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CpG Oligodeoxynucleotides Induces Apoptosis of Human Bladder Cancer Cells via Caspase-3-Bax/Bcl-2-p53 Axis

Yang Luo1, Xiaoyi Fu1, Ruizhen Ru1

  • 1School of Biosciences and Biopharmaceutics, Guangdong Pharmaceutical University, Guangzhou, China.

Archives of Medical Research
|March 7, 2020
PubMed
Abstract

Insights

Unmethylated cytosine-phosphorothioate-guanine (CpG) oligodeoxynucleotides (ODNs) show anti-cancer effects on human bladder cancer cells by decreasing viability and increasing apoptosis. CpG ODNs also promote normal urothelial cell proliferation, suggesting potential therapeutic applications.

Area of Science:

  • Immunology
  • Oncology
  • Molecular Biology

Background:

  • Bladder cancer remains a significant health concern.
  • Oligodeoxynucleotides (ODNs) containing unmethylated cytosine-phosphorothioate-guanine (CpG) motifs are known to activate immune responses.
  • The specific anti-cancer effects of CpG ODNs on human bladder cancer cells require further elucidation.

Purpose of the Study:

  • To investigate the anti-cancer effects of CpG ODNs on human bladder cancer cell lines.
  • To evaluate the impact of CpG ODNs on cell viability, apoptosis, and cell cycle progression.
  • To analyze the expression of key apoptosis-related proteins.

Main Methods:

  • Human bladder cancer cell lines (UM-UC-3, T24) and normal urothelial cells (SV-HUC-1) were treated with CpG ODNs.
  • Cell Counting Kit-8 (CCK-8) assay was used to assess cell viability.
  • Flow cytometry was employed to determine apoptosis rates and cell cycle distribution.
  • Western blot analysis was performed to detect the expression of caspase-3, p53, Bax, and Bcl-2.

Main Results:

  • CpG ODN treatment significantly decreased the viability of human bladder cancer cells (UM-UC-3, T24) in a time-dependent manner.
  • CpG ODNs increased the apoptosis rate and induced G0G1 phase arrest in UM-UC-3 cells.
  • The expression of pro-apoptotic factors (caspase-3, p53, Bax) was upregulated, while the anti-apoptotic factor (Bcl-2) was downregulated in UM-UC-3 cells upon CpG ODN treatment.
  • CpG ODNs promoted the proliferation of normal urothelial cells (SV-HUC-1).

Conclusions:

  • CpG ODNs exhibit a dual effect, inhibiting bladder cancer cell viability while promoting normal urothelial cell proliferation.
  • CpG ODNs induce apoptosis in human bladder cancer cells through a cascade involving caspase-3, p53, and Bax, and downregulating Bcl-2.
  • CpG ODNs affect cell cycle distribution, leading to G0G1 phase arrest in bladder cancer cells.
  • CpG ODNs represent a potential therapeutic candidate for human bladder cancer.
Keywords:
BaxBcl-2Caspase-3CpG ODNHuman bladder cancerp53

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