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  11. Targeting Lif-mediated Paracrine Interaction For Pancreatic Cancer Therapy And Monitoring

Targeting LIF-mediated paracrine interaction for pancreatic cancer therapy and monitoring

Yu Shi1, Weina Gao2,3, Nikki K Lytle4,5

  • 1Molecular and Cell Biology Laboratory, Salk Institute for Biological Studies, La Jolla, CA, USA. yshi@salk.edu.

Nature
|April 19, 2019

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View abstract on PubMed

Summary
This summary is machine-generated.

Leukaemia inhibitory factor (LIF) from pancreatic stellate cells drives pancreatic cancer progression and drug resistance. Blocking LIF or its receptor shows therapeutic potential and identifies LIF as a circulating biomarker for pancreatic ductal adenocarcinoma (PDAC).

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Area of Science:

  • Oncology
  • Cancer Biology
  • Tumor Microenvironment

Background:

  • Pancreatic ductal adenocarcinoma (PDAC) exhibits poor prognosis due to late diagnosis and drug resistance.
  • Activated pancreatic stellate cells (PSCs) create a dense stroma, promoting PDAC progression and resistance through cell-cell communication.
  • The interplay between PSCs and pancreatic cancer cells (PCCs) forms a vicious cycle, exacerbating tumorigenesis and treatment failure.

Purpose of the Study:

  • To investigate the paracrine communication between PSCs and PCCs as a therapeutic and diagnostic target in PDAC.
  • To identify key mediators and molecular mechanisms driving this crosstalk.
  • To evaluate the therapeutic potential of targeting this communication pathway.

Main Methods:

  • Systematic proteomic investigation of secreted factors between PSCs and PCCs.
  • Pharmacologic blockade of leukaemia inhibitory factor (LIF) and genetic deletion of its receptor (LIFR).
  • Assessment of tumour progression, chemotherapy efficacy, cancer cell differentiation, and epithelial-mesenchymal transition (EMT) in PDAC mouse models.
  • Analysis of LIF production in mouse models and human PDAC tissues, and correlation of circulating LIF levels with therapeutic response.

Main Results:

  • Leukaemia inhibitory factor (LIF) was identified as a key paracrine factor secreted by activated PSCs that acts on PCCs.
  • Pharmacologic LIF blockade and Lifr deletion significantly slowed tumour progression and enhanced chemotherapy efficacy in PDAC mouse models.
  • Targeting LIF modulated cancer cell differentiation and EMT status, prolonging survival.
  • Aberrant LIF production in the pancreas correlated with PDAC pathogenesis, and circulating LIF levels reflected treatment response.

Conclusions:

  • LIF plays a critical role in PDAC tumorigenesis and progression by mediating communication between PSCs and PCCs.
  • Targeting LIF presents a promising therapeutic strategy to overcome drug resistance and improve treatment outcomes in PDAC.
  • Circulating LIF levels serve as a potential biomarker for PDAC diagnosis and monitoring therapeutic response.