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Sparstolonin B inhibits pancreatic adenocarcinoma through the NF-κB signaling pathway

Yang Lyu1, Bowen Duan1, Ziming Liu1

  • 1Department of Gastroenterology, Shengjing Hospital of China Medical University, NO.36, Sanhao Street, Shenyang, Liaoning Province, 110004, PR China.

Experimental Cell Research
|May 20, 2022
PubMed

Insights

Sparstolonin B effectively inhibits pancreatic cancer cell growth and induces apoptosis. This natural compound targets the NF-κB pathway, showing potential as a novel therapeutic agent for pancreatic adenocarcinoma.

Area of Science:

  • Oncology
  • Pharmacology
  • Molecular Biology

Background:

  • Pancreatic adenocarcinoma is a lethal gastrointestinal malignancy with limited treatment options.
  • Sparstolonin B, an isocoumarin, exhibits promising anticancer properties.
  • Understanding Sparstolonin B's mechanism in pancreatic cancer is crucial for therapeutic development.

Purpose of the Study:

  • To investigate the antitumor effects of Sparstolonin B on pancreatic cancer cells.
  • To elucidate the molecular mechanisms underlying Sparstolonin B's action, focusing on the NF-κB pathway.
  • To evaluate Sparstolonin B's efficacy in a preclinical pancreatic cancer model.

Main Methods:

  • Network pharmacology was used to predict target genes and pathways.
  • In vitro assays (CCK-8, colony formation, Transwell) assessed cell viability, proliferation, migration, and invasion.
  • Flow cytometry analyzed cell cycle arrest and apoptosis.
  • Western blotting examined protein expression levels (Bax, Bcl-2, MMP2, IκBα, p65).
  • In vivo studies evaluated tumor growth in a xenograft model.

Main Results:

  • Sparstolonin B significantly reduced pancreatic cancer cell viability, proliferation, migration, and invasion.
  • It induced cell cycle arrest and apoptosis in cancer cells.
  • Sparstolonin B modulated apoptosis-related proteins (upregulated Bax, downregulated Bcl-2) and matrix metalloproteinases (downregulated MMP2).
  • The compound affected the NF-κB pathway by downregulating IκBα and upregulating p65 and IκBα phosphorylation, without altering total p65 levels.
  • NF-κB pathway inhibition reversed these effects.
  • In vivo, Sparstolonin B treatment suppressed tumor growth and reduced Ki-67 positive cells.

Conclusions:

  • Sparstolonin B exhibits significant antitumor activity against pancreatic cancer.
  • Its mechanism involves the induction of apoptosis and inhibition of proliferation, migration, and invasion via the NF-κB signaling pathway.
  • Sparstolonin B represents a potential novel therapeutic candidate for pancreatic adenocarcinoma treatment.
Keywords:
ApoptosisNuclear factor (NF)-Kappa BPancreatic adenocarcinomaSparstolonin B

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