Induction of apoptosis by<i>Dioscorea nipponica</i>Makino extracts in human SH-SY5Y neuroblastoma cells via mitochondria-mediated pathway

Saha

et al. 2020

Front. Cell Dev. Biol.

Self Cite

Autophagy, a cellular self-digestion process that is activated in response to stress, has a functional role in tumor formation and progression. Cancer stem cells (CSCs) accounting for a minor proportion of total cancer cells-have distinct self-renewal and differentiation abilities and promote metastasis. Researchers have shown that a numeral number of natural products using traditional experimental methods have been revealed to target CSCs. However, the specific role of autophagy with respect to CSCs and tumorigenesis using natural products are still unknown. Currently, CSCs are considered to be one of the causative reasons underlying the failure of anticancer treatment as a result of tumor recurrence, metastasis, and chemo-or radio-resistance. Autophagy may play a dual role in CSC-related resistance to anticancer treatment; it is responsible for cell fate determination and the targeted degradation of transcription factors via growth arrest. It has been established that autophagy promotes drug resistance, dormancy, and stemness and maintenance of CSCs. Surprisingly, numerous studies have also suggested that autophagy can facilitate the loss of stemness in CSCs. Here, we review current progress in research related to the multifaceted connections between autophagy modulation and CSCs control using natural products. Overall, we emphasize the importance of understanding the role of autophagy in the maintenance of different CSCs and implications of this connection for the development of new strategies for cancer treatment targeting natural products.

Section: Controlling Cancer Stem Cells Through Apoptosis Signaling Pamentioning

confidence: 99%

Molecular Insights Into Therapeutic Potential of Autophagy Modulation by Natural Products for Cancer Stem Cells

Saha

et al. 2020

Front. Cell Dev. Biol.

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“…Therapeutics that decrease the activation of the mitochondrial fission proteins such as Drp1, pTau, and Aβ can rescue the neurons from the toxic effects of those agents and their interconnection. A diversity of phytochemicals available in numerous plant sources demonstrate various pharmacological properties, including neuroprotection [ 93 , 94 ], apoptosis induction [ 95 , 96 , 97 , 98 , 99 , 100 , 101 , 102 ], autophagy activation [ 79 , 103 , 104 , 105 ], antioxidant [ 106 ] and anti-inflammatory action [ 107 ], and DNA repair function [ 13 ]. Because of these capabilities, phytochemicals are progressively considered as favorable therapeutic candidates for AD therapy [ 10 ] ( Figure 4 ).…”

Section: Therapeutic Applications Of Phytochemicals In Mitochondrimentioning

confidence: 99%

Potential Therapeutic Role of Phytochemicals to Mitigate Mitochondrial Dysfunctions in Alzheimer’s Disease

Biswas³

et al. 2020

Antioxidants

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Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by a decline in cognitive function and neuronal damage. Although the precise pathobiology of AD remains elusive, accumulating evidence suggests that mitochondrial dysfunction is one of the underlying causes of AD. Mutations in mitochondrial or nuclear DNA that encode mitochondrial components may cause mitochondrial dysfunction. In particular, the dysfunction of electron transport chain complexes, along with the interactions of mitochondrial pathological proteins are associated with mitochondrial dysfunction in AD. Mitochondrial dysfunction causes an imbalance in the production of reactive oxygen species, leading to oxidative stress (OS) and vice versa. Neuroinflammation is another potential contributory factor that induces mitochondrial dysfunction. Phytochemicals or other natural compounds have the potential to scavenge oxygen free radicals and enhance cellular antioxidant defense systems, thereby protecting against OS-mediated cellular damage. Phytochemicals can also modulate other cellular processes, including autophagy and mitochondrial biogenesis. Therefore, pharmacological intervention via neuroprotective phytochemicals can be a potential strategy to combat mitochondrial dysfunction as well as AD. This review focuses on the role of phytochemicals in mitigating mitochondrial dysfunction in the pathogenesis of AD.

“…Natural products and herbal medicine may be used for the management of neurodegeneration, cancer, and apoptosis [73][74][75][76][77][78][79][80] as well as autophagy inducer [81]. Recent studies revealed that active compounds in natural products exhibit curative effects against AD via a variety of mechanisms, including anti-cholinesterase activity, anti-apoptosis, and neuroprotective effects via antioxidation through targeting autophagy [82,83].…”

Section: Use Of Natural Compound To Modulate Autophagy In Admentioning

confidence: 99%

Promising Modulatory Effects of Autophagy on APP Processing as a Potential Treatment for Alzheimer's Disease

Rahman¹,

Rahman²,

Rahman³

et al. 2020

Preprint

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Autophagy refers to the degradation of cytoplasmic constituents by a lysosomal-mediated pathway, which plays a critical role in maintaining cellular homeostasis. Importantly, dysregulation of autophagy has been implicated in multiple neurodegenerative disorders. Previous studies reported that autophagy affects the processing of amyloid precursor protein (APP), thus stimulating β‐amyloid (Aβ) production in Alzheimer’s disease (AD) eventually. Although the mechanism of autophagy modulation on APP processing and its pathogenesis has not yet been fully elucidated at the molecular level, but modulation of autophagy has received considerable attention as a promising approach for the treatment of AD. In the early stage of AD, Aβ may prompt autophagy to facilitate its removal via mTOR‐independent as well as-dependent pathways. However, a recent study proposed that autophagy processes are not properly regulated as AD continues to progress, and consequently, the production of Aβ tends to accumulate rapidly. Meanwhile, a number of autophagy-related genes (Atg) as well as APP genes are also thought to influence the development of AD, which may serve as a bi‐directional link to autophagy and AD pathology. In this review, we summarized current observations related to autophagy regulation and APP processing, focusing on their dynamic modifications associated with the progression of AD. Recent findings together highlight the essential role of autophagy in the removal and clearance of APP and Aβ deposition in the pathological condition of AD.