Open AccessComparative analysis of ATP‐binding cassette (ABC) transporter gene expression levels in peripheral blood leukocytes and in liver with hepatocellular carcinoma
Author(s) -
Moustafa Mohsen A.,
Ogino Daisuke,
Nishimura Masuhiro,
Ueda Nobuhiko,
Naito Shinsaku,
Furukawa Motonobu,
Uchida Takafumi,
Ikai Iwao,
Sawada Hideki,
Fukumoto Manabu
Publication year - 2004
Publication title -
cancer science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 1347-9032
DOI - 10.1111/j.1349-7006.2004.tb03244.x
Subject(s) - hepatocellular carcinoma , atp binding cassette transporter , peripheral blood , transporter , gene expression , gene , medicine , biology , cancer research , biochemistry
ATP‐binding cassette (ABC) transporters comprise a superfamily of similar proteins involved in transmembrane transport of various substances. ABC transporter family members in the liver participate in bile formation and lipid metabolism. In order to assess whether peripheral blood leukocytes (PBL) are available as a surrogate for determination of the expression of ABC transporter genes in the liver, we compared ABC transporter gene expression levels in PBL with those in liver tissues from patients with hepatocellular carcinoma (HCC). We measured ABCA1, A2, B1‐B4 , C1°C5, G1 and G2 gene expression levels in PBL, and cancerous and non‐cancerous portions of liver from patients with hepatocellular carcinoma by means of real time reverse‐transcription (RT)‐PCR. We could not detect ABCC5 expression in any tissue of the liver. Close correlations between ABCA2, C1 and 67 in PBL and in non‐tumor tissues of the liver were found. Compared with the non‐tumor part, HCC tissue expressed lower levels of ABCA1, B4 and G2. We think monitoring of ABCA2, C1 and G7 gene expression levels in PBL will be useful for selection of anti cancer agents and monitoring of drug resistance of HCC. Administration of chemotherapeutic agents which are substrates of ABCA1, B4 and G2 should be effective for the treatment of HCC. (Cancer Sci 2004; 95: 530—536)