St. John’s Wort Suppresses Growth in Triple-Negative Breast Cancer Cell Line MDA-MB-231 by Inducing Prodeath Autophagy and Apoptosis

You, Mikyoung; Lee, Young-Hyun; Kim, Hwa-Jin; Kook, Ji Hyun; Kim, Hyeon-A

doi:10.3390/nu12103175

Cited by 10 publications

(4 citation statements)

References 50 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The cultured metabolic-imbalanced neurons at DIV 6 were treated with exendin-4 for 24 h. Protein levels and phosphorylation were analyzed using western blot analysis. An earlier study revealed that HFD induces insulin resistance through dephosphorylation of IRS-1 at tyrosine 612, AKT at serine 473, glycogen-synthase kinase-3beta (GSK-3β) at serine 9 in the brain 31 . In the present metabolic imbalanced model, it induced a similar dephosphorylation of IRS-1, AKT, GSK-3β in primary hippocampal and cortical neurons (Fig.…”

Section: Resultsmentioning

confidence: 99%

Exendin-4 improves long-term potentiation and neuronal dendritic growth in vivo and in vitro obesity condition

Wang

Yoon

Song

et al. 2021

Sci Rep

View full text Add to dashboard Cite

Metabolic syndrome, which increases the risk of obesity and type 2 diabetes has emerged as a significant issue worldwide. Recent studies have highlighted the relationship between metabolic imbalance and neurological pathologies such as memory loss. Glucagon-like peptide 1 (GLP-1) secreted from gut L-cells and specific brain nuclei plays multiple roles including regulation of insulin sensitivity, inflammation and synaptic plasticity. Although GLP-1 and GLP-1 receptor agonists appear to have neuroprotective function, the specific mechanism of their action in brain remains unclear. We investigated whether exendin-4, as a GLP-1RA, improves cognitive function and brain insulin resistance in metabolic-imbalanced mice fed a high-fat diet. Considering the result of electrophysiological experiments, exendin-4 inhibits the reduction of long term potentiation (LTP) in high fat diet mouse brain. Further, we identified the neuroprotective effect of exendin-4 in primary cultured hippocampal and cortical neurons in in vitro metabolic imbalanced condition. Our results showed the improvement of IRS-1 phosphorylation, neuronal complexity, and the mature of dendritic spine shape by exendin-4 treatment in metabolic imbalanced in vitro condition. Here, we provides significant evidences on the effect of exendin-4 on synaptic plasticity, long-term potentiation, and neural structure. We suggest that GLP-1 is important to treat neuropathology caused by metabolic syndrome.

show abstract

Section: Resultsmentioning

confidence: 99%

Exendin-4 improves long-term potentiation and neuronal dendritic growth in vivo and in vitro obesity condition

Wang

Yoon

Song

et al. 2021

Sci Rep

View full text Add to dashboard Cite

show abstract

“…St. John’s Wort was also found to induce autophagy and apoptosis in MDA-MB-231 cells [ 42 ]. Anti-apoptotic proteins were downregulated and the p-PI3K/PI3K and p-mTOR/mTOR ratios were also suppressed.…”

Section: Resultsmentioning

confidence: 99%

“…When autophagy was suppressed with 3-MA, cell proliferation increased and rates of apoptosis reversed, indicating that St. John’s Wort may work on the pro-death autophagy pathway. When studied in MDA-MG-231 xenografted athymic nude mice, administration of St. John’s Wort induced autophagy and apoptosis, as well as in vivo tumor growth inhibition [ 42 ].…”

