RETRACTED: Allicin promotes autophagy and ferroptosis in esophageal squamous cell carcinoma by activating AMPK/mTOR signaling

Guo, Zhanfang

doi:10.1016/j.heliyon.2022.e11005

Cited by 8 publications

(5 citation statements)

References 42 publications

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“…For example, the ubiquitin-specific peptidase 8 (USP8) inhibitor DUB-IN-1 can inhibit ESCC cell growth by stimulating autophagy through p53-dependent adenosine 5’-monophosphate (AMP)-activated protein kinase (AMPK) [ 55 ]. Allicin promotes cellular autophagy and ferroptosis in ESCC through activation of AMPK/mTOR [ 56 ]. Downregulation of fibulin-4 expression inhibits autophagy and promotes the sensitivity of ESCC cells to apatinib through activation of the Akt/mTOR signaling pathway [ 54 ].…”

Section: Cellular Regulation Mechanisms Of Radioresistancementioning

confidence: 99%

Mechanisms of radiotherapy resistance and radiosensitization strategies for esophageal squamous cell carcinoma

An,

Li,

Jia

2023

Mol Cancer

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Esophageal squamous cell carcinoma (ESCC) is the sixth most common cause of cancer-related mortality worldwide, with more than half of them occurred in China. Radiotherapy (RT) has been widely used for treating ESCC. However, radiation-induced DNA damage response (DDR) can promote the release of cytokines and chemokines, and triggers inflammatory reactions and changes in the tumor microenvironment (TME), thereby inhibiting the immune function and causing the invasion and metastasis of ESCC. Radioresistance is the major cause of disease progression and mortality in cancer, and it is associated with heterogeneity. Therefore, a better understanding of the radioresistance mechanisms may generate more reversal strategies to improve the cure rates and survival periods of ESCC patients. We mainly summarized the possible mechanisms of radioresistance in order to reveal new targets for ESCC therapy. Then we summarized and compared the current strategies to reverse radioresistance.

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Section: Cellular Regulation Mechanisms Of Radioresistancementioning

confidence: 99%

Mechanisms of radiotherapy resistance and radiosensitization strategies for esophageal squamous cell carcinoma

An,

Li,

Jia

2023

Mol Cancer

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“…GPX4 genetic knockdown mirrored RSL3 effect on mTOR pathway suppression. 551 Pancreatic cancer QD394 Phosphorylation STAT3 QD394 induces ferroptosis through inhibiting STAT3 phosphorylation, thereby inhibiting GPX4 548 ESCC Allicin Phosphorylation AMPK Allicin may induce ferritinophagy through increasing AMPK phosphorylation and decreasing mTOR 549 ALZ003 a curcumin analog, Anisomycin an agonist of p38 mitogen-activated protein kinase (MAPK), BC Breast cancer, ESCC esophageal squamous cell carcinoma, GBM Glioblastoma, DHA Dihydroartemisinin, DMOCPTL a derivative of natural product parthenolide, NN3 PARP1 proteolysis-targeted chimaera (PROTAC), OC ovarian cancer, Polyphyllin VI STAT3 inhibitor, QD394 a quinazolinedione reactive oxygen species inducer …”

Section: Modulation Of Epigenetic and Posttranslational Modifications...mentioning

confidence: 99%

“…Allicin may induce ferritinophagy by increasing AMPK phosphorylation and decreasing mTOR in ESCC. 549 …”

Section: Modulation Of Epigenetic and Posttranslational Modifications...mentioning

confidence: 99%

Targeting epigenetic and posttranslational modifications regulating ferroptosis for the treatment of diseases

