Cuprous oxide nanoparticles trigger reactive oxygen species-induced apoptosis through activation of erk-dependent autophagy in bladder cancer

Xiong, Qiao; Liu, Anwei; Ren, Qian; Xue, Yongping; Yu, Xiaowen; Ying, Yidie; Gao, Hongliang; Tan, Haoyuan; Zhang, Zhensheng; Li, Wei; Zeng, Shuxiong; Xu, Chuanliang

doi:10.1038/s41419-020-2554-5

Cited by 39 publications

(22 citation statements)

References 47 publications

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“…Several researchers have shown that the activation of the Erk/MAPK signaling pathway could promote the proliferation, invasion, and metastasis of liver cancer cells [56][57][58]. Furthermore, Erk/MAPK signaling pathway may be a vital pathway of autophagy in cancer [59][60][61]. In the present study, we found that p-Erk expression changed with PNO1 expression.…”

Section: Discussionsupporting

confidence: 57%

PNO1 regulates autophagy and apoptosis of hepatocellular carcinoma via the MAPK signaling pathway

Han¹,

Liu²,

Chen³

et al. 2021

Preprint

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Background Some studies have reported that the activated ribosomes are positively associated with malignant tumors, especially in hepatocellular carcinoma (HCC). The RNA-binding protein PNO1, as a critical ribosome has been rarely reported in human tumors. Thus, the roles of PNO1 in HCC should be explored. Methods We collected 150 formalin-fixed and paraffin-embedded (FFPE) samples and 8 fresh samples to explore the expression and prognosis of PNO1 in HCC by immunohistochemistry, Western Blotting and RT-PCR. Public databases (TCGA and GEO) were used to verify the expression and prognosis. The functions of PNO1 in HCC was verified by in vitro and in vivo experiments. The underlying molecular mechanisms of PNO1 were examined by RNA-seq analysis and a series of functional experiments. Results PNO1 expression was considerably higher in HCC tissues and the higher expression of PNO1 was associated with poor prognosis of HCC patients. In vitro experiments indicated that PNO1 overexpression promoted proliferation and depressed apoptosis of HCC cells. In addition, high expression of PNO1 increased autophagy of HCC cells. Consistent results were also observed in vivo experiments. The results of the RNA-seq analysis indicted that PNO1 as an oncogene promoted HCC progression through the MAPK signaling pathway. The results were also verified by in vivo experiments. Conclusions PNO1 was overexpressed in HCC, promoted autophagy and inhibited apoptosis of HCC cells via the MAPK signaling pathway.

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Section: Discussionsupporting

confidence: 57%

PNO1 regulates autophagy and apoptosis of hepatocellular carcinoma via the MAPK signaling pathway

Han¹,

Liu²,

Chen³

et al. 2021

Preprint

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show abstract

“…Several researchers have shown that the activation of the Erk/MAPK signaling pathway could promote the proliferation, invasion, and metastasis of liver cancer cells 56 – 58 . Furthermore, Erk/MAPK signaling pathway may be a vital pathway of autophagy in cancer 59 – 61 . In the present study, we found that p-Erk expression changed with PNO1 expression.…”

Section: Discussionmentioning

confidence: 99%

PNO1 regulates autophagy and apoptosis of hepatocellular carcinoma via the MAPK signaling pathway

et al. 2021

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Some studies have reported that activated ribosomes are positively associated with malignant tumors, especially in hepatocellular carcinoma (HCC). The RNA-binding protein PNO1 is a critical ribosome rarely reported in human tumors. This study aimed to explore the molecular mechanisms of PNO1 in HCC. Using 150 formalin-fixed and paraffin-embedded samples and 8 fresh samples, we found high PNO1 expression in HCC tumor tissues through Western blotting and RT-PCR. Moreover, the higher PNO1 expression was associated with poor HCC prognosis patients. In vitro and in vivo experiments indicated that PNO1 overexpression promoted the proliferation and depressed the apoptosis of HCC cells. High PNO1 expression also increased the autophagy of HCC cells. The molecular mechanisms underlying PNO1 were examined by RNA-seq analysis and a series of functional experiments. Results showed that PNO1 promoted HCC progression through the MAPK signaling pathway. Therefore, PNO1 was overexpressed in HCC, promoted autophagy, and inhibited the apoptosis of HCC cells through the MAPK signaling pathway.

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“…Xiong et al. 80 showed that cuprous oxide nanoparticles (CONPs) activated ERK-mediated autophagy, which triggered ROS-induced apoptosis in orthotopic xenografts and subcutaneous nude mouse bladder cancer models. Wang et al .…”

Section: Cell Death Effects Of Autophagy On Bladder Cancer Cellsmentioning

confidence: 99%

Contrast effects of autophagy in the treatment of bladder cancer

Konac

Kurman

Baltacı

2020

Exp Biol Med (Maywood)

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Bladder cancer is a disease that negatively affects patients’ quality of life, but treatment options have remained unchanged for a long time. Although promising results have been achieved with current bladder cancer treatments, cancer recurrence, progression, and therapy resistance are the most severe problems preventing the efficiency of bladder cancer treatments. Autophagy refers to an evolutionarily conserved catabolic process in which proteins, damaged organelles, and cytoplasmic components are degraded by lysosomal enzymes. Autophagy regulates the therapeutic response to the chemotherapy drugs, thus determining the effect of therapy on cancer cells. Autophagy is a stress-induced cell survival mechanism and its excessive stimulation can cause resistance of tumor cells to therapeutic agents. Depending on the conditions, an increase in autophagy may cause treatment resistance or autophagic cell death, and it is related to important anti-cancer mechanisms, such as apoptosis. Therefore, understanding the roles of autophagy under different conditions is important for designing effective anti-cancer agents. The dual role of autophagy in cancer has attracted considerable attention in respect of bladder cancer treatment. In this review, we summarize the basic characteristics of autophagy, including its mechanisms, regulation, and functions, and we present examples from current studies concerning the dual role of autophagy in bladder cancer progression and therapy. Impact statement Autophagy acts as an intracellular recycling system. Infection and mitochondrial damage, maintaining cellular homeostasis, orchestrating nutrient stress, hypoxia, and oxidative stress are some of the physiological roles associated with autophagy. Autophagy has also context-dependent roles in cancer. Autophagy has a significant impact on tumor initiation and promotion, with both tumor-suppressive and tumor-promoting roles. Unfortunately, conventional systemic chemotherapy for cancer therapy has been reported to have primary limitations such as chemo-resistance of targeted cells. The cytoprotective role of autophagy has been postulated as one of the causes of this resistance. Hence, combination therapy using autophagy inhibitors has recently started to emerge as a noteworthy strategy in the treatment of cancer. Therefore, targeting the autophagy pathways may be a potential therapeutic strategy for addressing cancer progression or therapy resistance in the near future. This review will provide a novel insight to understanding the paradoxical roles of autophagy in tumor suppression and tumor promotion.

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Cuprous oxide nanoparticles trigger reactive oxygen species-induced apoptosis through activation of erk-dependent autophagy in bladder cancer

Cited by 39 publications

References 47 publications

PNO1 regulates autophagy and apoptosis of hepatocellular carcinoma via the MAPK signaling pathway

PNO1 regulates autophagy and apoptosis of hepatocellular carcinoma via the MAPK signaling pathway

PNO1 regulates autophagy and apoptosis of hepatocellular carcinoma via the MAPK signaling pathway

Contrast effects of autophagy in the treatment of bladder cancer

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