Eicosapentaenoic acid induced SKOV-3 cell apoptosis through ERK1/2–mTOR–NF-κB pathways

Han, Lirong; Zhang, Yuanyuan; Meng, Meng; Cheng, Donghui

doi:10.1097/cad.0000000000000373

Cited by 14 publications

(8 citation statements)

References 34 publications

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“…A study conducted by Ge et al () once demonstrated that HTEA reduced myocardial cell apoptosis, decreased myocardial infraction size and myocardial abnormalities. Another previous study showed that mTOR/NF‐κB signaling pathway could act as a mediator to influence cell apoptosis (Han, Zhang, Meng, Cheng, & Wang, ). Besides, according to a relevant research, the inhibition of NF‐κB signaling pathway increased the anti‐apoptotic factor Bcl‐2 and decreased the pro‐apoptotic factors Bax and Fasl (Mattson, ).…”

Section: Discussionmentioning

confidence: 99%

Retracted: Effects of mTOR/NF‐κB signaling pathway and high thoracic epidural anesthesia on myocardial ischemia‐reperfusion injury via autophagy in rats

Huang

Wen

Lin

et al. 2018

Journal Cellular Physiology

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We investigated the role of mammalian target of rapamycin/nuclear factor-kappa B (mTOR/NF-κB) signaling pathway in high thoracic epidural anesthesia (HTEA) against myocardial ischemia-reperfusion (I/R) injury in rats. The rat model of myocardial I/R injury was established. Ninety rats were divided into the normal, sham, I/R, eHTEA, the PDTC, and HTEA + PDTC groups. ELISA was applied to detect cardiac function indexes. HE staining was conducted to observe histopathological changes of myocardial tissues, and TTC staining was performed to detect the myocardial infarction size. TUNEL staining was adopted to detect the cell apoptosis rate. The mRNA and protein levels of mTOR, NF-κB, Fasl, Bcl-2 and Bax, and LC3-I, LC3-II, BNIP3, and Atg5 were detected by RT-qPCR and Western blotting, respectively. The findings indicated that compared with the normal and sham groups, the I/R, PDTC, and HTEA groups showed the larger myocardial infarction size and increased cell apoptosis rate, while the results in the HTEA + PDTC group were opposite. Compared with the normal and sham groups, the I/R group showed reduced mRNA and protein levels of Bcl-2, LC3, BNIP3, and Atg5, and elevated mRNA and protein levels of mTOR, p50, p65, Bax, and Fasl, while the HTEA + PDTC group revealed the opposite results, and the PDTC and HTEA group revealed the increased mRNA and protein levels of Bcl-2, LC3, BNIP3, Atg5, mTOR, p50, p65, Bax, and Fasl. These results prove that the inhibition of mTOR/NF-κB signaling pathway potentiates HTEA against myocardial IR injury by autophagy and apoptosis in rats.

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Section: Discussionmentioning

confidence: 99%

Retracted: Effects of mTOR/NF‐κB signaling pathway and high thoracic epidural anesthesia on myocardial ischemia‐reperfusion injury via autophagy in rats

Huang

Wen

Lin

et al. 2018

Journal Cellular Physiology

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“…DHA reduced proliferation of the MHCC97L human metastatic hepatocarcinoma line through the inhibition of cyclin A/CDK2 [236]. EPA induced SKOV-3 ovarian cancer cells apoptosis via ERK1/2-mTOR-NF-κB pathways [237]. DHA and ALA decreased viability of ovarian cancer cells (SKOV3, A2780, HO8910), but only DHA also inhibited invasion and metastasis, via multiple molecular pathways [238].…”