Section: Resultsmentioning

confidence: 99%

A Review of Metabolic Targets of Anticancer Nutrients and Nutraceuticals in Pre-Clinical Models of Triple-Negative Breast Cancer

et al. 2022

View full text Add to dashboard Cite

Triple-negative breast cancer (TNBC) is a subtype of breast cancer that is notoriously aggressive and has poorer outcomes as compared with other breast cancer subtypes. Due to a lack of targeted therapies, TNBC is often treated with chemotherapeutics as opposed to hormone therapy or other targeted therapies available to individuals with estrogen receptor positive (ER+) breast cancers. Because of the lack of treatment options for TNBC, other therapeutic avenues are being explored. Metabolic reprogramming, a hallmark of cancer, provides potential opportunities to target cancer cells more specifically, increasing efficacy and reducing side effects. Nutrients serve a significant role in metabolic processes involved in DNA transcription, protein folding, and function as co-factors in enzyme activity, and may provide novel strategies to target cancer cell metabolism in TNBC. This article reviews studies that have investigated how nutrients/nutraceuticals target metabolic processes in TNBC cells alone or in combination with existing drugs to exert anticancer effects. These agents have been shown to cause perturbations in many metabolic processes related to glucose metabolism, fatty acid metabolism, as well as autophagy and oxidative stress-related metabolism. With this information, we present the potential of nutrients as metabolism-directed anticancer agents and the potential for using these agents alone or in cocktails as a new direction for TNBC therapy.

show abstract

“…As we all know, autophagy is very important for the maintenance of homeostasis, and it is responsible for the elimination of damaged or redundant macromolecules such as proteins, damaged organelles, and lipids (White, Mehnert, & Chan, 2015). In addition, excessive autophagy induces autophagic cell death (ACD) through excessive self‐digestion and degradation of essential cellular components (You, Lee, Kim, Kook, & Kim, 2020). Otherwise, some studies have shown that the regulation of autophagy can increase tumor cell sensitivity to chemotherapeutic agents (Santofimia‐Castaño & Iovanna, 2021; Tan et al, 2015).…”

Section: Introductionmentioning

confidence: 99%

Inhibition of fucoidan on breast cancer cells and potential enhancement of their sensitivity to chemotherapy by regulating autophagy

Zhang

Xue

Wang

et al. 2021

Phytotherapy Research

View full text Add to dashboard Cite

Fucoidan is a marine‐origin sulfated polysaccharide that has gained attention for its anticancer activities. However, the inhibitory effect of fucoidan on breast cancers by regulating autophagy and its mechanism are not clear, and the chemotherapeutic sensitization of fucoidan is largely unknown. In the present study, the anticancer potential of fucoidan was revealed in MCF‐7 and MDA‐MB‐231 cells. Additionally, we also studied the chemotherapeutic sensitization of fucoidan by combining chemotherapeutic drugs doxorubicin (ADM) and cisplatin (DDP) with fucoidan on breast cancer cells. In the two kinds of human breast cancer cells, cell viability was determined by 3‐(4,5‐dimethyl‐2‐thiazolyl)‐2,5‐diphenyl‐2H‐tetrazolium bromide (MTT) assay. Apoptosis was examined with flow cytometry. Transfection assay was used to examine autophagy flow. Western blot was used to examine the expressions of related proteins. Results suggested that fucoidan could induce autophagy and might enhance the sensitivity of breast cancer cells to chemotherapeutic drugs. Mechanistically, fucoidan induced autophagy in breast cancer cells by down‐regulating m‐TOR/p70S6K/TFEB pathway. In conclusion, our research revealed that fucoidan could induce autophagy of breast cancer cells by mediating m‐TOR/p70S6K/TFEB pathway, thus inhibiting tumor development. Furthermore, fucoidan might enhance the sensitivity of breast cancer cells to ADM and DDP, and this enhancement was related to autophagy.

show abstract

St. John’s Wort Suppresses Growth in Triple-Negative Breast Cancer Cell Line MDA-MB-231 by Inducing Prodeath Autophagy and Apoptosis

Cited by 10 publications

References 50 publications

Exendin-4 improves long-term potentiation and neuronal dendritic growth in vivo and in vitro obesity condition

Exendin-4 improves long-term potentiation and neuronal dendritic growth in vivo and in vitro obesity condition

A Review of Metabolic Targets of Anticancer Nutrients and Nutraceuticals in Pre-Clinical Models of Triple-Negative Breast Cancer

Inhibition of fucoidan on breast cancer cells and potential enhancement of their sensitivity to chemotherapy by regulating autophagy

Contact Info

Product

Resources

About