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.

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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