Autophagy flux in bladder cancer: Cell death crosstalk, drug and nanotherapeutics

Liu, Kuan; Chen, Huijing; Li, Yanhong; Wang, Bei; Li, Qian; Zhang, Lu; Liu, Xiaohui; Wang, Ce; Ertas, Yavuz Nuri; Shi, Hongyun

doi:10.1016/j.canlet.2024.216867

Cited by 4 publications

(1 citation statement)

References 216 publications

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“…In normal cells, autophagy plays a role in cellular homeostasis by aiding in the repair and renewal of cells, as well as helping them adapt to stress such as hypoxia and starvation [ 8 ]. However, in tumor cells, autophagy exhibits a dual role under different conditions [ 9 , 10 ]. Recent studies have shown that in pancreatic cancer, autophagy promotes and protects cancer cells and is closely associated with chemotherapy resistance [ 11 , 12 ].…”

Section: Introductionmentioning

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: Introductionmentioning

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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Exploring the oncogenic role of RGS19 in bladder cancer progression and prognosis

Yan,

Luo,

Han

et al. 2024

Acta Histochemica

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Non-coding RNAs in bladder cancer, a bridge between gut microbiota and host?

Zou,

Xu,

Luo

et al. 2024

Front. Immunol.

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In recent years, the role of gut microbiota (GM) in bladder cancer has attracted significant attention. Research indicates that GM not only contributes to bladder carcinogenesis but also influences the efficacy of adjuvant therapies for bladder cancer. Despite this, interventions targeting GM have not been widely employed in the prevention and treatment of bladder cancer, mainly due to the incomplete understanding of the complex interactions between the host and gut flora. Simultaneously, aberrantly expressed non-coding RNAs (ncRNAs) have been frequently associated with bladder cancer, playing crucial roles in processes such as cell proliferation, invasion, and drug resistance. It is widely known that the regulation of GM-mediated host pathophysiological processes is partly regulated through epigenetic pathways. At the same time, ncRNAs are increasingly regarded as GM signaling molecules involved in GM-mediated epigenetic regulation. Accordingly, this review analyzes the ncRNAs that are closely related to the GM in the context of bladder cancer occurrence and treatment, and summarizes the role of their interaction with the GM in bladder cancer-related phenotypes. The aim is to delineate a regulatory network between GM and ncRNAs and provide a new perspective for the study and prevention of bladder cancer.

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Autophagy flux in bladder cancer: Cell death crosstalk, drug and nanotherapeutics

Cited by 4 publications

References 216 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

Exploring the oncogenic role of RGS19 in bladder cancer progression and prognosis

Non-coding RNAs in bladder cancer, a bridge between gut microbiota and host?

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