Hydroxyl safflower yellow B combined with doxorubicin inhibits the proliferation of human breast cancer MCF-7 cells.

Doxorubicin (DOX) is currently the preferred chemotherapeutic agent for breast cancer, and hydroxyl safflower yellow B (HSYB) has a tumor growth-inhibiting activity. The present study aimed to investigate the effects of HSYB combined with DOX on the proliferation of human breast cancer MCF-7 cells and explore the underlying mechanism. MTT and cell colony formation assays revealed that the proliferation rate of MCF-7 cells was signifiscantly decreased after HSYB and DOX treatment.

Vitamin C induces human melanoma A375 cell apoptosis via Bax- and Bcl-2-mediated mitochondrial pathways.

Melanoma is the most malignant type of skin cancer and is resistant to numerous chemotherapeutic and radiotherapy-based treatment approaches due to the activation of rapid and reversible pro-survival signaling pathways. As a result, patients will often present with a poor prognosis. Therefore, novel preventive methods and treatments are urgently required for patients with melanoma.

Inhibitory Effect of Hydroxysafflor Yellow B on the Proliferation of Human Breast Cancer MCF-7 Cells.

Background: A recent patent has been issued for hydroxysafflor yellow A (HSYA) as a drug to prevent blood circulation disorders. Hydroxysafflor yellow B (HSYB), an isomer of HSYA with antioxidative effects, has been isolated from the florets of Carthamus tinctorius. The effects of HSYB on the proliferation of cancer cells and its mechanism of action have not been investigated.

Bufotalin induces cell cycle arrest and cell apoptosis in human malignant melanoma A375 cells.

Venenum bufonis has been used as an antitumor drug in China for many years. Bufotalin, as an active component of Venenum bufonis, has been proven to exhibit antitumor effects in cancer types. In the present study, the effect of bufotalin on the human melanoma skin cancer cell line A375 was analyzed using MTT and colony formation assays.

Isoliquiritigenin Induces Mitochondrial Dysfunction and Apoptosis by Inhibiting mitoNEET in a Reactive Oxygen Species-Dependent Manner in A375 Human Melanoma Cells.

The mitochondrial protein mitoNEET is a type of iron-sulfur protein localized to the outer membrane of mitochondria and is involved in a variety of human pathologies including cystic fibrosis, diabetes, muscle atrophy, and neurodegeneration. In the current study, we found that isoliquiritigenin (ISL), one of the components of the root of , could decrease the expression of mitoNEET in A375 melanoma cells. We also demonstrated that mitoNEET could regulate the content of reactive oxygen species (ROS), by showing that the ISL-mediated increase in the cellular ROS content could be mitigated by the mitoNEET overexpression.

Reprogramming induced by isoliquiritigenin diminishes melanoma cachexia through mTORC2-AKT-GSK3β signaling.

Isoliquiritigenin (ISL), a member of the flavonoids, is known to have anti-tumor activity in vitro and in vivo. The effect of ISL on reprogramming in cancer cells, however, remains elusive. In this study, we investigated the effect of ISL on reprogramming in human melanoma A375 cells.