Adenosine 5'‐monophosphate‐activated protein kinase‐dependent mTOR pathway is involved in flavokawain B‐induced autophagy in thyroid cancer cells

He, Qin; Liu, Wenping; Sha, Sha; Fan, Shanshan; Yu, Yajing; Chen, Li; Dong, Ming

doi:10.1111/cas.13699

Cited by 17 publications

(16 citation statements)

References 39 publications

(64 reference statements)

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“…During cytotoxicity of FKB, FKB induced autophagy by increasing LC3B-II and Beclin 1 expression and decreasing p62 expression. 121 In this study, Beclin 1 was activated by activating AMPK in a similar manner as in other studies. The antitumor effect of FKB was improved by inhibition of autophagy through 3-MA or cotreatment with Beclin 1 siRNA and ATG5 siRNA.…”

Section: Beclin 1 and Head And Neck Cancerssupporting

confidence: 77%

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<p>Autophagy-Related Beclin 1 and Head and Neck Cancers</p>

Hu¹,

Zhong²,

Gong³

et al. 2020

OTT

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Beclin 1, a positive regulator of autophagy, behaves as a double-edged sword in tumorigenesis. Beclin 1 contributes to tumor suppression by removing defective or damaged organelles and other cellular components; however, its activity can also stimulate cancer initiation and progression. In head and neck cancer, Beclin 1 overexpression promotes autophagy, which limits DNA damage and chromosomal instability and increases necrosis and inflammation by impacting apoptotic and autophagic pathways. This paper reviews the relationship between Beclin 1, carcinogenesis and head and neck cancer prognosis.

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Section: Beclin 1 and Head And Neck Cancerssupporting

confidence: 77%

“…The antitumor effect of FKB was improved by inhibition of autophagy through 3-MA or cotreatment with Beclin 1 siRNA and ATG5 siRNA. 121 …”

Section: Beclin 1 and Head And Neck Cancersmentioning

confidence: 99%

<p>Autophagy-Related Beclin 1 and Head and Neck Cancers</p>

Hu¹,

Zhong²,

Gong³

et al. 2020

OTT

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“…GFP-MAP 1LC3B (pBABEpuro, 22405)-expressing vectors were purchased from Addgene (Cambridge, MA, USA). The constructs, transfections, and lentiviral infections of GFP-MAP 1LC3B that we used have been described previously [24]. After treatments, we calculated the number of autophagic cells expressed as GFP-MAP 1LC3B dots (positive cells as ≥ 3 dots).…”

Section: Lentiviral Transfectionsmentioning

confidence: 99%

RETRACTED ARTICLE: Mesenchymal stem cell-derived exosomes exert ameliorative effects in type 2 diabetes by improving hepatic glucose and lipid metabolism via enhancing autophagy

He¹,

Wang²,

Zhao³

et al. 2020

Stem Cell Res Ther

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Background: Mesenchymal stem cell (MSC)-based therapy is currently considered to be an effective treatment strategy for diabetes and hepatic disorders, such as liver cirrhosis and non-alcoholic fatty liver disease. Exosomes are important mediators of cellular connections, and increasing evidence has suggested that exosomes derived from MSCs may be used as direct therapeutic agents; their mechanisms of action, however, remain largely unclear. Here, we evaluated the efficacy and molecular mechanisms of human umbilical cord MSC-derived exosomes (HucMDEs) on hepatic glucose and lipid metabolism in type 2 diabetes mellitus (T2DM). Methods: HucMDEs were used to treat T2DM rats, as well as palmitic acid (PA)-treated L-O2 cells, in order to determine the effects of HucMDEs on hepatic glucose and lipid metabolism. To evaluate the changes in autophagy and potential signaling pathways, autophagy-related proteins (BECN1, microtubule-associated protein 1 light chain 3 beta [MAP 1LC3B]), autophagy-related genes (ATGs, ATG5, and ATG7), AMP-activated protein kinase (AMPK), and phosphorylated AMPK (p-AMPK) were assessed by Western blotting. Results: HucMDEs promoted hepatic glycolysis, glycogen storage, and lipolysis, and reduced gluconeogenesis. Additionally, autophagy potentially contributed to the effects of HucMDE treatment. Transmission electron microscopy revealed an increased formation of autophagosomes in HucMDE-treated groups, and the autophagy marker proteins, BECN1 and MAP 1LC3B, were also increased. Moreover, autophagy inhibitor 3-methyladenine significantly reduced the effects of HucMDEs on glucose and lipid metabolism in T2DM rats. Based on its phosphorylation status, we found that the AMPK signaling pathway was activated and induced autophagy in T2DM rats and PA-treated L-O2 cells. Meanwhile, the transfection of AMPK siRNA or application of the AMPK inhibitor, Comp C, weakened the therapeutic effects of HucMDEs on glucose and lipid metabolism.

