elemene/유방암

OBJECTIVE To observe the synergistic effect of beta-elemene Injection (betaI) combined Paclitaxel Injection (PI) on breast cancer MB-468 cells and to study possible mechanisms. METHODS Breast cancer MB-468 cells were treated with betaI (2.5, 5.0, 10.0, 20.0, 40.0, 80.0, 160.0, 320.0, and 640.0

OBJECTIVE To study the reversal mechanism of adriamycin (ADM) resistance in human breast cancer cell line MCF-7/ADM by beta-elemene (beta-ELE), a wide spectrum anticancer drug derived from the Chinese herb Curcuma chaeocaulis. METHODS Sensitivity to ADM of MCF-7/ADM cells was studied by MTT assay.

Elemene (ELE), a natural plant drug extracted from Curcumae Rhizoma, has been widely used for cancer treatment in China for more than 20 years. Although it is reported to be a broad‑spectrum anticancer drug, the mechanism underlying the action of ELE in the treatment of breast cancer remains to be

BACKGROUND Currently, exosomes that act as mediators of intercellular communication are being researched extensively. Our previous studies confirmed that these exosomes contain microRNAs (miRNAs) that could alter chemo-susceptibility, which is partly attributed to the successful intercellular

Inactivation of E-cadherin results in cell migration and invasion, hence leading to cancer aggressiveness and metastasis. Downregulation of E-cadherin is closely correlated with a poor prognosis in invasive breast cancer. Thus, re-introducing E-cadherin is a novel strategy for cancer therapy. The

It has been approved for the clinical application of β-elemene to treat various cancers mainly brain tumors in China. In the present study, we found that β-elemene significantly inhibited the in vitro growth of human breast cancer cells by inducing apoptosis. In addition, β-elemene also induced the

Elemene has been approved for the treatment of advanced cancer in China, however, it inhibits cell growth only at high concentrations and is an essential oil with poor water solubility and stability. The discovery of new β-elemene derivatives is of increasing interest. We recently reported that the

Epithelial-mesenchymal transition (EMT) is the first step required for breast cancer to initiate metastasis. However, the potential of drugs to block and reverse the EMT process are not well explored. In the present study, we investigated the inhibitory effect of beta-elemene (ELE), an active

BACKGROUND Multidrug resistance (MDR) directly contributes to the clinical failure of chemotherapy in breast cancer (BCA). β-elemene is a natural antitumor drug from plants. We previously confirmed that MDR could be reversed by β-elemene. In this study, we intended to investigate the reversal effect

In order to explore the mechanism of the reversing multidrug resistance (MDR) phenotypes by β-elemene (β-ELE) in doxorubicin (DOX)-resistant breast cancer cells (MCF-7/DOX), both the functionality and quantity of the ABC transporters in MCF-7/DOX were studied. Bioluminescence imaging (BLI) was used

We examined expression differences in breast cancer stem cells (BCSCs) of the doxorubicin-resistant breast cancer cell line MCF-7/ADM and doxorubicin-sensitive cell line MCF-7/S. The effects of Chinese medicine β-elemene on BCSCs and resistance protein expression were determined. The serum-free cell

Pyruvate kinase M2 (PKM2), playing a central role in regulating aerobic glycolysis, was considered as a promising target for cancer therapy. However, its role in cancer metastasis is rarely known. Here, we found a tight relationship between PKM2 and breast cancer metastasis, demonstrated by the

Background: The most common chemotherapeutic drug for triple-negative breast cancer (TNBC) treatment is 5-fluorouracil (5-FU), but its therapeutic index is low due to its toxicity. β-Elemene (ELE) possesses antitumor activity against

BACKGROUND Multidrug resistance (MDR) presents a problem in cancer chemotherapy, and developing new agents to overcome MDR is important. This study intends to investigate the reversal effect of -elemene on MDR in human breast carcinoma MCF-7 and doxorubicin-resistant MCF-7 cells. METHODS MTT