Cantharidic acid induces apoptosis in human nasopharyngeal carcinoma cells through p38‐mediated upregulation of caspase activation

Chen, Yi‑Ching; Chen, Pei‐Ni; Lin, Chiao‐Wen; Yang, Wei‐En; Ho, Yu‐Ting; Chuang, Chun‐Yi

doi:10.1002/tox.22897

Cited by 6 publications

(11 citation statements)

References 42 publications

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“…Treatment with celastrol, a traditional Chinese medicinal plant, was also found to significantly increase the phosphorylation of p38 MAPK and JNK1/2 in cisplatin-resistant human NPC-039 and NPC-BM NPC cells, triggering cytotoxicity by activation of caspasemediated apoptotic pathways in these cells [119]. Cantharidic acid, a natural toxin secreted by beetles, has proven to reduce NPC cell viability through the upregulation of caspase activation in extrinsic and intrinsic apoptosis pathways, as well as the upregulation of p38 and JNK1/2 pathways [120]. Treatment with licochalcone A significantly promoted cell apoptosis by increasing p38 and JNK1/2 activation and upregulated caspase-3, caspase-8, caspase-9 activation, and cleaved-PARP expression [121].…”

Section: Tumor Suppressive Functions Of Jnk and P38 Mapk Signaling In...mentioning

confidence: 99%

Functional Roles of JNK and p38 MAPK Signaling in Nasopharyngeal Carcinoma

Pua

Chung

et al. 2022

IJMS

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c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK) family members integrate signals that affect proliferation, differentiation, survival, and migration in a cell context- and cell type-specific way. JNK and p38 MAPK activities are found upregulated in nasopharyngeal carcinoma (NPC). Studies have shown that activation of JNK and p38 MAPK signaling can promote NPC oncogenesis by mechanisms within the cancer cells and interactions with the tumor microenvironment. They regulate multiple transcription activities and contribute to tumor-promoting processes, ranging from cell proliferation to apoptosis, inflammation, metastasis, and angiogenesis. Current literature suggests that JNK and p38 MAPK activation may exert pro-tumorigenic functions in NPC, though the underlying mechanisms are not well documented and have yet to be fully explored. Here, we aim to provide a narrative review of JNK and p38 MAPK pathways in human cancers with a primary focus on NPC. We also discuss the potential therapeutic agents that could be used to target JNK and p38 MAPK signaling in NPC, along with perspectives for future works. We aim to inspire future studies further delineating JNK and p38 MAPK signaling in NPC oncogenesis which might offer important insights for better strategies in diagnosis, prognosis, and treatment decision-making in NPC patients.

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Section: Tumor Suppressive Functions Of Jnk and P38 Mapk Signaling In...mentioning

confidence: 99%

Functional Roles of JNK and p38 MAPK Signaling in Nasopharyngeal Carcinoma

Pua

Chung

et al. 2022

IJMS

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“…However, the activation of ERK can also induce cell apoptosis by regulating mitochondrial cytochrome c release and caspase-8 activation [ 42 ]. In our previous studies, many anticancer compounds were found to activate p-ERK and induce apoptosis in different types of cancer [ 38 , 43 ]. The activation of ERK can also reportedly induce cell-cycle arrest, which may cause apoptosis [ 44 ].…”

Section: Discussionmentioning

confidence: 99%

FLLL32 Triggers Caspase-Mediated Apoptotic Cell Death in Human Oral Cancer Cells by Regulating the p38 Pathway

Chuang

Chen

et al. 2021

IJMS

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Oral cancer is the most common oral malignant tumor in Taiwan. Although there exist several methods for treatment, oral cancer still has a poor prognosis and high recurrence. FLLL32, a synthetic analog of curcumin with antitumor activity, is currently known to induce melanoma apoptosis and inhibit tumor growth in various cancers. However, few studies have examined the mechanisms of FLLL32 in oral cancer. In this study, we explore whether FLLL32 induces apoptosis in oral cancer. We determined that FLLL32 can inhibit the cell viability of oral cancer. Next, we analyzed the effect of FLLL32 on the cell cycle of oral cancer cells and observed that the proportion of cells in the G2/M phase was increased. Additionally, annexin-V/PI double staining revealed that FLLL32 induced apoptosis in oral cancer cells. Data from the Human Apoptosis Array revealed that FLLL32 increases the expression of cleaved caspase-3 and heme oxygenase-1 (HO-1). FLLL32 activates proteins such as caspase-8, caspase-9, caspase-3, PARP, and mitogen-activated protein kinases (MAPKs) in apoptosis-related molecular mechanisms. Moreover, by using MAPK inhibitors, we suggest that FLLL32 induces the apoptosis of oral cancer cells through the p38 MAPK signaling pathway. In conclusion, our findings suggest that FLLL32 is a potential therapeutic agent for oral cancer by inducing caspase-dependent apoptosis and HO-1 activation through the p38 pathway. We believe that the activation of HO-1 and the p38 pathway by FLLL32 represent potential targets for further research in oral cancer.

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“…The ERK1/2, p38, and c‐Jun N‐terminal kinase 1/2 (JNK1/2) pathways were up‐regulated. These results indicated that CA treatment induced apoptosis of human NPC cells through up‐regulation of caspase activation, especially through p38 pathway‐mediated caspase activation (Chen et al., 2020).…”

Section: Natural Products That Target Nasopharyngeal Carcinomamentioning

confidence: 95%

“…Cantharidic acid (CA) is the product of hydrolysis of the acid anhydride cantharidin, which is a natural toxin secreted by several blister beetles (Chen et al., 2020). CA significantly reduced the viability of NPC cells and the activation of caspase in exogenous and endogenous apoptotic pathways.…”

Section: Natural Products That Target Nasopharyngeal Carcinomamentioning

confidence: 99%

The efficacy of natural products for the treatment of nasopharyngeal carcinoma

Ao,

Luo,

Zhang

et al. 2023

Chem Biol Drug Des

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Nasopharyngeal carcinoma (NPC) is a malignant tumor originating in the nasopharyngeal epithelium with a high incidence in southern China and parts of Southeast Asia. The current treatment methods are mainly radiotherapy and chemotherapy. However, they often have side effects and are not suitable for long‐term exposure. Natural products have received more and more attention in cancer prevention and treatment because of their its high efficiency, low toxic side effects, and low toxicity. Natural products can serve as a viable alternative, and this study aimed to review the efficacy and mechanisms of natural products in the treatment of NPC by examining previous literature. Most natural products act by inhibiting cell proliferation, metastasis, inducing cell cycle arrest, and apoptosis. Although further research is needed to verify their effectiveness and safety, natural products can significantly improve the treatment of NPC.

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Cantharidic acid induces apoptosis in human nasopharyngeal carcinoma cells through p38‐mediated upregulation of caspase activation

Cited by 6 publications

References 42 publications

Functional Roles of JNK and p38 MAPK Signaling in Nasopharyngeal Carcinoma

Functional Roles of JNK and p38 MAPK Signaling in Nasopharyngeal Carcinoma

FLLL32 Triggers Caspase-Mediated Apoptotic Cell Death in Human Oral Cancer Cells by Regulating the p38 Pathway

The efficacy of natural products for the treatment of nasopharyngeal carcinoma

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