Related Experiment Video

Updated: May 13, 2026

Quantitative Immunofluorescence Assay to Measure the Variation in Protein Levels at Centrosomes
09:39

Quantitative Immunofluorescence Assay to Measure the Variation in Protein Levels at Centrosomes

Published on: December 20, 2014

LGALS3BP regulates centriole biogenesis and centrosome hypertrophy in cancer cells

Marie-Laure Fogeron1, Hannah Müller, Sophia Schade

  • 1Department of Vertebrate Genomics, Max-Planck Institute for Molecular Genetics, 14195 Berlin, Germany.

Nature Communications
|February 28, 2013
PubMed

Insights

LGALS3BP protein dysregulation causes abnormal centrosome numbers and morphology in cancer cells. Its overexpression leads to enlarged centrosomes, while its depletion results in extra centriolar structures.

Area of Science:

  • Cell Biology
  • Cancer Research
  • Molecular Biology

Background:

  • Centrosome number and morphology are often altered in cancer cells, contributing to genomic instability.
  • Identifying key regulators of centrosome abnormalities is crucial for understanding cancer development.

Purpose of the Study:

  • To identify proteins functionally relevant to centrosome abnormalities in cancer.
  • To investigate the role of LGALS3BP in regulating centrosome structure and number.

Main Methods:

  • Construction of a protein-interaction network centered on centrosomal and cell-cycle proteins.
  • Analysis of protein deregulation in cancer.
  • Functional studies involving LGALS3BP overexpression and depletion in cancer cell lines and analysis of seminoma tissues.

Main Results:

  • LGALS3BP, a centriole- and basal body-associated protein, was identified as a key player.
  • Overexpression of LGALS3BP in SK-BR-3 cells caused centrosome hypertrophy.
  • Downregulation of LGALS3BP in seminoma tissues correlated with supernumerary centriole-like structures.
  • Depletion of LGALS3BP reversed centrosome hypertrophy, confirming its direct role.

Conclusions:

  • LGALS3BP plays a dual role in centrosome regulation: promoting hypertrophy when overexpressed and causing centriolar substructure accumulation when downregulated.
  • LGALS3BP appears to suppress the assembly of centriolar substructures; its depletion leads to the accumulation of complexes involving CPAP, acetylated tubulin, and centrin.

More Related Videos

Live Cell Imaging to Assess the Dynamics of Metaphase Timing and Cell Fate Following Mitotic Spindle Perturbations07:14

Live Cell Imaging to Assess the Dynamics of Metaphase Timing and Cell Fate Following Mitotic Spindle Perturbations

Published on: September 20, 2019

Exploring the Regulation of Lipid Droplet Catabolism through Lipophagy07:20

Exploring the Regulation of Lipid Droplet Catabolism through Lipophagy

Published on: January 31, 2025

Related Concept Videos

Centrosome Duplication02:25

Centrosome Duplication

The primary microtubule organizing center (MTOC) in animal cells is the centrosome. A centrosome has two cylindrical centrioles at its core. Each centriole consists of nine sets of three microtubules held together by proteins. The centrioles are positioned at right angles to each other and surrounded by a shapeless protein cloud called the pericentriolar matrix, or pericentriolar material (PCM).
To ensure that each daughter cell receives a centrosome after cell division, centrosome duplication...
Centrosome Duplication02:25

Centrosome Duplication

The primary microtubule organizing center (MTOC) in animal cells is the centrosome. A centrosome has two cylindrical centrioles at its core. Each centriole consists of nine sets of three microtubules held together by proteins. The centrioles are positioned at right angles to each other and surrounded by a shapeless protein cloud called the pericentriolar matrix, or pericentriolar material (PCM).
To ensure that each daughter cell receives a centrosome after cell division, centrosome duplication...
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...
Negative Regulator Molecules01:23

Negative Regulator Molecules

Positive regulators allow a cell to advance through cell cycle checkpoints. Negative regulators have an equally important role as they terminate a cell’s progression through the cell cycle—or pause it—until the cell meets specific criteria.
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...