Related Experiment Video

Updated: Sep 13, 2026

Application of Retinoic Acid to Obtain Osteocytes Cultures from Primary Mouse Osteoblasts
07:13

Application of Retinoic Acid to Obtain Osteocytes Cultures from Primary Mouse Osteoblasts

Published on: May 13, 2014

Retinoic acid inhibits phospholipid turnover and protein kinase C activity in RA-sensitive but not in RA-resistant

M C Vanier1, D Banerjee, B B Mukherjee

  • 1Department of Biology, McGill University, Montreal, Quebec, Canada.

FEBS Letters
|December 5, 1988
PubMed

Insights

Retinoic acid (RA) halts anchorage-independent growth in src-transformed cells by altering phospholipid metabolism and protein kinase C (PKC) activity. Ras-transformed cells show different responses, indicating distinct signaling pathways.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biochemistry

Background:

  • Anchorage-independent growth is a hallmark of cancer cells.
  • Retinoic acid (RA) is known to affect cell growth and differentiation.
  • Differential responses to RA in cancer cells suggest underlying variations in signaling pathways.

Purpose of the Study:

  • To investigate the differential effects of retinoic acid (RA) on src-transformed (RR1022) and ras-transformed (KNRK) cells.
  • To elucidate the mechanisms behind the varying responses, focusing on phospholipid turnover and protein kinase C (PKC) activity.
  • To understand how altered signal transduction pathways mediate the effects of RA on anchorage-independent growth.

Main Methods:

  • Treatment of RR1022 and KNRK cells with 10(-5) M retinoic acid (RA).
  • Analysis of 32P incorporation into phosphatidylinositol (PI), phosphatidic acid (PA), and phosphatidylcholine (PC) to assess phospholipid turnover.
  • Measurement of protein kinase C (PKC) activity in treated and untreated cells.

Main Results:

  • RA treatment caused loss of anchorage-independent growth in RR1022 cells but not KNRK cells.
  • In RR1022 cells, RA drastically inhibited PI and PA labeling, increased PC labeling, and significantly reduced PKC activity.
  • In KNRK cells, RA had minimal effects on PI, PA, and PC labeling, with only a small decrease in PKC activity.

Conclusions:

  • The differential effects of RA on anchorage-independent growth are linked to distinct alterations in phospholipid metabolism and PKC activity between src-transformed and ras-transformed cells.
  • These changes in phospholipid turnover and PKC activity are part of an altered signal transduction pathway that mediates RA's effects.
  • Understanding these specific pathways could offer insights into targeted cancer therapies.

More Related Videos

Identification of Mediators of T-cell Receptor Signaling via the Screening of Chemical Inhibitor Libraries08:49

Identification of Mediators of T-cell Receptor Signaling via the Screening of Chemical Inhibitor Libraries

Published on: January 22, 2019

Robust Differentiation of Human iPSCs into a Pure Population of Adipocytes to Study Adipocyte-Associated Disorders10:31

Robust Differentiation of Human iPSCs into a Pure Population of Adipocytes to Study Adipocyte-Associated Disorders

Published on: February 9, 2022

Related Concept Videos

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.
Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
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,...
Receptor Tyrosine Kinases01:26

Receptor Tyrosine Kinases

Receptor tyrosine kinases or RTKs are membrane-bound receptors that phosphorylate specific tyrosine on protein substrates. RTKs regulate cellular growth, differentiation, survival, and migration. They contain an extracellular ligand binding domain, a transmembrane domain, and a cytosolic tail with intrinsic kinase activity. Several extracellular signaling molecules activate RTKs in one or more ways and relay the signal downstream. Ligands such as platelet-derived growth factor (PDGF) or...
The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
Inhibition of CDK Activity02:34

Inhibition of CDK Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...