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Mebendazole Impedes the Proliferation and Migration of Pancreatic Cancer Cells through SK1 Inhibition Dependent

Khem Raj Limbu1, Rashmi Bhandari Chhetri1, Yoon Sin Oh2

  • 1College of Pharmacy, Mokpo National University, Mokpo 58554, Republic of Korea.

Molecules (Basel, Switzerland)
|December 11, 2022
PubMed

Insights

The study found that mebendazole (MBZ) inhibits cancer cell growth and migration in pancreatic cancer by targeting sphingosine kinase activity and lowering S1P production. This suggests MBZ as a potential therapeutic agent for pancreatic ductal adenocarcinoma (PDAC).

Area of Science:

  • Oncology
  • Biochemistry
  • Pharmacology

Background:

  • Pancreatic ductal adenocarcinoma (PDAC) has high mortality rates, with chemotherapy resistance limiting treatment efficacy.
  • Sphingosine 1-phosphate (S1P), produced by sphingosine kinase (SK), is crucial in cancer progression, metastasis, and drug resistance.
  • Targeting S1P production offers a potential strategy to overcome treatment resistance in PDAC.

Purpose of the Study:

  • To investigate if mebendazole (MBZ), an anthelmintic, can inhibit SK activity and reduce S1P production.
  • To determine MBZ's effects on PDAC cell proliferation, invasion, metastasis, and drug resistance.
  • To elucidate the molecular pathways involved in MBZ's anti-cancer effects.

Main Methods:

  • MBZ was tested for its ability to inhibit SK1 and SK2 activity and regulate sphingolipid levels.
  • PDAC cell lines were treated with MBZ to assess effects on proliferation and migration.
  • Experiments involving S1P treatment were conducted to confirm S1P-mediated effects of MBZ.
  • Key signaling pathways, including JAK2/STAT3/Bcl-2 and S1P/FAK/vimentin, were analyzed.

Main Results:

  • MBZ selectively inhibited SK1 over SK2, altering sphingolipid profiles.
  • MBZ demonstrated significant inhibition of PDAC cell proliferation and migration.
  • MBZ counteracted S1P-induced cancer cell growth and regulated the JAK2/STAT3/Bcl-2 pathway.
  • MBZ inhibited FAK phosphorylation, indicating regulation of migration via the S1P/FAK/vimentin pathway.

Conclusions:

  • The anthelmintic mebendazole (MBZ) shows potential as a therapeutic agent for pancreatic ductal adenocarcinoma (PDAC).
  • MBZ exerts anti-cancer effects by inhibiting sphingosine kinase (SK) activity, reducing S1P production, and modulating key signaling pathways.
  • Further studies on MBZ analogs are warranted for structural synthesis and enhanced therapeutic applications in PDAC treatment.
Keywords:
mebendazolepancreatic ductal adenocarcinomasphingosine 1-phosphatesphingosine kinase

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