Hispolon induces apoptosis in oral squamous cell carcinoma cells through <scp>JNK</scp>/<scp>HO</scp>‐1 pathway activation

Yang, Wei‐En; Chen, Yi‐Tzu; Su, Chung‐Kuang; Chen, Mu‐Kuan; Yeh, Chia‐Ming; Chen, Yen‐Lin; Tsai, Meng‐Ying; Yang, Shun‐Fa; Lin, Chiao‐Wen

doi:10.1111/jcmm.17729

Cited by 11 publications

(6 citation statements)

References 53 publications

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“…The results of several studies have supported the anticancer role of JNK alone or synergistically with downstream molecules in OSCC. Yang et al reported that hispolon may activate the JNK pathway to induce caspase-dependent apoptosis ( Yang et al, 2023 ). Chen et al also demonstrated that triptolide can induce apoptosis of OSCC cell lines SCC-25 and OEC-M1 in vivo by activating caspase-25 and caspase-1 ( Chen et al, 2009 ).…”

Section: Discussionmentioning

confidence: 99%

Network pharmacology and experiment validation investigate the potential mechanism of triptolide in oral squamous cell carcinoma

Hao,

Zhang,

Liu

et al. 2024

Front. Pharmacol.

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Objective: This study aimed to investigate the molecular mechanism of triptolide in the treatment of oral squamous cell carcinoma (OSCC) via network pharmacology and experimental validation.Methods: The network pharmacological method was used to predict the key targets, detect the signal pathways for the treatment of OSCC, and screen the critical components and targets for molecular docking. Predicted targets were validated in cellular and xenograft mouse model.Results: In this study, we predicted action on 17 relevant targets of OSCC by network pharmacology. PPI network demonstrated that Jun, MAPK8, TP53, STAT3, VEGFA, IL2, CXCR4, PTGS2, IL4 might be the critical targets of triptolide in the treatment of OSCC. These potential targets are mainly closely related to JAK-STAT and MAPK signaling pathways. The analysis of molecular docking showed that triptolide has high affinity with Jun, MAPK8 and TP53. Triptolide can suppress the growth of OSCC cells and xenograft mice tumor, and downregulate the expression of Jun, MAPK8, TP53, STAT3, VEGFA, IL2, CXCR4, PTGS2 to achieve the therapeutic effect of OSCC.Conclusion: Through network pharmacological methods and experimental studies, we predicted and validated the potential targets and related pathways of triptolide for OSCC treatment. The results suggest that triptolide can inhibit the growth of OSCC via several key targets.

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Section: Discussionmentioning

confidence: 99%

Network pharmacology and experiment validation investigate the potential mechanism of triptolide in oral squamous cell carcinoma

Hao,

Zhang,

Liu

et al. 2024

Front. Pharmacol.

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“…The captured proteins were detected with biotinylated detection antibodies and deposited on the nitrocellulose membrane and visualized with chemiluminescent detection reagents. 30 …”

Section: Methodsmentioning

confidence: 99%

Apoptotic effect and cell arrest of deoxyshikonin in human osteosarcoma cells through the p38 pathway

Hsieh

Chou

et al. 2023

J Cellular Molecular Medi

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Osteosarcoma is the most common primary bone cancer that affects adolescents with early metastatic potential and drastically reduces their long‐term survival rate if pulmonary metastases are detected at diagnosis. The natural naphthoquinol compound deoxyshikonin exhibits anticancer properties, so we hypothesized that it has an apoptotic effect on osteosarcoma U2OS and HOS cells and studied its mechanisms. After deoxyshikonin treatment, dose‐dependent decreases in cell viability, induction of cell apoptosis and arrest in the sub‐G1 phase of U2OS and HOS cells were observed. The increases in cleaved caspase 3 expression and the decreases in X‐chromosome‐linked IAP (XIAP) and cellular inhibitors of apoptosis 1 (cIAP‐1) expressions after deoxyshikonin treatment in the human apoptosis array were identified in HOS cells, and dose‐dependent expression changes of IAPs and cleaved caspase 3, 8 and 9 were verified by Western blotting in U2OS and HOS cells. Phosphorylation of extracellular signal‐regulated protein kinases (ERK)1/2, c‐Jun N‐terminal kinases (JNK)1/2 and p38 expressions in U2OS and HOS cells was also increased by deoxyshikonin in a dose‐dependent manner. Subsequently, cotreatment with inhibitors of ERK (U0126), JNK (JNK‐IN‐8) and p38 (SB203580) was performed to show that p38 signalling is responsible for deoxyshikonin‐induced apoptosis in U2OS and HOS cells, but not via the ERK and JNK pathways. These discoveries demonstrate that deoxyshikonin may be a possible chemotherapeutic candidate to induce cell arrest and apoptosis by activating extrinsic and intrinsic pathways through p38 for human osteosarcoma.

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“…Notably, Hispolon, a compound derived from specific fungi, has demonstrated its capability to induce apoptosis in OSCC cells through the JNK/HO-1 pathway and caspase-dependent mechanisms. This underscores its potential as an anticancer agent with promising implications for OSCC treatment [ 32 ]. In addition, investigations have shed light on the influence of various genes and signalling pathways, including BCLAF1 and the Fas-mediated apoptosis pathway, in shaping the apoptotic responses of OSCC cells [ 33 , 34 ].…”

Section: Reviewmentioning

confidence: 99%

Role of Cathepsin B Expression in Oral Squamous Cell Carcinoma: A Comprehensive Review

Sagar,

Gadkari,

Hiwale

et al. 2024

Cureus

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This comprehensive review delves into the intricate landscape of oral squamous cell carcinoma (OSCC) by examining the role of cathepsin B expression in its pathogenesis. OSCC, a prevalent and clinically significant oral malignancy, poses a considerable global health burden, necessitating a thorough exploration of its underlying molecular mechanisms. Cathepsin B, a lysosomal cysteine protease, emerges as a critical player in OSCC, influencing tumour initiation, invasion, and metastasis. The review begins with a brief overview of OSCC, emphasizing its epidemiological and clinical features, followed by exploring the significance of studying cathepsin B expression in this context. In the manuscript, the structure and function of cathepsin B are elucidated, providing a foundation for understanding its aberrant expression in OSCC. Clinical studies revealing correlations with tumour grade and stage, along with prognostic significance, are scrutinized, offering insights into the potential diagnostic and prognostic utility of cathepsin B. The biological functions of cathepsin B in OSCC, including its impact on tumour invasion and modulation of apoptosis, are comprehensively discussed. The Therapeutic Implications section explores targeting cathepsin B as a potential strategy, emphasizing the need for future research to overcome associated challenges. In the Conclusion section, the review synthesizes key findings, delineates implications for future research, and highlights the potential impact of cathepsin B on OSCC diagnosis and treatment, contributing to the ongoing efforts to advance our understanding of this complex malignancy, which is associated with a high mortality rate and improve clinical outcomes.

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Hispolon induces apoptosis in oral squamous cell carcinoma cells through JNK/HO‐1 pathway activation

Cited by 11 publications

References 53 publications

Network pharmacology and experiment validation investigate the potential mechanism of triptolide in oral squamous cell carcinoma

Network pharmacology and experiment validation investigate the potential mechanism of triptolide in oral squamous cell carcinoma

Apoptotic effect and cell arrest of deoxyshikonin in human osteosarcoma cells through the p38 pathway

Role of Cathepsin B Expression in Oral Squamous Cell Carcinoma: A Comprehensive Review

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