Triptolide induces apoptosis and cytoprotective autophagy by ROS accumulation via directly targeting peroxiredoxin 2 in gastric cancer cells

Chen, Pengchen; Zhong, Xiaoru; Song, Yali; Zhong, Wenbin; Wang, Sisi; Wang, Jinyan; Huang, Pan; Niu, Yaping; Yang, Wenyue; Ding, Ziyang; Luo, Qingming; Yang, Chuanbin; Wang, Jigang; Zhang, Wei

doi:10.1016/j.canlet.2024.216622

Cited by 8 publications

(1 citation statement)

References 42 publications

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“…The generation of reactive oxygen species (ROS) is not only a significant factor in activating autophagy but also in inducing cell apoptosis, as demonstrated in various tumor cells [ 25 , 26 ]. Therefore, we examined the levels of ROS in pancreatic cancer cells after treatment with TET using fluorescence microscopy and a fluorescence microplate reader.…”

Section: Resultsmentioning

confidence: 99%

Inhibition of autophagy induced by tetrandrine promotes the accumulation of reactive oxygen species and sensitizes efficacy of tetrandrine in pancreatic cancer

Wang,

Xu,

Wang

et al. 2024

Cancer Cell Int

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Pancreatic cancer, characterized by its poor prognosis, exhibits a marked resistance to conventional chemotherapy and immunotherapy, underscoring the urgent need for more effective treatment modalities. In light of this, the present study is designed to assess the potential antineoplastic efficacy of a combined regimen involving tetrandrine, a plant-derived alkaloid, and autophagy inhibitors in the context of pancreatic cancer. Electron microscopy and immunoblots showed that tetrandrine promoted the formation of autophagosomes and the upregulation of LC3II and the downregulation of p62 expression, indicating that tetrandrine induced autophagy in pancreatic cancer cells. Western blot revealed that tetrandrine inhibited the phosphorylation of AKT and mTOR, as well as the expression of Bcl-2, while upregulating Beclin-1 expression. Moreover, tetrandrine promoted the transcription and protein expression of ATG7. Following the combination of autophagy inhibitors and tetrandrine, the apoptotic rate and cell death significantly increased in pancreatic cancer cells. Consistent results were obtained when ATG7 was silenced. Additionally, tetrandrine induced the generation of ROS, which was involved in the activation of autophagy and apoptosis. Further investigation revealed that upon autophagy inhibition, ROS accumulated in pancreatic cancer cells, resulting in decreased mitochondrial membrane potential and further induction of apoptosis. The results of treating subcutaneous xenograft tumors with a combination of tetrandrine and chloroquine validated that autophagy inhibition enhances the toxicity of tetrandrine against pancreatic cancer in vivo. Altogether, our study demonstrates that tetrandrine induces cytoprotective autophagy in pancreatic cancer cells. Inhibiting tetrandrine-induced autophagy promotes the accumulation of ROS and enhances its toxicity against pancreatic cancer.

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Section: Resultsmentioning

confidence: 99%

Inhibition of autophagy induced by tetrandrine promotes the accumulation of reactive oxygen species and sensitizes efficacy of tetrandrine in pancreatic cancer

Wang,

Xu,

Wang

et al. 2024

Cancer Cell Int

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Plant‐Derived Phytochemicals and Their Nanoformulations for Inducing Programed Cell Death in Cancer

Wang,

Wang

et al. 2024

Advanced Therapeutics

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Phytochemicals are a diverse class of compounds found in various plant‐based foods and beverages that have displayed the capacity to exert powerful anticancer effects through the induction of programed cell death (PCD) in malignancies. PCD is a sophisticated process that maintains in upholding tissue homeostasis and eliminating injured or neoplastic cells. Phytochemicals have shown the potential to induce PCD in malignant cells through various mechanisms, including modulation of cell signaling pathways, regulation of reactive oxygen species (ROS), and interaction with critical targets in cells such as DNA. Moreover, recent studies have suggested that nanomaterials loaded with phytochemicals may enhance cell death in tumors, which can also stimulate antitumor immunity. In this review, a comprehensive overview of the current understanding of the anticancer effects of phytochemicals and their potential as a promising approach to cancer therapy, is provided. The impacts of phytochemicals such as resveratrol, curcumin, apigenin, quercetin, and some approved plant‐derived drugs, such as taxanes on the regulation of some types of PCD, including apoptosis, pyroptosis, anoikis, autophagic cell death, ferroptosis, and necroptosis, are discussed. The underlying mechanisms and the potential of nanomaterials loaded with phytochemicals to enhance PCD in tumors are also explained.

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Immune escape between endoplasmic reticulum stress-related cancer cells and exhausted CD8+T cells leads to neoadjuvant chemotherapy resistance in ovarian cancer

Zhang,

Song

et al. 2024

Biochemical and Biophysical Research Communications

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Triptolide induces apoptosis and cytoprotective autophagy by ROS accumulation via directly targeting peroxiredoxin 2 in gastric cancer cells

Cited by 8 publications

References 42 publications

Inhibition of autophagy induced by tetrandrine promotes the accumulation of reactive oxygen species and sensitizes efficacy of tetrandrine in pancreatic cancer

Inhibition of autophagy induced by tetrandrine promotes the accumulation of reactive oxygen species and sensitizes efficacy of tetrandrine in pancreatic cancer

Plant‐Derived Phytochemicals and Their Nanoformulations for Inducing Programed Cell Death in Cancer

Immune escape between endoplasmic reticulum stress-related cancer cells and exhausted CD8+T cells leads to neoadjuvant chemotherapy resistance in ovarian cancer

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