Related Experiment Video

Updated: Apr 11, 2026

Glycan Node Analysis: A Bottom-up Approach to Glycomics
11:36

Glycan Node Analysis: A Bottom-up Approach to Glycomics

Published on: May 22, 2016

11.3K

COSMC knockdown mediated aberrant O-glycosylation promotes oncogenic properties in pancreatic cancer

Bianca T Hofmann1,2, Laura Schlüter3, Philip Lange4

  • 1Department of General, Visceral and Thoracic Surgery, University Medical Center Hamburg-Eppendorf, Martinistrasse 52, 20246, Hamburg, Germany. bi.hofmann@uke.de.

Molecular Cancer
|May 30, 2015
PubMed
Abstract

Insights

Altering O-linked glycosylation by inhibiting COSMC promotes pancreatic cancer cell migration and reduces apoptosis. O-GalNAc modified Nucleolin is a new prognostic marker for PDAC patients.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Oncology

Background:

  • Pancreatic ductal adenocarcinoma (PDAC) is a lethal malignancy with limited treatment options.
  • Aberrant O-linked N-acetylgalactosamine (GalNAc) glycosylation, specifically Tn antigen expression, is common in PDAC.
  • The role of Tn antigen in PDAC progression is not fully understood.

Purpose of the Study:

  • To investigate the impact of COSMC-mediated Tn antigen expression on PDAC cell oncogenic properties.
  • To identify novel O-GalNAc modified proteins in PDAC cells.
  • To evaluate the prognostic significance of Tn antigen and Nucleolin co-expression in PDAC patients.

Main Methods:

  • Lentiviral-mediated knockdown of COSMC to induce Tn antigen expression in PDAC cell lines (Panc-1, L3.6pl).
  • Analysis of O-GalNAc glycosylation using Western blot, Far-Western blot, and immunocytochemistry.
  • Assessment of cell viability, migration, and apoptosis.
  • Mass spectrometry to identify O-GalNAc modified proteins.
  • Immunohistochemical evaluation of Tn antigen and Nucleolin in patient samples.

Main Results:

  • COSMC knockdown led to Tn antigen expression and altered O-glycosylation.
  • PDAC cell proliferation decreased, while migration increased and apoptosis decreased.
  • Nucleolin was identified as an O-GalNAc modified protein.
  • Co-expression of Tn antigen and Nucleolin correlated with poor patient survival.

Conclusions:

  • Altered O-glycan expression, including Tn/STn antigens, influences PDAC's oncogenic properties.
  • O-GalNAc modified Nucleolin serves as a novel prognostic marker for pancreatic cancer.

More Related Videos

Syngeneic Mouse Orthotopic Allografts to Model Pancreatic Cancer06:20

Syngeneic Mouse Orthotopic Allografts to Model Pancreatic Cancer

Published on: October 4, 2022

4.3K
Mimicking and Manipulating Pancreatic Acinar-to-Ductal Metaplasia in 3-dimensional Cell Culture08:16

Mimicking and Manipulating Pancreatic Acinar-to-Ductal Metaplasia in 3-dimensional Cell Culture

Published on: February 11, 2019

9.5K

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...
5.1K
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

1.7K
Induced Pluripotent Stem Cells01:06

Induced Pluripotent Stem Cells

Stem cells are undifferentiated cells that divide and produce different cell types. Ordinarily, cells that have differentiated into a specific cell type are terminally differentiated; however, scientists have found a way to reprogram these mature cells so that they dedifferentiate and return to an unspecialized, proliferative state. These cells are pluripotent like embryonic stem cells—able to produce all cell types—and are called induced pluripotent stem cells (iPSCs).
Somatic...
6.3K
Cancer-Critical Genes I: Proto-oncogenes01:33

Cancer-Critical Genes I: Proto-oncogenes

Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
12.1K
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...
5.4K
Adaptive Mechanisms in Cancer Cells02:53

Adaptive Mechanisms in Cancer Cells

Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
7.5K