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Mol. Cells 2009; 28(6): 509-513

Published online December 31, 2009

https://doi.org/10.1007/s10059-009-0160-6

© The Korean Society for Molecular and Cellular Biology

Distinct Roles for JNK1 and JNK3 During TNF-α- or
Etoposide-Induced Apoptosis in HeLa Cells

Young-Mi Ham, Jin-Hee Lim, and Seung-Ki Lee

Received: December 17, 2009; Revised: October 11, 2009; Accepted: October 12, 2009

Abstract

Here, we show that JNK1 and JNK3 have different roles in TNF-α- or etoposide-induced apoptosis in HeLa cells. Dominant negative JNK1 inhibited TNF-α- or etoposide-induced apoptosis, while dominant negative JNK3 promoted TNF-α- or etoposide-induced apoptosis. During TNF-α-induced apoptosis, JNK1 was activated in a biphasic manner, exhibiting both transient and sustained activity, whereas JNK3 was activated early and in a transient manner. The role of JNK3 activation was an anti-apoptotic effect, while the role of JNK1 activation was a pro-apoptotic effect. These results suggest that the anti-apoptotic mechanism of JNK3 in TNF-α-induced apoptosis originates before the apoptotic machinery is triggered.

Keywords : anti-apoptotic, apoptosis, etoposide, JNK1, JNK3, survival, TNF-α

Article

Research Article

Mol. Cells 2009; 28(6): 509-513

Published online December 31, 2009 https://doi.org/10.1007/s10059-009-0160-6

Copyright © The Korean Society for Molecular and Cellular Biology.

Distinct Roles for JNK1 and JNK3 During TNF-α- or
Etoposide-Induced Apoptosis in HeLa Cells

Young-Mi Ham, Jin-Hee Lim, and Seung-Ki Lee

Received: December 17, 2009; Revised: October 11, 2009; Accepted: October 12, 2009

Abstract

Here, we show that JNK1 and JNK3 have different roles in TNF-α- or etoposide-induced apoptosis in HeLa cells. Dominant negative JNK1 inhibited TNF-α- or etoposide-induced apoptosis, while dominant negative JNK3 promoted TNF-α- or etoposide-induced apoptosis. During TNF-α-induced apoptosis, JNK1 was activated in a biphasic manner, exhibiting both transient and sustained activity, whereas JNK3 was activated early and in a transient manner. The role of JNK3 activation was an anti-apoptotic effect, while the role of JNK1 activation was a pro-apoptotic effect. These results suggest that the anti-apoptotic mechanism of JNK3 in TNF-α-induced apoptosis originates before the apoptotic machinery is triggered.

Keywords: : anti-apoptotic, apoptosis, etoposide, JNK1, JNK3, survival, TNF-&alpha,

Mol. Cells
Sep 30, 2023 Vol.46 No.9, pp. 527~572
COVER PICTURE
Chronic obstructive pulmonary disease (COPD) is marked by airspace enlargement (emphysema) and small airway fibrosis, leading to airflow obstruction and eventual respiratory failure. Shown is a microphotograph of hematoxylin and eosin (H&E)-stained histological sections of the enlarged alveoli as an indicator of emphysema. Piao et al. (pp. 558-572) demonstrate that recombinant human hyaluronan and proteoglycan link protein 1 (rhHAPLN1) significantly reduces the extended airspaces of the emphysematous alveoli by increasing the levels of TGF-β receptor I and SIRT1/6, as a previously unrecognized mechanism in human alveolar epithelial cells, and consequently mitigates COPD.

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