Related Experiment Video

Updated: Jun 1, 2026

Evaluating Autophagy Levels in Two Different Pancreatic Cell Models Using LC3 Immunofluorescence
08:07

Evaluating Autophagy Levels in Two Different Pancreatic Cell Models Using LC3 Immunofluorescence

Published on: April 28, 2023

Omeprazole inhibits proliferation and modulates autophagy in pancreatic cancer cells

Andrej Udelnow1, Andreas Kreyes, Stefan Ellinger

  • 1Department of General, Visceral and Transplantation Surgery, University Hospital of Ulm, Ulm, Germany.

Plos One
|June 2, 2011
PubMed
Abstract

Insights

Omeprazole inhibits pancreatic cancer cell growth by modulating autophagy and lysosomal pathways, potentially overcoming chemoresistance. This proton pump inhibitor shows promise for new clinical applications in cancer therapy.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Pancreatic tumors exhibit significant chemoresistance, necessitating novel therapeutic strategies.
  • Omeprazole's role in tumor chemoresistance is debated, requiring further investigation into its mechanisms.

Purpose of the Study:

  • To investigate the pharmacodynamic, morphological, and biochemical effects of omeprazole on pancreatic cancer cell lines.
  • To elucidate the molecular mechanisms by which omeprazole may modulate pancreatic cancer chemoresistance.

Main Methods:

  • Dose-effect analyses of omeprazole and chemotherapeutics (gemcitabine, 5-fluorouracil) on pancreatic cancer cell lines.
  • Electron microscopy, proton NMR spectroscopy, Western blot analysis, and acridine orange staining to assess cellular effects and pathway modulation.
  • Gene expression analysis of autophagy-related and drug resistance markers.

Main Results:

  • Omeprazole inhibited pancreatic cancer cell proliferation at non-toxic concentrations and reversed 5-fluorouracil resistance.
  • Omeprazole induced autophagosome accumulation and programmed cell death, modulating lysosomal transport and autophagy pathways.
  • Intracellular omeprazole was identified, and its interaction with v-ATPase regulatory functions, without inhibiting pump activity, was suggested.

Conclusions:

  • Omeprazole modulates pancreatic cancer cell autophagy and lysosomal transport, leading to programmed cell death.
  • This mechanism may circumvent common pancreatic cancer resistance pathways.
  • Findings suggest potential new clinical applications for omeprazole in pancreatic cancer treatment.

More Related Videos

Cell-Based Drug Screening for Inhibitors of Autophagy Related 4B Cysteine Peptidase09:51

Cell-Based Drug Screening for Inhibitors of Autophagy Related 4B Cysteine Peptidase

Published on: June 30, 2023

Related Concept Videos

mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
Autophagic Cell Death01:18

Autophagic Cell Death

Christian de Duve discovered “autophagy,” a process in which cellular components are engulfed by membrane-bound organelles called autophagosomes. The autophagosomes then fuse with lysosomes to digest the enclosed contents. Autophagy is generally activated in cells to prevent cell death. However, cell death is triggered when the damage is beyond repair.
Autophagy and Apoptosis
Autophagy can activate apoptosis. In normal conditions, the autophagy activating protein Beclin-1 and pro-apoptotic...
Autophagy01:27

Autophagy

Autophagy is a self-digesting process by which a cell protects itself from threats both within and outside the cell, ranging from abnormal proteins to invading bacteria. In this process, obsolete components of the cell and invading microbes are degraded by hydrolytic enzymes active in an acidic environment of the lysosomal lumen.
An autophagic pathway consists of a series of signaling events activated in response to diverse stress and physiological conditions such as food deprivation,...
Peptic Ulcer Disease IV: Management01:26

Peptic Ulcer Disease IV: Management

Medical treatment strategies for peptic ulcers encompass various methods. The primary goal of treatment is to diminish gastric acidity and strengthen mucosal defense mechanisms.
The therapeutic approach involves ensuring adequate rest, implementing drug therapy, promoting smoking cessation, making dietary modifications, and emphasizing long-term follow-up care.
Pharmacological management
The prevailing therapy for peptic ulcers involves a combination of managing the patient's current medication...
Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...