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“…Flavokavain B was reported to have significant anti-tumor effects on several carcinoma cell lines both in vitro and in lab animal models. Similar to flavokavain A, flavokavain B was reported to inhibit cancer cell proliferation [ 118 ], metastasis [ 128 , 129 ] and angiogenesis [ 130 ], and induce apoptosis [ 128 , 129 , 131 , 132 , 133 , 134 , 135 , 136 ], G2/M [ 128 , 132 , 136 , 137 ], G0/G1 [ 138 ] cell cycle arrest, autophagy [ 134 , 139 , 140 , 141 , 142 ], and the immune responses [ 143 ]. Unlike flavokavain A, flavokavain B induced G2/M cell cycle arrest in cancer cells regardless of the p53 status [ 128 , 131 , 132 , 134 , 136 , 137 ], which is intriguing given their similar structures ( Figure 2 ).…”

Section: Kava and Cancermentioning

confidence: 99%

Kava as a Clinical Nutrient: Promises and Challenges

et al. 2020

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Kava beverages are typically prepared from the root of Piper methysticum. They have been consumed among Pacific Islanders for centuries. Kava extract preparations were once used as herbal drugs to treat anxiety in Europe. Kava is also marketed as a dietary supplement in the U.S. and is gaining popularity as a recreational drink in Western countries. Recent studies suggest that kava and its key phytochemicals have anti-inflammatory and anticancer effects, in addition to the well-documented neurological benefits. While its beneficial effects are widely recognized, rare hepatotoxicity had been associated with use of certain kava preparations, but there are no validations nor consistent mechanisms. Major challenges lie in the diversity of kava products and the lack of standardization, which has produced an unmet need for quality initiatives. This review aims to provide the scientific community and consumers, as well as regulatory agencies, with a broad overview on kava use and its related research. We first provide a historical background for its different uses and then discuss the current state of the research, including its chemical composition, possible mechanisms of action, and its therapeutic potential in treating inflammatory and neurological conditions, as well as cancer. We then discuss the challenges associated with kava use and research, focusing on the need for the detailed characterization of kava components and associated risks such as its reported hepatotoxicity. Lastly, given its growing popularity in clinical and recreational use, we emphasize the urgent need for quality control and quality assurance of kava products, pharmacokinetics, absorption, distribution, metabolism, excretion, and foundational pharmacology. These are essential in order to inform research into the molecular targets, cellular mechanisms, and creative use of early stage human clinical trials for designer kava modalities to inform and guide the design and execution of future randomized placebo controlled trials to maximize kava’s clinical efficacy and to minimize its risks.

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Adenosine 5'‐monophosphate‐activated protein kinase‐dependent mTOR pathway is involved in flavokawain B‐induced autophagy in thyroid cancer cells

Cited by 17 publications

References 39 publications

<p>Autophagy-Related Beclin 1 and Head and Neck Cancers</p>

<p>Autophagy-Related Beclin 1 and Head and Neck Cancers</p>

RETRACTED ARTICLE: Mesenchymal stem cell-derived exosomes exert ameliorative effects in type 2 diabetes by improving hepatic glucose and lipid metabolism via enhancing autophagy

Kava as a Clinical Nutrient: Promises and Challenges

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