Gamma linolenic acid suppresses hypoxia-induced proliferation and invasion of non-small cell lung cancer cells by inhibition of HIF1α

Wang, Yan; Shi, Jian; Gong, Liya

doi:10.1007/s13258-020-00961-5

Cited by 11 publications

(7 citation statements)

References 22 publications

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“…Similar to our results, PA treatment significantly increased the apoptosis level, upregulated mRNA expression levels of BAX , caspase 3, and caspase 9, and inhibited autophagy, degrading autophagy-related protein Beclin-1, in human hepatocytes. In this study, GLA moderated PA-induced apoptosis in AML-12, decreasing the apoptosis cell percentage with high expression of BCL2. − Consequently, GLA can protect against lipid metabolism disorders by balancing autophagy and apoptosis in PA-treated hepatocytes.…”

Section: Discussionmentioning

confidence: 62%

γ-Linolenic Acid Prevents Lipid Metabolism Disorder in Palmitic Acid-Treated Alpha Mouse Liver-12 Cells by Balancing Autophagy and Apoptosis via the LKB1-AMPK-mTOR Pathway

Liang

Zhang

et al. 2021

J. Agric. Food Chem.

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Excessive fat deposition is the main character in nonalcoholic fatty liver disease (NAFLD), while γ-linolenic acid (GLA) is a polyunsaturated fatty acid that can reduce lipid deposition. This study investigated the effect and regulatory mechanism of GLA (100 μM) on lipid metabolism in alpha mouse liver 12 (AML-12) cells treated by 400 μM palmitic acid (PA). GLA reduced lipid content and increased fatty acid β oxidation, as indicated by decreasing triglyceride and cholesterol contents and increasing mRNA and protein expressions of CPT1α and PPARα. GLA relieved oxidative stress caused by PA, upregulated mRNA levels of superoxide dismutase and glutathione peroxidase, and decreased reactive oxygen species content. GLA reduced apoptosis, as indicated by decreases in the BAX/BCL2 expression level and apoptosis percentage. GLA activated autophagy, autophagosome-lysosome fusion, and LKB1-AMPK-mTOR signaling and upregulated mRNA and protein expressions of Beclin-1, autophagy-related 5, and liver kinase B1 (LKB1). These effects of GLA on lipid metabolism disorders of PA-treated hepatocytes were reversed by autophagy inhibitor 3MA and AMPK inhibitor compound C, confirming our conclusions. Overall, GLA can protect AML-12 cells from lipid metabolism disorder caused by PA via balancing autophagy and apoptosis mediated by the LKB1-AMPK-mTOR pathway. Consequently, GLA, as a dietary supplement, can help to prevent and treat NAFLD by regulating lipid metabolism and autophagy.

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Section: Discussionmentioning

confidence: 62%

γ-Linolenic Acid Prevents Lipid Metabolism Disorder in Palmitic Acid-Treated Alpha Mouse Liver-12 Cells by Balancing Autophagy and Apoptosis via the LKB1-AMPK-mTOR Pathway

Liang

Zhang

et al. 2021

J. Agric. Food Chem.

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“…Dietary supplementation with gamma-linolenic acid was shown to inhibit the growth of a human lung carcinoma implanted in nude mice [ 76 ]. In vitro experiments also confirmed that gamma-linolenic acid was effective in inhibiting the migration and invasion of NSCLC cells [ 77 ].…”

Section: Discussionmentioning

confidence: 99%

Identification of Candidate lncRNA and Pseudogene Biomarkers Associated with Carbon-Nanotube-Induced Malignant Transformation of Lung Cells and Prediction of Potential Preventive Drugs

