Astragalus polysaccharide alleviated hepatocyte senescence via autophagy pathway

Background: The development of cancer stem-like cells (CSCs) is one of the main causes of ovarian cancer tolerance to radiotherapy. Autophagy is an adaptive process by which cells repair damage due to radiation. As a metabolite of riboflavin, lumiflavin can enhance the chemotherapeutic effects of cisplatin on ovarian cancer CSCs. Objective: This study aimed to investigate the synergistic effects of lumiflavin and ionising radiation on ovarian cancer CSCs and explore the association of this metabolite with autophagy. Methods: CSCs of human ovarian cancer cell lines HO8910 were treated with lumiflavin and rapamycin and then subjected to irradiation at a cumulative dose of 8 Gy. Cell proliferation ability, clonal formation ability, apoptosis rate, autophagy changes and autophagy-related protein changes were detected. Results: Lumiflavin and ionising radiation synergistically reduced cell vitality and clone formation and increased the apoptosis of CSCs compared with irradiation alone. In addition, ionising radiation increased autophagy and the expression of associated proteins, whereas lumiflavin reduced those changes in autophagy progression. Moreover, rapamycin, an autophagy inhibitor, was observed to block the synergistic effects of lumiflavin and ionising radiation on CSC apoptosis. Conclusion: Lumiflavin can enhance the effects of ionising radiation on ovarian cancer CSCs. The mechanism by which these effects are exerted is related to blocking the autophagy pathway.

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Berberine-photodynamic induced apoptosis by activating endoplasmic reticulum stress-autophagy pathway involving CHOP in human malignant melanoma cells

Biochemical and Biophysical Research Communications ◽

10.1016/j.bbrc.2021.02.147 ◽

2021 ◽

Vol 552 ◽

pp. 183-190

Author(s):

Jiaping Fang ◽

Xuan Huang ◽

Yun Yang ◽

Xiaotong Wang ◽

Xin Liang ◽

...

Keyword(s):

Endoplasmic Reticulum ◽

Malignant Melanoma ◽

Endoplasmic Reticulum Stress ◽

Melanoma Cells ◽

Human Malignant Melanoma ◽

Autophagy Pathway ◽

Induced Apoptosis

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Epigenomic Analysis of RAD51 ChIP-seq Data Reveals cis-regulatory Elements Associated with Autophagy in Cancer Cell Lines

Cancers ◽

10.3390/cancers13112547 ◽

2021 ◽

Vol 13 (11) ◽

pp. 2547

Author(s):

Keunsoo Kang ◽

Yoonjung Choi ◽

Hyeonjin Moon ◽

Chaelin You ◽

Minjin Seo ◽

...

Keyword(s):

Gene Regulation ◽

Homologous Recombination ◽

Cell Lines ◽

Regulatory Elements ◽

Binding Motif ◽

Genome Wide ◽

E Box ◽

Autophagy Pathway ◽

Mcf 7

RAD51 is a recombinase that plays a pivotal role in homologous recombination. Although the role of RAD51 in homologous recombination has been extensively studied, it is unclear whether RAD51 can be involved in gene regulation as a co-factor. In this study, we found evidence that RAD51 may contribute to the regulation of genes involved in the autophagy pathway with E-box proteins such as USF1, USF2, and/or MITF in GM12878, HepG2, K562, and MCF-7 cell lines. The canonical USF binding motif (CACGTG) was significantly identified at RAD51-bound cis-regulatory elements in all four cell lines. In addition, genome-wide USF1, USF2, and/or MITF-binding regions significantly coincided with the RAD51-associated cis-regulatory elements in the same cell line. Interestingly, the promoters of genes associated with the autophagy pathway, such as ATG3 and ATG5, were significantly occupied by RAD51 and regulated by RAD51 in HepG2 and MCF-7 cell lines. Taken together, these results unveiled a novel role of RAD51 and provided evidence that RAD51-associated cis-regulatory elements could possibly be involved in regulating autophagy-related genes with E-box binding proteins.

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Astragalus Polysaccharide Protects Against Cadmium-Induced Autophagy Injury Through Reactive Oxygen Species (ROS) Pathway in Chicken Embryo Fibroblast

Biological Trace Element Research ◽

10.1007/s12011-021-02628-y ◽

2021 ◽

Author(s):

Xudong Shen ◽

Zequn Tang ◽

Yu Bai ◽

Meishuo Wan ◽

Miao Yu ◽

...

Keyword(s):

Reactive Oxygen Species ◽

Chicken Embryo ◽

Chicken Embryo Fibroblast ◽

Reactive Oxygen ◽

Oxygen Species ◽

Astragalus Polysaccharide

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Marliolide Derivative Induces Melanosome Degradation via Nrf2/p62-Mediated Autophagy

International Journal of Molecular Sciences ◽

10.3390/ijms22083995 ◽

2021 ◽

Vol 22 (8) ◽

pp. 3995

Author(s):

Cheong-Yong Yun ◽

Nahyun Choi ◽

Jae Un Lee ◽

Eun Jung Lee ◽

Ji Young Kim ◽

...

Keyword(s):

Related Factor ◽

Melanin Pigmentation ◽

Microtubule Associated Proteins ◽

Melanocyte Stimulating Hormone ◽

Associated Proteins ◽

Autophagy Pathway ◽

Nrf2 Activator ◽

Promising Therapeutic Agent

Nuclear factor erythroid 2-related factor 2 (Nrf2), which is linked to autophagy regulation and melanogenesis regulation, is activated by marliolide. In this study, we investigated the effect of a marliolide derivative on melanosome degradation through the autophagy pathway. The effect of the marliolide derivative on melanosome degradation was investigated in α-melanocyte stimulating hormone (α-MSH)-treated melanocytes, melanosome-incorporated keratinocyte, and ultraviolet (UV)B-exposed HRM-2 mice (melanin-possessing hairless mice). The marliolide derivative, 5-methyl-3-tetradecylidene-dihydro-furan-2-one (DMF02), decreased melanin pigmentation by melanosome degradation in α-MSH-treated melanocytes and melanosome-incorporated keratinocytes, evidenced by premelanosome protein (PMEL) expression, but did not affect melanogenesis-associated proteins. The UVB-induced hyperpigmentation in HRM-2 mice was also reduced by a topical application of DMF02. DMF02 activated Nrf2 and induced autophagy in vivo, evidenced by decreased PMEL in microtubule-associated proteins 1A/1B light chain 3B (LC3)-II-expressed areas. DMF02 also induced melanosome degradation via autophagy in vitro, and DMF02-induced melanosome degradation was recovered by chloroquine (CQ), which is a lysosomal inhibitor. In addition, Nrf2 silencing by siRNA attenuated the DMF02-induced melanosome degradation via the suppression of p62. DMF02 induced melanosome degradation in melanocytes and keratinocytes by regulating autophagy via Nrf2-p62 activation. Therefore, Nrf2 activator could be a promising therapeutic agent for reducing hyperpigmentation.

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