Related Experiment Video
Updated: Dec 18, 2025
Author Spotlight: Exploring Salidroside's Molecular Mechanisms in Breast Cancer Treatment
Published on: June 9, 2023
Silibinin suppresses epithelial-mesenchymal transition in human non-small cell lung cancer cells by restraining
Suyan Xu1, Hongyan Zhang1, Aifeng Wang1
1Department of Pharmacy, Henan Provincial People Hospital, Department of Pharmacy of Central China Fuwai Hospital, Central China Fuwai Hospital of Zhengzhou University, Zhengzhou, 450003 Henan China.
Background:
Rhomboid domain containing 1 (RHBDD1) plays a crucial role in tumorigenesis. Silibinin, which is a natural extract from milk thistle, has shown anti-tumor effects against various tumors. Here, we investigate whether silibinin affects the function of RHBDD1 in non-small cell lung cancer (NSCLC) cell proliferation, migration and invasion.
Methods:
The Oncomine database and an immunohistochemistry (IHC) assay were used to determine the RHBDD1 expression levels in lung cancer tissues. The associations between RHBDD1 and overall survival rate or clinicopathological parameters were respectively assessed using the Kaplan-Meier overall survival analysis or Chi-squared test. CCK-8 and Transwell assays were applied to analyze cell proliferation, migration and invasion. A549 cells were incubated with increasing concentrations of silibinin. RHBDD1 knockdown and overexpression were achieved via transfection with si-RHBDD1 or RHBDD1 overexpression plasmid, respectively. Western blotting was performed to measure the expressions of epithelial-mesenchymal transition (EMT) markers.
Results:
We found that overexpression of RHBDD1 in lung cancer tissues correlates with a poor prognosis of survival. Clinical specimen analysis showed that upregulation of RHBDD1 correlates remarkably well with TNM stage and lymph node metastasis. Silibinin suppresses A549 cell proliferation, migration, invasion and EMT in a dose-dependent manner. Importantly, RHBDD1 was downregulated in silibinin-treated A549 cells. RHBDD1 overexpression reversed the suppressive effects of silibinin on A549 cell proliferation, migration, invasion and EMT expression, while its knockdown enhanced them.
Conclusions:
These findings shown an anti-tumor impact of silibinin on NSCLC cells via repression of RHBDD1.
Insights
Silibinin, a milk thistle extract, inhibits non-small cell lung cancer (NSCLC) growth by downregulating RHBDD1. This natural compound suppresses tumor cell proliferation, migration, and invasion, offering a potential therapeutic strategy for NSCLC.
Area of Science:
- Oncology
- Molecular Biology
- Natural Product Chemistry
Background:
- Rhomboid domain containing 1 (RHBDD1) is implicated in tumorigenesis.
- Silibinin, a milk thistle extract, exhibits anti-tumor properties.
- The role of RHBDD1 in non-small cell lung cancer (NSCLC) requires further investigation.
Purpose of the Study:
- To investigate the effect of silibinin on RHBDD1 expression and function in NSCLC.
- To determine the impact of silibinin on NSCLC cell proliferation, migration, and invasion.
- To elucidate the mechanism by which silibinin exerts its anti-cancer effects in NSCLC.
Main Methods:
- RHBDD1 expression analysis in lung cancer tissues using Oncomine and immunohistochemistry.
- Correlation analysis of RHBDD1 with patient survival and clinicopathological parameters.
- In vitro assays (CCK-8, Transwell) to assess cell proliferation, migration, and invasion in silibinin-treated A549 cells with RHBDD1 manipulation (knockdown/overexpression).
- Western blotting to evaluate epithelial-mesenchymal transition (EMT) markers.
Main Results:
- RHBDD1 overexpression in lung cancer correlates with poor prognosis, advanced TNM stage, and lymph node metastasis.
- Silibinin dose-dependently suppresses A549 cell proliferation, migration, invasion, and EMT.
- Silibinin treatment downregulates RHBDD1 expression in A549 cells.
- RHBDD1 overexpression counteracted silibinin's suppressive effects, while RHBDD1 knockdown enhanced them.
Conclusions:
- Silibinin demonstrates an anti-tumor effect on NSCLC cells.
- The anti-tumor activity of silibinin in NSCLC is mediated through the repression of RHBDD1.
- Targeting RHBDD1 with silibinin presents a potential therapeutic avenue for NSCLC treatment.
Related Concept Videos
02:23Abnormal Proliferation
01:20The Retinoblastoma Gene
The first-ever tumor suppressor gene called Rb was identified in retinoblastoma - a rare eye tumor in children. In inherited forms of the disease, a child inherits one defective copy of the Rb gene, which predisposes them to retinoblastoma. However,...