Abstract
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.
Highlights
Nasopharyngeal carcinoma (NPC) is a malignancy arising from nasopharyngeal epithelial cells
We studied the molecular mechanism by which dimethyl celecoxib (DMC) caused apoptosis and autophagic cell death, which was controlled by the reactive oxygen species (ROS)/Jun N-terminal kinase (JNK) signaling axis
We investigated that DMC induced apoptosis and autophagic cell death are regulated by the ROS/JNK signaling
Summary
Nasopharyngeal carcinoma (NPC) is a malignancy arising from nasopharyngeal epithelial cells. Despite the fact that the incidence and mortality of NPC are decreasing as a result of advances in neoadjuvant chemoradiotherapy, patients’ 5-year survival rates remain poor [3, 4]. The antipyretic, analgesic, and anti-inflammatory are the properties of 2,5-dimethyl celecoxib (DMC), a structural counterpart of celecoxib that cannot occupy cyclooxygenase-2 (COX-2) [6]. It has a number of characteristics that make it a good candidate for repurposing as an anti-cancer treatment in the same way as celecoxib is. Whether DMC exhibits anti-tumor effect against NPC is not yet investigated. We investigated the effect of DMC on NPC in vitro and in vivo, as well as the underlying molecular mechanism that underpins it
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