and expression of NO are closely related to breast cancer. NO-related cell signal transduction significantly affects the occurrence and development of breast cancer. However, the understanding of the relationship between NO and breast cancer associated cell signal transduction needs to be further improved. In this paper, the related studies on NO-related cellular signal transduction in breast cancer were reviewed with a view to improving the understanding of the development and progression of breast cancer.
ABSTRACT
Objective: In order to reveal the mechanisms of rh-endostatin and its suppression effect on HUVECs at different activating levels. Methods: Three types of HUVEC were prepared. We detected the ex-pression of CD105 and CD62E on the surface of adhering HUVEC, HUVEC of exponential phase of growth, and HUVEC activated with TNF-alpha. The effect of endostatin on these three types of HUVEC was indicated by the variation in the expression of CD105 and CD62E on the cells. The relationship of the changes in cell markers with the time and the concentration of endostatin was analyzed by SPSS 11.5. Results: The expres-sion of CD105 was correlated with time and dose of endostar in all groups. The expression of CD62E was cor-related with the dose of endostar in HUVEC treated with TNF-α for 24h. Conclusion: Endostatin of a certain dose can inhibit the activation of endothelial cells but it cannot induce cell apoptosis.