TY - JOUR
T1 - 2,5-dimethyl celecoxib induces apoptosis and autophagy via activation of ROS/JNK axis in nasopharyngeal carcinoma cells
AU - Tan, Tan
AU - Fu, Xiangjie
AU - Qu, Jiaquan
AU - Zhang, Miao
AU - Chen, He
AU - Wang, Yaochun
AU - Wang, Bo
AU - Li, Juan
AU - Liu, Jie
AU - Liu, Peijun
N1 - Publisher Copyright:
© 2021 Tan et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
PY - 2021/9/15
Y1 - 2021/9/15
N2 - 2,5-dimethyl celecoxib (DMC), a close derivative of celecoxib, has also been reported to have anticancer effects. However, the effects and underlying molecular mechanisms of DMC with respect to nasopharyngeal carcinoma are still largely unknown. In this study, we present that DMC has displayed anticancer potency in nasopharyngeal carcinoma in vitro and in vivo. Mechanistically, we found DMC induced apoptosis and autophagy for anticancer therapy against nasopharyngeal carcinoma. Furthermore, DMC-induced autophagy could remarkably attenuate after the treatment of reactive oxygen species (ROS) scavenger N-acetyl cysteine (NAC) and c-Jun N-terminal kinase (JNK) inhibitor SP600125 (SP). Taken together, these results suggested DMC induced apoptosis and autophagic death via activation of ROS/JNK axis in NPC cells, which providing us new insights into developing potential therapeutic agents for nasopharyngeal carcinoma patients.
AB - 2,5-dimethyl celecoxib (DMC), a close derivative of celecoxib, has also been reported to have anticancer effects. However, the effects and underlying molecular mechanisms of DMC with respect to nasopharyngeal carcinoma are still largely unknown. In this study, we present that DMC has displayed anticancer potency in nasopharyngeal carcinoma in vitro and in vivo. Mechanistically, we found DMC induced apoptosis and autophagy for anticancer therapy against nasopharyngeal carcinoma. Furthermore, DMC-induced autophagy could remarkably attenuate after the treatment of reactive oxygen species (ROS) scavenger N-acetyl cysteine (NAC) and c-Jun N-terminal kinase (JNK) inhibitor SP600125 (SP). Taken together, these results suggested DMC induced apoptosis and autophagic death via activation of ROS/JNK axis in NPC cells, which providing us new insights into developing potential therapeutic agents for nasopharyngeal carcinoma patients.
KW - 2
KW - 5-dimethyl celecoxib
KW - apoptosis
KW - autophagy
KW - nasopharyngeal carcinoma
UR - https://www.scopus.com/pages/publications/85115643435
U2 - 10.18632/aging.203488
DO - 10.18632/aging.203488
M3 - 文章
C2 - 34511433
AN - SCOPUS:85115643435
SN - 1945-4589
VL - 13
SP - 21483
EP - 21496
JO - Aging
JF - Aging
IS - 17
ER -