SHCBP1 promotes cisplatin induced apoptosis resistance, migration and invasion through activating Wnt pathway

Area of Science:

• Oncology
• Molecular Biology
• Cancer Research

Background:

• Lung cancer is a leading cause of cancer mortality, often due to resistance to existing treatments.
• Understanding the mechanisms of therapy resistance is crucial for improving lung cancer treatment outcomes.

Purpose of the Study:

• To investigate the role of SHC binding and spindle associated 1 (SHCBP1) in cisplatin resistance in lung cancer.
• To elucidate the molecular mechanisms by which SHCBP1 influences lung cancer progression and treatment response.

Main Methods:

• Analysis of SHCBP1 expression in lung cancer tissues and cells.
• Assessment of apoptosis, migration, and invasion using apoptosis assays and transwell assays.
• Evaluation of Wnt pathway activation, including beta-catenin nuclear translocation.
• Inhibition of the Wnt pathway to determine its role in SHCBP1-mediated effects.

Main Results:

• SHCBP1 was found to be upregulated in lung cancer tissues and cells, correlating with poor patient prognosis.
• SHCBP1 overexpression enhanced resistance to cisplatin-induced apoptosis, promoted migration and invasion.
• SHCBP1 knockdown reversed these effects, sensitizing cells to cisplatin.
• SHCBP1 was shown to activate the Wnt pathway by promoting beta-catenin nuclear translocation.
• Inhibition of the Wnt pathway abrogated the pro-cancer effects of SHCBP1 overexpression.
• A positive correlation was observed between SHCBP1 expression and Wnt pathway activity in lung cancer samples.

Conclusions:

• SHCBP1 promotes cisplatin resistance, migration, and invasion in lung cancer by activating the Wnt pathway.
• SHCBP1 represents a potential therapeutic target for overcoming treatment resistance in lung cancer.