Wang,

Hu,

et al. 2023

Sig Transduct Target Ther

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Ferroptosis, a unique modality of cell death with mechanistic and morphological differences from other cell death modes, plays a pivotal role in regulating tumorigenesis and offers a new opportunity for modulating anticancer drug resistance. Aberrant epigenetic modifications and posttranslational modifications (PTMs) promote anticancer drug resistance, cancer progression, and metastasis. Accumulating studies indicate that epigenetic modifications can transcriptionally and translationally determine cancer cell vulnerability to ferroptosis and that ferroptosis functions as a driver in nervous system diseases (NSDs), cardiovascular diseases (CVDs), liver diseases, lung diseases, and kidney diseases. In this review, we first summarize the core molecular mechanisms of ferroptosis. Then, the roles of epigenetic processes, including histone PTMs, DNA methylation, and noncoding RNA regulation and PTMs, such as phosphorylation, ubiquitination, SUMOylation, acetylation, methylation, and ADP-ribosylation, are concisely discussed. The roles of epigenetic modifications and PTMs in ferroptosis regulation in the genesis of diseases, including cancers, NSD, CVDs, liver diseases, lung diseases, and kidney diseases, as well as the application of epigenetic and PTM modulators in the therapy of these diseases, are then discussed in detail. Elucidating the mechanisms of ferroptosis regulation mediated by epigenetic modifications and PTMs in cancer and other diseases will facilitate the development of promising combination therapeutic regimens containing epigenetic or PTM-targeting agents and ferroptosis inducers that can be used to overcome chemotherapeutic resistance in cancer and could be used to prevent other diseases. In addition, these mechanisms highlight potential therapeutic approaches to overcome chemoresistance in cancer or halt the genesis of other diseases.

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“…Inhibited the proliferation and promoted apoptosis of various colorectal cancer cells. [36,37] Antibacterial Inhibited DNA gyrase activity in bacteria and has natural antibacterial properties. [38] Anti-cardiovascular and cerebrovascular diseases Decreased serum levels of IL-1β, IL-6, and TNF-α, improved calcium homeostasis in cardiomyocytes, and downregulated calcium transport related CaMK II and inflammation related NF-κB and NLRP3, inhibited the activation of CaMK II/NF-κB pathway and protected hypertensive vascular and cardiac remodeling in spontaneously hypertensive rats.…”

Section: Anticancermentioning

confidence: 99%

Pungency Perception and the Interaction with Basic Taste Sensations: An Overview

Liang

Zhang

2023

Foods

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The perception of pungency can be attributed to the combination of pain and heat, and it has critical impacts on food flavor and food consumption preferences. Many studies have reported a variety of pungent ingredients with different Scoville heat units (SHU), and the mechanism of pungent perception was revealed in vivo and in vitro. The worldwide use of spices containing pungent ingredients has led to an increasing awareness of their effects on basic tastes. However, the interaction between basic tastes and pungency perception based on structure-activity relationship, taste perception mechanism and neurotransmission lacks review and summary, considering its brighter prospects in food flavor. Thus, in this review, common pungency substances and pungency evaluation methods, and the mechanism of pungency perception is presented, and the interaction between basic tastes and pungency perception and the possible factors of their interaction are reviewed in detail. Pungent stimuli are mainly transduced through transient receptor potential vanilloid 1 (TRPV1) and transient receptor potential fixed hormone isoform (TRPA1) activated by stimulants. Using modern detection techniques combined with sensory standards, different substances produce different degrees of pungent stimulation, ranging from 104 to 107 SHU/g. Pungent stimuli can affect taste receptor or channel protein conformation and regulate taste bud cell sensitivity by producing neurotransmission products. The products of neurotransmission and taste receptor cell activation in turn act on taste perception. When there are simultaneous effects of taste perception, pungency stimulation may enhance the perception of salty at a certain concentration, with a mutual inhibition effect with sour, sweet, and bitter taste, while its interaction with umami taste is not obvious. However, due to the complexity of perception and the uncertainty of many perceptual receptors or channels, the current studies of interactions are still controversial. Based on the understanding of the mechanism and influencing factors, the availability of pungency substances is proposed in the perspective of food industry in order to achieve new development.

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RETRACTED: Allicin promotes autophagy and ferroptosis in esophageal squamous cell carcinoma by activating AMPK/mTOR signaling

Cited by 8 publications

References 42 publications

Mechanisms of radiotherapy resistance and radiosensitization strategies for esophageal squamous cell carcinoma

Mechanisms of radiotherapy resistance and radiosensitization strategies for esophageal squamous cell carcinoma

Targeting epigenetic and posttranslational modifications regulating ferroptosis for the treatment of diseases

Pungency Perception and the Interaction with Basic Taste Sensations: An Overview

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