Long non-coding RNA CASC2 enhances cisplatin sensitivity in oral squamous cell cancer cells by the miR-31-5p/KANK1...

Area of Science:

• Oncology
• Molecular Biology
• Genetics

Background:

• Oral squamous cell cancer (OSCC) is a prevalent head and neck malignancy.
• Chemotherapeutic resistance, particularly to cisplatin (DDP), poses a significant clinical challenge in OSCC treatment.
• Long non-coding RNAs (lncRNAs) are increasingly recognized for their roles in cancer progression and drug resistance.

Purpose of the Study:

• To investigate the role and underlying mechanism of lncRNA CASC2 in conferring DDP resistance in OSCC.
• To elucidate the molecular interactions between CASC2, miR-31-5p, and KANK1 in DDP-resistant OSCC cells.
• To evaluate the therapeutic potential of CASC2 in overcoming DDP resistance in OSCC.

Main Methods:

• Quantitative real-time PCR (qRT-PCR) to assess expression levels of CASC2, miR-31-5p, and KANK1.
• Cell Counting Kit-8 (CCK-8) and flow cytometry to determine DDP sensitivity and apoptosis.
• Dual-luciferase reporter and RNA immunoprecipitation (RIP) assays to validate molecular interactions.
• In vivo xenograft experiments to confirm the role of CASC2 in DDP resistance.

Main Results:

• CASC2 and KANK1 expression were significantly downregulated, while miR-31-5p was upregulated in DDP-resistant OSCC tissues and cells.
• Overexpression of CASC2 enhanced DDP sensitivity and promoted apoptosis in DDP-resistant OSCC cells.
• CASC2 functions as a molecular sponge for miR-31-5p, thereby upregulating KANK1 expression and restoring DDP sensitivity.

Conclusions:

• CASC2 plays a critical role in overcoming DDP resistance in OSCC by upregulating KANK1 through sponging miR-31-5p.
• The CASC2/miR-31-5p/KANK1 axis represents a promising therapeutic strategy for DDP-resistant OSCC.
• CASC2 holds potential as a novel therapeutic target for improving treatment outcomes in DDP-resistant OSCC patients.