Anacardic acid induces cell apoptosis of prostatic cancer through autophagy by ER stress/DAPK3/Akt signaling pathway

Tan, Jianxin; Jiang, Xianzhen; Yin, Guangming; He, Leye; Liu, Jianye; Long, Zhi; Jiang, Ziying; Yao, Kun

doi:10.3892/or.2017.5841

Cited by 37 publications

(28 citation statements)

References 31 publications

(43 reference statements)

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“…In breast cancer cells, AA inhibited cell proliferation by modulating mitochondrial bioenergetics (Radde, Alizadeh‐Rad, Price, Schultz, & Klinge, ). Similar anticancer effects have also been observed in prostate cancer cells (Park et al, ; Tan et al, ). Therefore, AA, a natural compound, may be able to prevent metabolic diseases such as diabetes and cancer.…”

Section: Discussionsupporting

confidence: 74%

Anacardic acid mitigates liver fat accumulation and impaired glucose tolerance in mice fed a high‐fat and high‐sucrose diet

Chung

Shin

Choi

et al. 2020

Food Science & Nutrition

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In this study, we evaluated the effects of anacardic acid (AA), a phenolic lipid found in cashew nuts (Anacardium occidentale), on metabolic disorders related to obesity, fatty liver disease, and diabetes using both in vitro and in vivo models. The application of AA led to a reduction in lipid accumulation in 3T3‐L1 cells without observable cytotoxicity. Results from Western blot analysis revealed that AA treatment also led to decreased expression of fatty acid synthase and peroxisome proliferator‐activated receptor gamma. In vivo studies were performed to evaluate the effects of AA treatment on fatty liver disease and diabetes. Mice fed a high‐fat and high‐sucrose diet had significantly higher body and liver weights, and higher levels of liver fat, cholesterol, fasting glucose, and homeostasis model assessment of insulin resistance (HOMA‐IR). However, 12 weeks of oral treatment with 500 μg/kg BW AA slowed down lipid accumulation rates in the liver and mitigated insulin resistance in these mice. Thus, AA may reduce lipid levels and have an antidiabetic effect.

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Section: Discussionsupporting

confidence: 74%

Anacardic acid mitigates liver fat accumulation and impaired glucose tolerance in mice fed a high‐fat and high‐sucrose diet

Chung

Shin

Choi

et al. 2020

Food Science & Nutrition

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show abstract

“…and apoptosis ( 26 ). Overexpression of p-AKT is associated with advanced human prostate cancer ( 33 ). mTOR, a protein downstream of AKT, also serves a vital role in regulating cell proliferation, growth, differentiation and survival.…”

Section: Discussionmentioning

confidence: 99%

Long noncoding RNA HOTAIR promotes the proliferation and metastasis of osteosarcoma cells through the AKT/mTOR signaling pathway

Zhao

et al. 2017

Exp Ther Med

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It has been proven that long non-coding (lnc)RNAs serve an important role in the tumorigenesis and development of several types of human malignancy. Previous studies have demonstrated that the lncRNA Hox transcript antisense intergenic RNA (HOTAIR) is involved in the development various types of cancer, including osteosarcoma (OS). However, the underlying mechanisms by which it has an affect are still largely unknown. In the present study, it was observed that the expression of HOTAIR was significantly upregulated in OS tissues compared to matched adjacent normal tissues, using reverse transcription-quantitative polymerase chain reaction analysis. HOTAIR was silenced using specific small interfering RNA (siRNA/siR), siR-HOTAIR, in order to investigate its role in regulating OS cell proliferation, apoptosis, migration and invasion. siR-HOTAIR inhibited the proliferation of MG-63 cells due to the induction of G1 phase arrest. In addition, the results of in vitro assays demonstrated that the suppression of HOTAIR in MG-63 OS cells significantly reduced migration and invasion. The silencing of HOTAIR also significantly decreased the expression of matrix metalloproteinase (MMP) 2 and MMP9, but increased E-cadherin expression through regulating the RAC α serine/threonine protein kinase-mammalian target of rapamycin signaling pathway. The results indicated that siR-HOTAIR may be a potential OS therapy.

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“…However, whether TTF1-NP induces autophagy in human hepatoma and the relationship between autophagy and apoptosis remain unknown. Autophagy and apoptosis are topics of considerable interest in tumor research (18)(19)(20). In our study, TTF1-NP induced apoptosis, including changes to cell morphology and activation of the apoptosis-related protein caspase-3.…”

Section: Discussionmentioning

confidence: 61%

TTF1‑NP induces protective autophagy during apoptosis by inhibiting the Akt/mTOR pathway and activating JNK in human liver cancer cells

Zhang

Xiao

et al. 2018

Oncol Rep

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TTF1‑NP is a flavonoid nanoparticle based on 5,2',4'‑trihydroxy‑6,7,5'‑trimethoxyflavone (TTF1), which is derived from the medicinal plant Sorbaria sorbifolia that grows in the Changbai Mountain. We previously demonstrated antitumor effects of TTF1‑NP in human hepatoma including induction of apoptosis and inhibition of angiogenesis, migration and invasion. Herein, we examined the effects of TTF1‑NP on autophagy and its relationship with apoptosis, and explored potential underlying mechanisms in human hepatoma cell lines. We conducted cell viability assays, Annexin V/propidium iodide double staining, Hoechst staining, monodansylcadaverine staining, transmission electron microscopy, green fluorescent protein‑light chain 3 plasmid transfection and western blots. We found that TTF1‑NP induced apoptosis and autophagy in HepG2 and SMMC‑7721 cells. Pretreatment with the autophagy inhibitor 3‑methyladenine promoted TTF1‑NP‑induced apoptosis. TTF1‑NP decreased levels of phosphorylated (p)‑Akt, p‑mTOR and p‑ERK1/2 and increased p‑JNK levels in the two cell lines. Treating cells with insulin, SP600125 and U0126 indicated that the Akt/mTOR pathway and JNK were involved in TTF1‑NP‑induced autophagy. Together, these findings suggest that TTF1‑NP induced protective apoptosis‑related autophagy by modulating the Akt/mTOR and JNK pathways in HepG2 and SMMC‑7721 cells. Therefore, autophagy may be a potential target for TTF1‑NP in human hepatoma therapy.

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Anacardic acid induces cell apoptosis of prostatic cancer through autophagy by ER stress/DAPK3/Akt signaling pathway

Cited by 37 publications

References 31 publications

Anacardic acid mitigates liver fat accumulation and impaired glucose tolerance in mice fed a high‐fat and high‐sucrose diet

Anacardic acid mitigates liver fat accumulation and impaired glucose tolerance in mice fed a high‐fat and high‐sucrose diet

Long noncoding RNA HOTAIR promotes the proliferation and metastasis of osteosarcoma cells through the AKT/mTOR signaling pathway

TTF1‑NP induces protective autophagy during apoptosis by inhibiting the Akt/mTOR pathway and activating JNK in human liver cancer cells

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