التفاصيل البيبلوغرافية
العنوان: |
Ginsenoside Rh1 Prevents Migration and Invasion through Mitochondrial ROS-Mediated Inhibition of STAT3/NF-κB Signaling in MDA-MB-231 Cells |
المؤلفون: |
Yujin Jin, Diem Thi Ngoc Huynh, Chang-Seon Myung, Kyung-Sun Heo |
المصدر: |
International Journal of Molecular Sciences; Volume 22; Issue 19; Pages: 10458 |
بيانات النشر: |
Multidisciplinary Digital Publishing Institute |
سنة النشر: |
2021 |
المجموعة: |
MDPI Open Access Publishing |
مصطلحات موضوعية: |
metastasis, ginsenoside Rh1, mitochondrial ROS, STAT3, NF-κB, triple-negative breast cancer cells |
جغرافية الموضوع: |
agris |
الوصف: |
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. |
نوع الوثيقة: |
text |
وصف الملف: |
application/pdf |
اللغة: |
English |
Relation: |
Molecular Pharmacology; https://dx.doi.org/10.3390/ijms221910458 |
DOI: |
10.3390/ijms221910458 |
الاتاحة: |
https://doi.org/10.3390/ijms221910458 |
Rights: |
https://creativecommons.org/licenses/by/4.0/ |
رقم الانضمام: |
edsbas.64ECAF2A |
قاعدة البيانات: |
BASE |