ALC1 knockdown enhances cisplatin cytotoxicity of esophageal squamous cell carcinoma cells by inhibition of glycolysis through PI3K/Akt pathway

Li, Fangfang; Zhang, Zhen; Wang, Peng; Wen, Penghao; Xu, Quanxiao; Wang, Yunlong; Pan, Ping-Ying; Ma, Lei

doi:10.1016/j.lfs.2019.116679

Cited by 12 publications

(8 citation statements)

References 29 publications

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“…To investigate whether EA mediated protection of MCs following HG treatment via regulating the PI3K/Akt signaling pathway, HG-stimulated MCs were treated with EA (40 µM) and/or 740Y-P (10 µM) for 24 h ( 18 ). The results revealed that 740Y-P further increased intranuclear p-NF-κB levels and the phosphorylation of PI3K and Akt and decreased intranuclear FOXO3a and SOD2 expression levels.…”

Section: Resultsmentioning

confidence: 99%

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Ellagic acid inhibits high glucose‑induced injury in rat mesangial cells via the PI3K/Akt/FOXO3a signaling pathway

et al. 2021

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The pathological damage of mesangial cells serves an important role in the occurrence and development of diabetic nephropathy. Ellagic acid has been reported to possess antioxidant, antitumor, antiviral and anti-inflammatory properties in several diseases, but the roles of ellagic acid in diabetic nephropathy are unclear. The main aim of the present study was to investigate the effect of ellagic acid on high glucose-induced mesangial cell damage. The results revealed that high glucose could induce the hyperproliferation of mesangial cells, decrease the activity of superoxide dismutase, increase the malondialdehyde content, the level of reactive oxygen species, the secretion of inflammatory factors (TNF-α, IL-1β and IL-6) and the synthesis of extracellular matrix (Fibronectin, MMP-9 and TIMP-1) and activate the PI3K/Akt/FOXO3a signaling pathway. Ellagic acid could attenuate the injury of mesangial cells induced by high glucose in a concentration-dependent manner and its effect was consistent with that of a PI3K inhibitor (LY294002). Moreover, a PI3K agonist (740Y-P) reversed the protective effect of ellagic acid on mesangial cells induced by high glucose. In conclusion, ellagic acid protected mesangial cells from high glucose-induced injury in a concentration-dependent manner. The mechanism may be associated with ellagic acid inhibiting the activation of the PI3K/Akt signaling pathway and reducing the expression levels of downstream transcription factor FOXO3a.

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Section: Resultsmentioning

confidence: 99%

“…To examine whether EA mediated protection of MCs following HG treatment via the PI3K/Akt signaling pathway, HG-stimulated MCs were treated with EA (40 µM) and/or the PI3K agonist 740Y-P (10 µM, MedChemExpress) at 37˚C for 24 h ( 18 ).…”

Section: Methodsmentioning

confidence: 99%

Ellagic acid inhibits high glucose‑induced injury in rat mesangial cells via the PI3K/Akt/FOXO3a signaling pathway

et al. 2021

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“…Cisplatin, paclitaxel, and 5‐fluorouracil are widely used chemotherapeutic drugs for ESCC in clinics, but drug resistances occur commonly and reduce their therapeutic efficacy 26–28 . Previous research reported that many signaling pathways, such as AKT 29 and NFκB, 30 and biological processes such as glycolysis 31,32 influence cisplatin resistance in ESCC. In this paper, we detected whether CMA influences the chemoresistance of ESCC cells too.…”

Section: Discussionmentioning

confidence: 99%

Chaperone‐mediated autophagy affects tumor cell proliferation and cisplatin resistance in esophageal squamous cell carcinoma

et al. 2021

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Background Chaperone‐mediated autophagy (CMA) is a lysosomal degradation pathway of selective soluble proteins. Lysosomal membrane associated protein 2a (LAMP2a) is the lysosomal membrane receptor of CMA and influences CMA activity. Although it has been suggested that higher expression of LAMP2a is associated with more advanced tumor node metastasis (TNM) stages and shorter survival time in patients with esophageal squamous cell carcinoma (ESCC), the underlying mechanism has not been known yet. Methods In this study, we modulated the activity of CMA through LAMP2a or small molecular compounds in human ESCC cells to investigate its role in ESCC. Results We found that down‐regulating the activity of CMA could inhibit the proliferation and colony formation of ESCC cells as well as increase their sensitivity to cisplatin. Conclusions Our results promote better understanding of how CMA affects human ESCC and provide a new therapeutic target against ESCC through down‐regulating LAMP2a.

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“…In osteosarcoma tumour stem cells, PKM2 is highly expressed and downregulated with metformin, which reduces the uptake of glucose and the production of lactic acid and ATP, thereby increasing cell sensitivity to cisplatin (Shang et al, 2017). The oncogene ALC1 can promote cisplatin resistance in oesophageal cancer cells by activating glycolysis (F. Li et al, 2019). Glycolysis levels increased significantly in cisplatin-resistant T24 cells of bladder cancer, promoting acetate and fatty acid synthesis (Wen et al, 2019).…”

Section: Glycometabolism and Cisplatin Resistancementioning

confidence: 99%

The Role of Tumour Metabolism in Cisplatin Resistance

Wang

Zhao

et al. 2021

Front. Mol. Biosci.

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Cisplatin is a chemotherapy drug commonly used in cancer treatment. Tumour cells are more sensitive to cisplatin than normal cells. Cisplatin exerts an antitumour effect by interfering with DNA replication and transcription processes. However, the drug-resistance properties of tumour cells often cause loss of cisplatin efficacy and failure of chemotherapy, leading to tumour progression. Owing to the large amounts of energy and compounds required by tumour cells, metabolic reprogramming plays an important part in the occurrence and development of tumours. The interplay between DNA damage repair and metabolism also has an effect on cisplatin resistance; the molecular changes to glucose metabolism, amino acid metabolism, lipid metabolism, and other metabolic pathways affect the cisplatin resistance of tumour cells. Here, we review the mechanism of action of cisplatin, the mechanism of resistance to cisplatin, the role of metabolic remodelling in tumorigenesis and development, and the effects of common metabolic pathways on cisplatin resistance.

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ALC1 knockdown enhances cisplatin cytotoxicity of esophageal squamous cell carcinoma cells by inhibition of glycolysis through PI3K/Akt pathway

Cited by 12 publications

References 29 publications

Ellagic acid inhibits high glucose‑induced injury in rat mesangial cells via the PI3K/Akt/FOXO3a signaling pathway

Ellagic acid inhibits high glucose‑induced injury in rat mesangial cells via the PI3K/Akt/FOXO3a signaling pathway

Chaperone‐mediated autophagy affects tumor cell proliferation and cisplatin resistance in esophageal squamous cell carcinoma

The Role of Tumour Metabolism in Cisplatin Resistance

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