
Downregulation of microRNAs‐143 and ‐145 in B‐cell malignancies
Author(s) -
Akao Yukihiro,
Nakagawa Yoshihito,
Kitade Yukio,
Kinoshita Tomohiro,
Naoe Tomoki
Publication year - 2007
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.1349-7006.2007.00618.x
Subject(s) - microrna , carcinogenesis , lymphoma , b cell , cell culture , cancer research , raji cell , cell , cell growth , biology , downregulation and upregulation , cancer , burkitt's lymphoma , b cell lymphoma , epstein–barr virus , immunology , virus , gene , antibody , genetics
Recently, it has been found that inappropriate expression of microRNAs (miRNAs) is strongly associated with carcinogenesis. In this study, we demonstrated that the expression of miRNAs (miRs) ‐143 and ‐145, the levels of which were previously shown to be reduced in colon cancers and various kinds of established cancer cell lines, was also decreased in most of the B‐cell malignancies examined, including chronic lymphocytic leukemias (CLL), B‐cell lymphomas, Epstein‐Barr virus (EBV)‐transformed B‐cell lines, and Burkitt lymphoma cell lines. All samples from 13 CLL patients and eight of nine B‐cell lymphoma ones tested exhibited an extremely low expression of miRs‐143 and ‐145. The expression levels of miRs‐143 and ‐145 were consistently low in human Burkitt lymphoma cell lines and were inversely associated with the cell proliferation observed in the EBV‐transformed B‐cell lines. Moreover, the introduction of either precursor or mature miR‐143 and ‐145 into Raji cells resulted in a significant growth inhibition that occurred in a dose‐dependent manner and the target gene of miRNA‐143 was determined to be ERK5, as previously reported in human colon cancer DLD‐1 cells. Taken together, these findings suggest that miRs‐143 and ‐145 may be useful as biomarkers that differentiate B‐cell malignant cells from normal cells and contribute to carcinogenesis in B‐cell malignancies by a newly defined mechanism. ( Cancer Sci 2007; 98: 1914–1920)