Section: ω-3 Pufasmentioning

confidence: 99%

Dietary Fat and Cancer—Which Is Good, Which Is Bad, and the Body of Evidence

Bojková

Winklewski

Wszędybył-Winklewska

2020

IJMS

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A high-fat diet (HFD) induces changes in gut microbiota leading to activation of pro-inflammatory pathways, and obesity, as a consequence of overnutrition, exacerbates inflammation, a known risk factor not only for cancer. However, experimental data showed that the composition of dietary fat has a greater impact on the pathogenesis of cancer than the total fat content in isocaloric diets. Similarly, human studies did not prove that a decrease in total fat intake is an effective strategy to combat cancer. Saturated fat has long been considered as harmful, but the current consensus is that moderate intake of saturated fatty acids (SFAs), including palmitic acid (PA), does not pose a health risk within a balanced diet. In regard to monounsaturated fat, plant sources are recommended. The consumption of plant monounsaturated fatty acids (MUFAs), particularly from olive oil, has been associated with lower cancer risk. Similarly, the replacement of animal MUFAs with plant MUFAs decreased cancer mortality. The impact of polyunsaturated fatty acids (PUFAs) on cancer risk depends on the ratio between ω-6 and ω-3 PUFAs. In vivo data showed stimulatory effects of ω-6 PUFAs on tumour growth while ω-3 PUFAs were protective, but the results of human studies were not as promising as indicated in preclinical reports. As for trans FAs (TFAs), experimental data mostly showed opposite effects of industrially produced and natural TFAs, with the latter being protective against cancer progression, but human data are mixed, and no clear conclusion can be made. Further studies are warranted to establish the role of FAs in the control of cell growth in order to find an effective strategy for cancer prevention/treatment.

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“…The alterations induced by ω-3 PUFA in membranes can substantially modulate important signaling pathways for cancer development. As a result, they can reduce the expression/activity of the nuclear transcription factor-κB (NF-κB) in several kinds of cancer cells, thus inducing apoptosis [ 53 , 54 , 55 , 56 ]. ω-3 PUFA can also inhibit cancer cell growth by altering the levels of several factors involved in the progression of the cell cycle, such as cyclins, cyclin-dependent kinases and retinoblastoma protein [ 31 ].…”

Section: ω-3 Pufa and Cancermentioning

confidence: 99%

Protective Effects of ω-3 PUFA in Anthracycline-Induced Cardiotoxicity: A Critical Review

Serini

Vasconcelos

Gomes

et al. 2017

IJMS

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It has been demonstrated that ω-3 polyunsaturated fatty acids (ω-3 PUFA) may exert a beneficial role as adjuvants in the prevention and treatment of many disorders, including cardiovascular diseases and cancer. Particularly, several in vitro and in vivo preclinical studies have shown the antitumor activity of ω-3 PUFA in different kinds of cancers, and several human studies have shown that ω-3 PUFA are able to decrease the risk of a series of cardiovascular diseases. Several mechanisms have been proposed to explain their pleiotropic beneficial effects. ω-3 PUFA have also been shown to prevent harmful side-effects (including cardiotoxicity and heart failure) induced by conventional and innovative anti-cancer drugs in both animals and patients. The available literature regarding the possible protective effects of ω-3 PUFA against anthracycline-induced cardiotoxicity, as well as the mechanisms involved, will be critically discussed herein. The study will analyze the critical role of different levels of ω-3 PUFA intake in determining the results of the combinatory studies with anthracyclines. Suggestions for future research will also be considered.

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Eicosapentaenoic acid induced SKOV-3 cell apoptosis through ERK1/2–mTOR–NF-κB pathways

Cited by 14 publications

References 34 publications

Retracted: Effects of mTOR/NF‐κB signaling pathway and high thoracic epidural anesthesia on myocardial ischemia‐reperfusion injury via autophagy in rats

Retracted: Effects of mTOR/NF‐κB signaling pathway and high thoracic epidural anesthesia on myocardial ischemia‐reperfusion injury via autophagy in rats

Dietary Fat and Cancer—Which Is Good, Which Is Bad, and the Body of Evidence

Protective Effects of ω-3 PUFA in Anthracycline-Induced Cardiotoxicity: A Critical Review

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