ginsenoside-rh1 has been researched along with Triple-Negative-Breast-Neoplasms* in 2 studies
2 other study(ies) available for ginsenoside-rh1 and Triple-Negative-Breast-Neoplasms
| Article | Year |
|---|---|
Ginsenoside Rh1 inhibits tumor growth in MDA-MB-231 breast cancer cells via mitochondrial ROS and ER stress-mediated signaling pathway.
Ginsenoside-Rh1 (Rh1) is a ginseng-derived compound that has been reported to exert anticancer effects by regulating cell cycle arrest and apoptosis according to reactive oxygen species (ROS) production. However, the effects of Rh1 on mitochondrial dysfunction are involved in triple negative breast cancer (TNBC) cell apoptosis, and the related molecular mechanisms remain unknown. Rh1 treatment induced cell toxicity less than 50% at 50 μM. In addition, Rh1 induced apoptosis in TNBC cells through cleaved caspase-3 activation and G1/S arrest. The Rh1-treated TNBC cells showed a significant increase in mitochondrial ROS (mtROS), which in turn increased protein expression of mitochondrial molecules, such as Bak and cytochrome C, and caused the loss of mitochondrial membrane potential. Pretreatment with mitochondria-targeted antioxidant Mito-TEMPO alters the Rh1-reduced rate of mito- and glycol-ATP. Furthermore, Rh1 induces ER stress-mediated calcium accumulation via PERK/eIF2α/ATF4/CHOP pathway. Inhibition of ATF4 by siRNA transfection significantly inhibited Rh1-mediated apoptosis and calcium production. Interestingly, Mito-TEMPO treatment significantly reduced apoptosis and ER stress induced by Rh1. Finally, Rh1 at 5 mg/kg suppressed tumor growth through increased levels of ROS production, cleaved caspase-3, and ATF4 more than 5-fluorouracil treated group. Overall, our results suggest that Rh1 has potential for use in TNBC treatment. Topics: Ginsenosides; Humans; Mitochondria; Reactive Oxygen Species; Signal Transduction; Triple Negative Breast Neoplasms | 2022 |
Ginsenoside Rh1 Prevents Migration and Invasion through Mitochondrial ROS-Mediated Inhibition of STAT3/NF-κB Signaling in MDA-MB-231 Cells.
Breast cancer (BC) a very common cancer in women worldwide. Triple negative breast cancer (TNBC) has been shown to have a poor prognosis with a high level of tumor metastatic spread. Here, the inhibitory effects of ginsenoside-Rh1 (Rh1) on BC metastasis, and its underlying signaling pathway in TNBC were investigated. Rh1-treated MDA-MB-231 cells were analyzed for metastasis using a wound healing assay, transwell migration and invasion assay, western blotting, and qRT-PCR. Rh1 treatment significantly inhibited BC metastasis by inhibiting the both protein and mRNA levels of MMP2, MMP9, and VEGF-A. Further, Rh1-mediated inhibitory effect on BC migration was associated with mitochondrial ROS generation. Rh1 treatment significantly eliminated STAT3 phosphorylation and NF-κB transactivation to downregulate metastatic factors, such as MMP2, MMP9, and VEGF-A. In addition, Mito-TEMPO treatment reversed Rh1 effects on the activation of STAT3, NF-κB, and their transcriptional targets. Rh1 further enhanced the inhibitory effects of STAT3 or NF-κB specific inhibitor, stattic or BAY 11-7082 on MMP2, MMP9, and VEGF-A expression, respectively. In summary, our results revealed the potent anticancer effect of Rh1 on TNBC migration and invasion through mtROS-mediated inhibition of STAT3 and NF-κB signaling. Topics: Antineoplastic Agents; Cell Line, Tumor; Cell Movement; Female; Ginsenosides; Humans; Mitochondria; Neoplasm Invasiveness; NF-kappa B; Reactive Oxygen Species; Signal Transduction; STAT3 Transcription Factor; Triple Negative Breast Neoplasms | 2021 |