Effect of all-trans retinoic acid (ATRA) on syndecan-1 expression and its chemoprotective effect in benzo(α)pyrene-induced lung cancer mice model.

Abstract

All-trans retinoic acid (ATRA), an active metabolite of retinal, has been shown to exert anti-cancer activities in a number of cancer cells and tissues. Syndecan-1 is a proteoglycan, mediate cell-cell adhesion and prevent invasion in epithelial cells. The aim of the present study was to examine the level of syndecan-1 expression and the chemopreventive effect of ATRA during lung cancer development in BALB/c mice. Syndecan-1 expression was examined by immunohistochemistry using mouse monoclonal anti-human syndecan-1 antibody. In this study, benzo(α)pyrene [B(α)P] was used to induce lung cancer. The results indicated that ATRA has anti-cancer effect against B(α)P-induced lung tumor development as induced by number of tumor nodules and histopathologic report. The loss of syndecan-1 expression in the epithelial cell membrane is associated with tumor cell growth and invasiveness. Our study for syndecan-1 indicated a chemoprotective effect of ATRA against changes in lung epithelial cell membrane syndecan-1 expression in B(α)P-induced lung cancer model. Therefore ATRA could serve as effective chemotherapeutic agent against cancer invasion/metastasis, at least in the lungs.

• Authors: D Ramya, Siddikuzzaman, V M Berlin Grace
• Journal: Immunopharmacology and immunotoxicology (Immunopharmacol Immunotoxicol) Vol. 34 Issue 6 Pg. 1020-7 (Dec 2012) ISSN: 1532-2513 [Electronic] England
• PMID: 22686587 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Antibodies, Monoclonal, Murine-Derived
• Antineoplastic Agents
• Neoplasm Proteins
• SDC1 protein, human
• Sdc1 protein, mouse
• Syndecan-1
• Benzo(a)pyrene
• Tretinoin

Topics

• Animals
• Antibodies, Monoclonal, Murine-Derived (chemistry)
• Antineoplastic Agents (pharmacology)
• Benzo(a)pyrene (toxicity)
• Cell Membrane (metabolism, pathology)
• Epithelial Cells (metabolism, pathology)
• Gene Expression Regulation, Neoplastic (drug effects)
• Humans
• Immunohistochemistry
• Lung Neoplasms (chemically induced, metabolism, pathology, prevention & control)
• Mice
• Mice, Inbred BALB C
• Neoplasm Invasiveness
• Neoplasm Proteins (biosynthesis)
• Neoplasms, Experimental (metabolism, pathology, prevention & control)
• Respiratory Mucosa (metabolism, pathology)
• Syndecan-1 (biosynthesis)
• Tretinoin (pharmacology)