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Characterization of MLKL-mediated Plasma Membrane Rupture in Necroptosis
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Salecan Suppresses Pancreatic Cancer Progression by Promoting Necroptosis via the RIPK1/MLKL Pathway

Wenya Du1, Rong Xu1, Pengfei Chen1

  • 1School of Food and Bioengineering, Food Microbiology Key Laboratory of Sichuan Province, Chongqing Key Laboratory of Specialty Food Co-Built by Sichuan and Chongqing, Xihua University, Chengdu 610039, China.

Nutrients
|October 16, 2025
PubMed

Insights

Salecan, a natural beta-glucan, inhibits pancreatic cancer growth and metastasis without harming normal cells. It triggers programmed necrosis (necroptosis) via the RIPK1/MLKL pathway, offering a potential new strategy for pancreatic cancer treatment.

Area of Science:

  • Oncology
  • Pharmacology
  • Natural Products

Background:

  • Pancreatic ductal adenocarcinoma (PDAC) presents significant treatment challenges due to drug resistance and severe side effects of current therapies.
  • There is an urgent need for novel strategies for PDAC prevention and treatment.
  • Salecan, a naturally occurring polysaccharide, is explored for its therapeutic potential.

Purpose of the Study:

  • To evaluate the antitumor activities of Salecan against human pancreatic cancer cells.
  • To elucidate the mechanism by which Salecan inhibits pancreatic cancer progression.
  • To assess Salecan's potential as a functional food component for PDAC management.

Main Methods:

  • In vitro assessment of Salecan on pancreatic cancer cell lines, including viability, colony formation, migration, and invasion assays.
  • Flow cytometry, caspase-3 activity assays, qRT-PCR, and Western blotting were employed.
  • RNA sequencing (RNA-seq) was utilized to uncover the underlying molecular mechanisms.

Main Results:

  • Salecan significantly inhibited pancreatic cancer cell proliferation and migration while showing no toxicity to normal cells.
  • Salecan impeded cancer cell migration and invasion by affecting the epithelial-to-mesenchymal transition (EMT) pathway.
  • Mechanistically, Salecan induced necroptosis (programmed necrosis) rather than apoptosis, mediated by the RIPK1/MLKL signaling pathway.

Conclusions:

  • Salecan demonstrates efficacy in inhibiting pancreatic cancer cell proliferation, migration, and invasion in vitro.
  • Salecan accelerates cancer cell death through necroptosis induction via the MLKL/RIPK1 pathway.
  • These findings suggest Salecan holds promise as a functional food component for PDAC prevention and therapy.
Keywords:
RNA-seqSalecannecroptosispancreatic cancer

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