Tuberous sclerosis complex 2 loss-of-function mutation regulates reactive oxygen species production through Rac1 activation.

Abstract:

:The products of the TSC1 (hamartin) and TCS2 (tuberin) tumor suppressor genes negatively regulate cell growth by inhibiting mTOR signaling. Recent research has led to the postulation that tuberin and/or hamartin are involved in tumor migration, presumably through Rho activation. Here we show that LEF-8 cells, which contain a Y1571 missense mutation in tuberin, express higher Rac1 activity than tuberin negative and positive cells. We also provide evidence of obvious lamellipodia formation in LEF-8 cells. Since the production of TSC2(Y1571H) cannot form a hetero-complex with hamartin, we further analyzed another mutant, TSC2(R611Q), which also lacks the ability to form a complex with hamartin. Introducing both forms of mutated TSC2 into COS-1 cells increased Rac1 activity as well as cell motility. We also found these two mutants interacted with Rac1. We further demonstrated that the introduction of mutated TSC2 into COS-1 cells can generate higher reactive oxygen species (ROS). These results indicate that loss-of-function mutated tuberin can activate Rac1 and thereby increase ROS production.

authors

Suzuki T,Das SK,Inoue H,Kazami M,Hino O,Kobayashi T,Yeung RS,Kobayashi K,Tadokoro T,Yamamoto Y

doi

10.1016/j.bbrc.2008.01.077

subject

Has Abstract

pub_date

2008-03-28 00:00:00

pages

132-7

issue

1

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(08)00097-1

journal_volume

368

pub_type

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