2. Academic Validation
  3. Apoptotic effects of dehydrocrenatidine via JNK and ERK pathway regulation in oral squamous cell carcinoma

Apoptotic effects of dehydrocrenatidine via JNK and ERK pathway regulation in oral squamous cell carcinoma

  • Biomed Pharmacother. 2021 May;137:111362. doi: 10.1016/j.biopha.2021.111362.
Hsin-Yu Ho 1,  Chia-Chieh Lin 1,  Yi-Ching Chuang 1,  Yu-Sheng Lo 1,  Ming-Ju Hsieh 2,  Mu-Kuan Chen 3
Affiliations

Affiliations

  • 1 Oral Cancer Research Center, Changhua Christian Hospital, Changhua 500, Taiwan.
  • 2 Oral Cancer Research Center, Changhua Christian Hospital, Changhua 500, Taiwan; Institute of Medicine, Chung Shan Medical University, Taichung 402, Taiwan; Department of Holistic Wellness, Mingdao University, Changhua 52345, Taiwan; Graduate Institute of Biomedical Sciences, China Medical University, Taichung 404, Taiwan. Electronic address: [email protected].
  • 3 Department of Otorhinolaryngology, Head and Neck Surgery, Changhua Christian Hospital, Changhua 500, Taiwan. Electronic address: [email protected].
PMID: 33578238 DOI: 10.1016/j.biopha.2021.111362
Abstract

Dehydrocrenatidine, a β-carboline alkaloid isolated from Picrasma quassioides, has been demonstrated to exert analgesic effects and play essential roles in janus kinase inhibition and exert analgesic effects through the suppression of neuronal excitability. Alkaloids such as paclitaxel and vincristine had been well explored to be chemotherapeutic agents. However, the Anticancer effects of dehydrocrenatidine remain unclear. In the present study, we found that dehydrocrenatidine induced Apoptosis in human oral Cancer cells through both extrinsic and intrinsic pathways involving proteins such as Caspase-3, Caspase-8, caspase-9, poly (adenosine diphosphate-ribose) polymerase, and members of the Bcl-2 Family. Cotreatment with dehydrocrenatidine and mitogen-activated protein kinase (MAPK) inhibitors indicated that dehydrocrenatidine induced Apoptosis through the activation of extracellular signal-regulated kinases (ERK) and c-Jun N-terminal kinases (JNK). The findings provide insight into the potential of dehydrocrenatidine for a new perspective on molecular regulation.

Keywords

Apoptosis; Dehydrocrenatidine; MAPK pathway; Oral cancer.

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