let-7 microRNA functions as a potential growth suppressor in human colon cancer cells

Yukihiro Akao, Yoshihito Nakagawa, Tomoki Naoe

Research output: Contribution to journalArticle

499 Citations (Scopus)

Abstract

MicroRNAs (miRNAs) are endogenously expressed RNAs, 18-25 nucleotides in length, that repress protein translation through binding to target mRNAs. miRNAs have been implicated in many cellular processes including cell proliferation, differentiation, and death. Recently, let-7 miRNAs were found to regulate human RAS oncogene expression and to be often down-regulated in human lung tumors. In this study, we examined the expression of let-7 miRNAs in human colon cancer tumors and cell lines, with the result that 2 of 6 cases and 1 of 3 cell lines showed reduced expression of let-7. When let-7 low-expressing DLD-1 human colon cancer cells were transfected with let-7a-1 precursor miRNA, which is located at chromosome 9q22.3, the cells underwent significant growth suppression. At that time, the levels of RAS and c-myc proteins were lowered after the transfection, whereas the levels of both of their mRNAs remained almost unchanged. These findings suggest the involvement of let-7 miRNA in the growth of colon cancer cells. Thus, miRNAs might provide a basis for novel RNA anti-cancer agents.

Original languageEnglish
Pages (from-to)903-906
Number of pages4
JournalBiological and Pharmaceutical Bulletin
Volume29
Issue number5
DOIs
Publication statusPublished - 01-05-2006

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MicroRNAs
Colonic Neoplasms
Growth
RNA
Proto-Oncogene Proteins c-myc
Messenger RNA
Protein Biosynthesis
Tumor Cell Line
Oncogenes
Transfection
Cell Differentiation
Neoplasms
Cell Death
Nucleotides
Chromosomes
Cell Proliferation
Cell Line
Lung

All Science Journal Classification (ASJC) codes

  • Pharmacology
  • Pharmaceutical Science

Cite this

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let-7 microRNA functions as a potential growth suppressor in human colon cancer cells. / Akao, Yukihiro; Nakagawa, Yoshihito; Naoe, Tomoki.

In: Biological and Pharmaceutical Bulletin, Vol. 29, No. 5, 01.05.2006, p. 903-906.

Research output: Contribution to journalArticle

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