Inhibition of amino acid-mTOR signaling by a leucine derivative induces G1 arrest in Jurkat cells

Sujuti Hidayat; Ken Ichi Yoshino; Chiharu Tokunaga; Kenta Hara; Masafumi Matsuo; Kazuyoshi Yonezawa

doi:10.1016/S0006-291X(02)03052-8

Inhibition of amino acid-mTOR signaling by a leucine derivative induces G1 arrest in Jurkat cells

Sujuti Hidayat
, Ken Ichi Yoshino
, Chiharu Tokunaga
, Kenta Hara
, Masafumi Matsuo
, Kazuyoshi Yonezawa^*

^*Corresponding author for this work

Research output: Contribution to journal › Article › peer-review

50 Citations (Scopus)

Abstract

We have previously demonstrated that N-acetylleucine amide, a derivative of L-leucine, inhibits leucine-induced p70^S6k activation in a rat hepatoma cell line. In the present study, we investigated whether N-acetylleucine amide is capable of inhibiting amino acid-mTOR signaling. N-Acetylleucine amide caused cell cycle arrest at G1 stage in Jurkat cells, a human leukemia T cell line, concomitant with the inhibition of serum-induced p70^S6k activation and p27 degradation. Treatment of Jurkat cells with this compound also exhibited dephosphorylation of retinoblastoma protein. These effects are similar to the inhibitory effects of rapamycin on amino acid-mTOR signaling pathway and suggest that N-acetylleucine amide acts as a rapamycin-like reagent to inhibit cell cycle progression in Jurkat cells.

Original language	English
Pages (from-to)	417-423
Number of pages	7
Journal	Biochemical and Biophysical Research Communications
Volume	301
Issue number	2
DOIs	https://doi.org/10.1016/S0006-291X(02)03052-8
Publication status	Published - 7 Feb 2003
Externally published	Yes

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

SDG 3 Good Health and Well-being

Keywords

Cell cycle
Leucine
N-Acetylleucine amide
Rapamycin
mTOR
p27 and retinoblastoma protein
p70 S6 kinase

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10.1016/S0006-291X(02)03052-8

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title = "Inhibition of amino acid-mTOR signaling by a leucine derivative induces G1 arrest in Jurkat cells",

abstract = "We have previously demonstrated that N-acetylleucine amide, a derivative of L-leucine, inhibits leucine-induced p70S6k activation in a rat hepatoma cell line. In the present study, we investigated whether N-acetylleucine amide is capable of inhibiting amino acid-mTOR signaling. N-Acetylleucine amide caused cell cycle arrest at G1 stage in Jurkat cells, a human leukemia T cell line, concomitant with the inhibition of serum-induced p70S6k activation and p27 degradation. Treatment of Jurkat cells with this compound also exhibited dephosphorylation of retinoblastoma protein. These effects are similar to the inhibitory effects of rapamycin on amino acid-mTOR signaling pathway and suggest that N-acetylleucine amide acts as a rapamycin-like reagent to inhibit cell cycle progression in Jurkat cells.",

keywords = "Cell cycle, Leucine, N-Acetylleucine amide, Rapamycin, mTOR, p27 and retinoblastoma protein, p70 S6 kinase",

author = "Sujuti Hidayat and Yoshino, \{Ken Ichi\} and Chiharu Tokunaga and Kenta Hara and Masafumi Matsuo and Kazuyoshi Yonezawa",

year = "2003",

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doi = "10.1016/S0006-291X(02)03052-8",

language = "English",

volume = "301",

pages = "417--423",

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TY - JOUR

T1 - Inhibition of amino acid-mTOR signaling by a leucine derivative induces G1 arrest in Jurkat cells

AU - Hidayat, Sujuti

AU - Yoshino, Ken Ichi

AU - Tokunaga, Chiharu

AU - Hara, Kenta

AU - Matsuo, Masafumi

AU - Yonezawa, Kazuyoshi

PY - 2003/2/7

Y1 - 2003/2/7

N2 - We have previously demonstrated that N-acetylleucine amide, a derivative of L-leucine, inhibits leucine-induced p70S6k activation in a rat hepatoma cell line. In the present study, we investigated whether N-acetylleucine amide is capable of inhibiting amino acid-mTOR signaling. N-Acetylleucine amide caused cell cycle arrest at G1 stage in Jurkat cells, a human leukemia T cell line, concomitant with the inhibition of serum-induced p70S6k activation and p27 degradation. Treatment of Jurkat cells with this compound also exhibited dephosphorylation of retinoblastoma protein. These effects are similar to the inhibitory effects of rapamycin on amino acid-mTOR signaling pathway and suggest that N-acetylleucine amide acts as a rapamycin-like reagent to inhibit cell cycle progression in Jurkat cells.

AB - We have previously demonstrated that N-acetylleucine amide, a derivative of L-leucine, inhibits leucine-induced p70S6k activation in a rat hepatoma cell line. In the present study, we investigated whether N-acetylleucine amide is capable of inhibiting amino acid-mTOR signaling. N-Acetylleucine amide caused cell cycle arrest at G1 stage in Jurkat cells, a human leukemia T cell line, concomitant with the inhibition of serum-induced p70S6k activation and p27 degradation. Treatment of Jurkat cells with this compound also exhibited dephosphorylation of retinoblastoma protein. These effects are similar to the inhibitory effects of rapamycin on amino acid-mTOR signaling pathway and suggest that N-acetylleucine amide acts as a rapamycin-like reagent to inhibit cell cycle progression in Jurkat cells.

KW - Cell cycle

KW - Leucine

KW - N-Acetylleucine amide

KW - Rapamycin

KW - mTOR

KW - p27 and retinoblastoma protein

KW - p70 S6 kinase

UR - https://www.scopus.com/pages/publications/0037423752

U2 - 10.1016/S0006-291X(02)03052-8

DO - 10.1016/S0006-291X(02)03052-8

M3 - Article

C2 - 12565877

AN - SCOPUS:0037423752

SN - 0006-291X

VL - 301

SP - 417

EP - 423

JO - Biochemical and Biophysical Research Communications

JF - Biochemical and Biophysical Research Communications

IS - 2

ER -

Inhibition of amino acid-mTOR signaling by a leucine derivative induces G1 arrest in Jurkat cells

Abstract

UN SDGs

Keywords

Access to Document

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