AMPK-ERK/CARM1 Signaling Pathways Affect Autophagy of Hepatic Cells in Samples of Liver Cancer Patients

Qin, Qiu-Fang; Li, Xiaojun; Li, Yu-Sang; Zhang, Wei Kevin; Tian, Guihua; Shang, Hongcai; Tang, He-Bin

doi:10.3389/fonc.2019.01247

Cited by 15 publications

(8 citation statements)

References 44 publications

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“…On the other hand, oxidized biomaterials such as damaged mitochondria are targeted by autophagy for lysosomal degradation [6,16]. Hence, ROS and autophagy constitute a negative feedback mechanism that mitigates oxidative stress and promotes cell survival [17]. However, single treatment with antioxidant or autophagy activator has defects on treating diseases with autophagy dysfunction and antioxidative stress.…”

Section: Introductionmentioning

confidence: 99%

Reactive Oxygen Species as a Link between Antioxidant Pathways and Autophagy

Ding

et al. 2021

Oxidative Medicine and Cellular Longevity

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Reactive oxygen species (ROS) are highly reactive molecules that can oxidize proteins, lipids, and DNA. Under physiological conditions, ROS are mainly generated in the mitochondria during aerobic metabolism. Under pathological conditions, excessive ROS disrupt cellular homeostasis. High levels of ROS result in severe oxidative damage to the cellular machinery. However, a low/mild level of ROS could serve as a signal to trigger cell survival mechanisms. To prevent and cope with oxidative damage to biomolecules, cells have developed various antioxidant and detoxifying mechanisms. Meanwhile, ROS can initiate autophagy, a process of self-clearance, which helps to reduce oxidative damage by engulfing and degrading oxidized substance. This review summarizes the interactions among ROS, autophagy, and antioxidant pathways. The effects of natural phytochemicals on autophagy induction, antioxidation, and dual-function are also discussed.

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Section: Introductionmentioning

confidence: 99%

Reactive Oxygen Species as a Link between Antioxidant Pathways and Autophagy

Ding

et al. 2021

Oxidative Medicine and Cellular Longevity

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“…Autophagy has an important role in cell survival in neuronal cells and elimination of abnormal protein. Moreover, autophagy was down-regulated in neurodegenerative diseases in accordance with the regulation of ERK [64,65]. AMPK, which is upstream of ERK in autophagy, induces autophagy activation [66].…”

Section: Discussionmentioning

confidence: 99%

Neuroprotective Effect of Cudrania tricuspidata Fruit Extracts on Scopolamine-Induced Learning and Memory Impairment

Jee

Lee

Kim

et al. 2020

IJMS

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Cudrania tricuspidata has diverse biological activities, such as antioxidant, anti-inflammatory, anticancer, and neuroprotective effects. This study investigated the protective effects of C. tricuspidata fruit extracts (CTFE) against scopolamine (SCO)-induced neuron impairment. The neuroprotective effects of CTFE on SCO-induced memory dysfunction were confirmed in mice using the Barnes maze test. The results showed that co-treatment of SCO and CTFE increased the stay time in the target zone compared with SCO treatment alone. Similarly, the results obtained by the fear conditioning test revealed that SCO-CTFE co-treatment induced the freezing action time under both the contextual fear condition and the cued fear condition compared with SCO treatment alone. Moreover, we showed that CTFE reduced the SCO-induced acetylcholinesterase (AChE) activity, thereby increasing the acetylcholine concentration in mice hippocampal tissues. Consistent with the improvement of memory and recognition function in vivo, our in vitro results showed that CTFE induced cAMP response element binding protein (CREB) and extracellular regulated kinase 1/2 (ERK1/2) activity in PC12 cells and reduced SCO-induced AChE activity. In addition, the microarray results of the hippocampal tissue support our data showing that CTFE affects gene expressions associated with neurogenesis and neuronal cell differentiation markers such as spp1 and klk6. Overall, CTFE exerts a neuroprotective effect via regulation of the CREB and ERK1/2 signaling pathways and could be a therapeutic candidate for neurodegenerative diseases.

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“…All pathological tissue samples were collected and manipulated with the approval of the Committee on Ethics of Experiments of the South-Central University for Nationalities, China (Permit Number: 2017-SCUEC-MEC-007). 40 …”

Section: Methodsmentioning

confidence: 99%

Testosterone Exacerbates the Formation of Liver Cancer Induced by Environmental N-Nitrosamines Exposure: Potential Mechanisms and Implications for Human Health

Yin,

Gu,

Ning

et al. 2024

OTT

Self Cite

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Background Humans are frequently exposed to N-nitrosamines through various sources, including diet, cigarette smoking, contaminated water, the atmosphere, and endogenous nitrosation. Exposure to these carcinogens may also contribute to the gender-specific incidence of liver cancer, which is significantly higher in males than in females, possibly due to the influence of endogenous hormones such as testosterone. However, the effect of testosterone on N-nitrosamine-induced liver cancer and its underlying mechanism remains unclear. Purpose To investigate the effect of testosterone on the development of liver cancer induced by N-nitrosamines exposure. Patients and Methods Histopathological and immunohistochemical staining techniques were employed to analyze the expression levels and nuclear localizations of key signaling molecules, including androgen receptor (AR), β-catenin, and HMGB1, in both tumor and non-tumor regions of liver samples obtained from human patients and mice. Results The findings demonstrated a strong correlation between AR and β-catenin in the nuclear region of tumor areas. AR also showed a significant correlation with HMGB1 in the cytoplasmic region of non-tumor areas in both human and mice samples. The study further analyzed the expression levels and patterns of these three proteins during the progression of liver tumors. Conclusion This study confirms that AR has the ability to modulate the expression levels and patterns of β-catenin and HMGB1 in vivo, thereby exacerbating the progression of liver cancer induced by environmental N-nitrosamines exposure. Importantly, the effect of testosterone on the formation of liver cancer induced by environmental N-nitrosamine exposure intensifies this progression. These findings have important implications for drug safety in clinical practice and emphasize the significance of reducing N-nitrosamines exposure through conscious choices regarding diet and lifestyle to ensure environmental safety.

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AMPK-ERK/CARM1 Signaling Pathways Affect Autophagy of Hepatic Cells in Samples of Liver Cancer Patients

Cited by 15 publications

References 44 publications

Reactive Oxygen Species as a Link between Antioxidant Pathways and Autophagy

Reactive Oxygen Species as a Link between Antioxidant Pathways and Autophagy

Neuroprotective Effect of Cudrania tricuspidata Fruit Extracts on Scopolamine-Induced Learning and Memory Impairment

Testosterone Exacerbates the Formation of Liver Cancer Induced by Environmental N-Nitrosamines Exposure: Potential Mechanisms and Implications for Human Health

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