The Interaction Between SMAD1 and YAP1 Is Correlated with Increased Resistance of Gastric Cancer Cells to Cisplatin
Wanjing Chen1, Jingtao Hu2, Yawei He1
1Department of General Surgery, The Second Hospital of Anhui Medical University, No. 678, Furong Road, Economic and Technological Development District, Hefei, 230601, Anhui, People's Republic of China.
Abstract:
Drug resistance is a major obstacle leading to treating failure and poor outcome in gastric cancer (GC). This study explores the interaction between SMAD family member 1 (SMAD1) and Yes1-associated transcriptional regulator (YAP1) and their roles in cisplatin (DDP) resistance in GC. Transcriptome analysis predicted that SMAD1 is highly expressed in DDP-resistant cells. Elevated SMAD1 expression was detected in GC tissue and cells, especially in DDP-resistant cells (MKN-45/DDP and AGS/DDP). SMAD1 downregulation in cells decreased 50% inhibition value of DDP, reduced proliferation, migration, and invasion, and promoted cell cycle arrest and apoptosis. A protein-protein interaction network suggested a possible SMAD1 and YAP1 interaction in GC. The SMAD1 and YAP1 interaction was validated by chromatin immunoprecipitation (ChIP), co-immunoprecipitation (Co-IP), and luciferase assays. SMAD1 bound to YAP1 and activated its transcription. SMAD1 formed complexes with YAP1 in nucleus, and YAP1 upregulation enhanced SMAD1 activity as well. Upregulation of YAP1 restored the malignant behaviors of GC cells suppressed by SMAD1 silencing. In vivo, SMAD1 silencing suppressed growth and DDP resistance of xenograft tumors in nude mice, and this suppression was blocked by YAP1 overexpression again. In conclusion, this study demonstrates that SMAD1 can interact with YAP1 to enhance the DDP resistance of GC cells.
Insights
SMAD1 and YAP1 interaction enhances cisplatin resistance in gastric cancer (GC). Silencing SMAD1 reduces resistance, while YAP1 upregulation reverses this effect, highlighting a key pathway in GC drug resistance.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Drug resistance is a significant challenge in gastric cancer (GC) treatment.
- Understanding molecular mechanisms of resistance is crucial for improving patient outcomes.
Purpose of the Study:
- To investigate the interaction between SMAD family member 1 (SMAD1) and Yes1-associated transcriptional regulator (YAP1).
- To elucidate their roles in cisplatin (DDP) resistance in gastric cancer.
Main Methods:
- Transcriptome analysis to predict SMAD1 expression.
- Cellular and molecular assays including chromatin immunoprecipitation (ChIP), co-immunoprecipitation (Co-IP), and luciferase assays.
- In vivo xenograft tumor models in nude mice.
Main Results:
- SMAD1 was highly expressed in DDP-resistant GC cells and tissues.
- SMAD1 downregulation decreased DDP resistance, reduced proliferation, migration, and invasion, and promoted apoptosis.
- SMAD1 directly interacted with and activated YAP1 transcription, forming nuclear complexes.
- YAP1 upregulation restored malignant behaviors suppressed by SMAD1 silencing.
- SMAD1 silencing inhibited tumor growth and DDP resistance in vivo, an effect reversed by YAP1 overexpression.
Conclusions:
- SMAD1 interacts with YAP1 to enhance cisplatin resistance in gastric cancer.
- Targeting the SMAD1-YAP1 interaction may offer a therapeutic strategy for overcoming DDP resistance in GC.
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