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Effect of PLK1 inhibition on cisplatin-resistant gastric cancer cells

Zihao Chen1,2, Yanling Chai3, Ting Zhao1

  • 1Graduate School of Hebei Medical University, Shijiazhuang, China.

Journal of Cellular Physiology
|November 30, 2018
PubMed
Abstract

Insights

Polo-like kinase 1 (PLK1) overexpression drives cisplatin resistance in gastric cancer (GC). Inhibiting PLK1 restores sensitivity to chemotherapy, offering a potential new treatment strategy for GC patients.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Gastric cancer (GC) exhibits resistance to cisplatin (DDP) chemotherapy.
  • Polo-like kinase 1 (PLK1) is implicated in cancer cell proliferation and survival.

Purpose of the Study:

  • To investigate the role of PLK1 in DDP-resistant GC cells.
  • To evaluate the therapeutic potential of PLK1 inhibition in overcoming DDP resistance.

Main Methods:

  • Quantitative reverse-transcription polymerase chain reaction (qRT-PCR) and western blot were used to measure PLK1 expression.
  • Cell viability, proliferation, cell cycle, and apoptosis were assessed using MTT assays, EdU staining, and flow cytometry.
  • Autophagosome formation was tracked using a GFP-LC3 vector.

Main Results:

  • DDP-resistant GC cells (SGC-7901/DDP) showed increased autophagy and PLK1 expression.
  • PLK1 inhibition (using BI2536 or si-PLK1) resensitized cells to DDP, suppressed proliferation and autophagy, and enhanced apoptosis.
  • PLK1 inhibition downregulated cell division regulators CDC25C and cyclin B1.

Conclusions:

  • Aberrant PLK1 overexpression contributes to DDP resistance in GC.
  • Targeting PLK1 can restore chemosensitivity in DDP-resistant GC cells, highlighting its potential as a therapeutic target in GC chemotherapy.
Keywords:
BI2536PLK1autophagycisplatingastric cancer

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