Related Experiment Video

Updated: Jul 17, 2026

Utilizing 18F-FDG PET/CT Imaging and Quantitative Histology to Measure Dynamic Changes in the Glucose Metabolism in Mouse Models of Lung Cancer
06:51

Utilizing 18F-FDG PET/CT Imaging and Quantitative Histology to Measure Dynamic Changes in the Glucose Metabolism in Mouse Models of Lung Cancer

Published on: July 21, 2018

Insulin-like growth factor binding protein-related protein 1 (IGFBP-rP1) has potential tumour-suppressive activity in

Y Chen1, M Pacyna-Gengelbach, F Ye

  • 1Institute of Pathology, University Hospital Charité, Schumannstr 20-21, D-10098 Berlin, Germany.

The Journal of Pathology
|January 20, 2007
PubMed

Insights

Insulin-like growth factor binding protein-related protein 1 (IGFBP-rP1) is downregulated in lung cancer. Its low expression correlates with aggressive tumors and is linked to DNA methylation, suggesting IGFBP-rP1 acts as a tumor suppressor.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • The role of insulin-like growth factor binding protein-related protein 1 (IGFBP-rP1) in lung cancer is not well understood.
  • Previous studies indicate reduced IGFBP-rP1 expression in various tumors.

Purpose of the Study:

  • To investigate the expression and function of IGFBP-rP1 in human lung cancer.
  • To determine if IGFBP-rP1 acts as a tumor suppressor and if its inactivation is linked to DNA methylation.

Main Methods:

  • Immunohistochemistry on lung cancer tissues and cell lines.
  • Treatment with 5-aza-2'-deoxycytidine to assess gene expression restoration.
  • DNA methylation analysis using bisulfite sequencing.
  • Stable transfection of IGFBP-rP1 in a lung cancer cell line.
  • Assessment of tumor growth, apoptosis, and caspase-3 activation in vivo and in vitro.

Main Results:

  • Reduced IGFBP-rP1 expression was observed in 42% of primary lung tumors compared to normal lung tissues.
  • Low IGFBP-rP1 expression significantly correlated with high-grade squamous cell lung cancer.
  • DNA methylation was identified as a mechanism for IGFBP-rP1 silencing.
  • Restoration of IGFBP-rP1 suppressed colony formation, tumor growth, and induced apoptosis in lung cancer cells.

Conclusions:

  • IGFBP-rP1 functions as a tumor suppressor in human lung cancer.
  • Inactivation of IGFBP-rP1 by DNA methylation is a key event in lung tumorigenesis.

Related Concept Videos

PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a rapamycin-insensitive companion...
The Retinoblastoma Gene01:20

The Retinoblastoma Gene

Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
The first-ever tumor suppressor gene called Rb was identified in retinoblastoma - a rare eye tumor in children. In inherited forms of the disease, a child inherits one defective copy of the Rb gene, which predisposes them to retinoblastoma. However,...
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...
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...
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.
Regulation of Angiogenesis and Blood Supply01:24

Regulation of Angiogenesis and Blood Supply

Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl hydroxylase and factor...