Chang

Xie

et al. 2022

IJERPH

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Mounting evidence has linked carbon nanotube (CNT) exposure with malignant transformation of lungs. Long non-coding RNAs (lncRNAs) and pseudogenes are important regulators to mediate the pathogenesis of diseases, representing potential biomarkers for surveillance of lung carcinogenesis in workers exposed to CNTs and possible targets to develop preventive strategies. The aim of this study was to screen crucial lncRNAs and pseudogenes and predict preventive drugs. GSE41178 (small airway epithelial cells exposed to single- or multi-walled CNTs or dispersant control) and GSE56104 (lung epithelial cells exposed to single-walled CNTs or dispersant control) datasets were downloaded from the Gene Expression Omnibus database. Weighted correlation network analysis was performed for these two datasets, and the turquoise module was preserved and associated with CNT-induced malignant phenotypes. In total, 24 lncRNAs and 112 pseudogenes in this module were identified as differentially expressed in CNT-exposed cells compared with controls. Four lncRNAs (MEG3, ARHGAP5-AS1, LINC00174 and PVT1) and five pseudogenes (MT1JP, MT1L, RPL23AP64, ZNF826P and TMEM198B) were predicted to function by competing endogenous RNA (MEG3/RPL23AP64-hsa-miR-942-5p-CPEB2/PHF21A/BAMBI; ZNF826P-hsa-miR-23a-3p-SYNGAP1, TMEM198B-hsa-miR-15b-5p-SYNGAP1/CLU; PVT1-hsa-miR-423-5p-PSME3) or co-expression (MEG3/MT1L/ZNF826P/MT1JP-ATM; ARHGAP5-AS1-TMED10, LINC00174-NEDD4L, ARHGAP5-AS1/PVT1-NIP7; MT1L/MT1JP-SYNGAP1; MT1L/MT1JP-CLU) mechanisms. The expression levels and prognosis of all genes in the above interaction pairs were validated using lung cancer patient samples. The receiver operating characteristic curve analysis showed the combination of four lncRNAs, five pseudogenes or lncRNAs + pseudogenes were all effective for predicting lung cancer (accuracy >0.8). The comparative toxicogenomics database suggested schizandrin A, folic acid, zinc or gamma-linolenic acid may be preventive drugs by reversing the expression levels of lncRNAs or pseudogenes. In conclusion, this study highlights lncRNAs and pseudogenes as candidate diagnostic biomarkers and drug targets for CNT-induced lung cancer.

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“…Afterwards, the cells were incubated with 0.5 mg/mL of MTT solution for 3 h before being dissolved in DMSO. Optical density was detected at 540 nm by a microplate reader (VERSA Max, Molecular Device Co., Sunnyvale, CA, USA) as previously described [ 54 ]. The cellular morphology was observed using an inverted microscope (Carl Zeiss, Oberkochen, Germany).…”

Section: Methodsmentioning

confidence: 99%

Spermidine Attenuates Oxidative Stress-Induced Apoptosis via Blocking Ca2+ Overload in Retinal Pigment Epithelial Cells Independently of ROS

Kim

Kim²,

Hwangbo

et al. 2021

IJMS

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Retinal pigment epithelial (RPE) cells occupy the outer layer of the retina and perform various biological functions. Oxidative damage to RPE cells is a major risk factor for retinal degeneration that ultimately leads to vision loss. In this study, we investigated the role of spermidine in a hydrogen peroxide (H2O2)-induced oxidative stress model using human RPE cells. Our findings showed that 300 μM H2O2 increased cytotoxicity, apoptosis, and cell cycle arrest in the G2/M phase, whereas these effects were markedly suppressed by 10 μM spermidine. Furthermore, spermidine significantly reduced H2O2-induced mitochondrial dysfunction including mitochondrial membrane potential and mitochondrial activity. Although spermidine displays antioxidant properties, the generation of intracellular reactive oxygen species (ROS) upon H2O2 insult was not regulated by spermidine. Spermidine did suppress the increase in cytosolic Ca2+ levels resulting from endoplasmic reticulum stress in H2O2-stimulated human RPE cells. Treatment with a cytosolic Ca2+ chelator markedly reversed H2O2-induced cellular dysfunction. Overall, spermidine protected against H2O2-induced cellular damage by blocking the increase of intracellular Ca2+ independently of ROS. These results suggest that spermidine protects RPE cells from oxidative stress, which could be a useful treatment for retinal diseases.

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Gamma linolenic acid suppresses hypoxia-induced proliferation and invasion of non-small cell lung cancer cells by inhibition of HIF1α

Cited by 11 publications

References 22 publications

γ-Linolenic Acid Prevents Lipid Metabolism Disorder in Palmitic Acid-Treated Alpha Mouse Liver-12 Cells by Balancing Autophagy and Apoptosis via the LKB1-AMPK-mTOR Pathway

γ-Linolenic Acid Prevents Lipid Metabolism Disorder in Palmitic Acid-Treated Alpha Mouse Liver-12 Cells by Balancing Autophagy and Apoptosis via the LKB1-AMPK-mTOR Pathway

Identification of Candidate lncRNA and Pseudogene Biomarkers Associated with Carbon-Nanotube-Induced Malignant Transformation of Lung Cells and Prediction of Potential Preventive Drugs

Spermidine Attenuates Oxidative Stress-Induced Apoptosis via Blocking Ca2+ Overload in Retinal Pigment Epithelial Cells Independently of ROS

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