Your browser doesn't support javascript.
Mostrar: 20 | 50 | 100
Resultados 1 - 2 de 2
Mais filtros

Base de dados
Intervalo de ano de publicação
Aging (Albany NY) ; 13(17): 21483-21496, 2021 09 12.
Artigo em Inglês | MEDLINE | ID: mdl-34511433


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.

Cancer Manag Res ; 12: 4595-4604, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32606952


Cancer is the leading cause of death, placing a substantial global health burden. The development of the most effective treatment regimen is the unmet clinical need for cancer. Inflammation plays a role in tumorigenesis and progression, and anti-inflammation may be a promising option for cancer management and prevention. Emerging studies have shown that non-steroidal anti-inflammatory drugs (NSAIDs) display anticarcinogenic and chemopreventive properties through the regulation of autophagy in certain types of cancer. In this review, we summarize the pharmacological functions and side effects of NSAIDs as chemotherapeutic agents, and focus on its mode of action on autophagy regulation, which increases our knowledge of NSAIDs and cancer-related inflammation, and contributes to a putative addition of NSAIDs in the chemoprevention and treatment of cancer.