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LY6K Promotes Proliferation and Energy Metabolism of Lung Adenocarcinoma Cells by Regulating Aerobic Glycolysis

LY6K Promotes Proliferation and Energy Metabolism of Lung Adenocarcinoma Cells by Regulating Aerobic Glycolysis

Yan Wang1,2*, Lin Liu3, Na Li4, Yijun Zong1, Wei Liu1, Wenhua Xu1, Qi Wang1, Peijuan Zhang1 and Huiling Feng2,5*

1Department of Medical Nursing, College of Nursing, Hebei University of Chinese Medicine, China
2Key Laboratory for Health Care with Chinese Medicine of Hebei Province, Hebei University of Chinese Medicine, China
3Department of Biochemistry and Molecular Biology, College of Basic Medicine, Hebei University of Chinese Medicine, China
4Department of Oncology, Hebei General Hospital, China
5Department of Surgical Nursing, College of Nursing, Hebei University of Chinese Medicine, China
 
Yan Wang and Lin Liu contributed equally to this study.
 
* Corresponding author: wangyan_wy2022@126.com

ABSTRACT

The main objective of this study was to investigate the effects of lymphocyte antigen 6-complex K (LY6K) on aerobic glycolysis and proliferation of lung adenocarcinoma cells. Database analysis confirmed the association between LY6K expression and survival prognosis. Western blot was used to detect the protein expression of proteins. RT-PCR was used to detect the mRNA expression level of genes. Cell proliferation was discovered using the CCK8 test and plate cloning. The impact on the cell cycle was examined by using flow cytometry. The production of glycolytic enzymes and the significance of LY6K in the development of lung cancer in naked mice were both noted. The effects of LY6K knockdown on glucose uptake rate, lactic acid and energy metabolism of A549 cells were determined by UV spectrophotometry. According to data analysis from GEPIA2, TCGA, and Kaplan Meier plotter, lung adenocarcinoma exhibits high levels of LY6K expression and is associated with a poor prognosis. The expression of LY6K was most significant in A549 cells. In A549 cells, LY6K knockdown significantly inhibited cell proliferation and plate clonal formation (all p < 0.05), and inhibited tumor formation in nude mice (p < 0.01). The protein expression levels of GLUT1, HK2, PFKL, ALDOA, PGK-1, PKM2 and LDHA were down-regulated (all p < 0.05), and the glucose consumption and the contents of lactic acid and ATP were decreased (all p<0.05). To conclusion by regulating the production of enzymes involved in aerobic glycolysis, LY6K may encourage the proliferation and energy metabolism of A549 cells.

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Pakistan Journal of Zoology

June

Pakistan J. Zool., Vol. 56, Iss. 3, pp. 1001-1500

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