Inhibition of cell proliferation and induction of autophagy by KDM2B/FBXL10 knockdown in gastric cancer cells

Zhao, Erhu; Tang, Chunling; Jiang, Xiaolan; Weng, Xiong; Zhong, Xiaoxia; Zhang, Dunke; Hou, Jingyao; Wang, Feng; Huang, Mengying; Cui, Hongjuan

doi:10.1016/j.cellsig.2017.05.011

Cited by 32 publications

(23 citation statements)

References 39 publications

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“…The rats were randomly allocated to experimental groups. The left anterior descending (LAD) coronary artery was ligated to reproduce myocardial I/R model, as described before [9].…”

Section: Animals and Groupsmentioning

confidence: 99%

“…Some researchers reported FBXL10 exerted its H3K36 demethylase activity at different genome sites, and played an important role in anti-tumor activities by regulating cell proliferation and inhibiting apoptosis [8]. Furthermore, the deletion of the full-length isform of FBXL10 leads to an abnormal increase in cell proliferation and apoptosis [9], accompanied by neural tube defects, suggesting that FBXL10 is involved in the regulation of proliferation and apoptosis in the early stages of neurogenesis. Although the protective role of FBXL10 in inhibiting apoptosis in cerebrovascular disease and tumors has been demonstrated, the potential protective effect in cardiovascular disease is still unclear.…”

Section: Introductionmentioning

confidence: 99%

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Protective effect of FBXL10 in myocardial ischemia reperfusion injury via inhibiting endoplasmic reticulum stress

Gao

Guo

Liu

et al. 2020

Respiratory Medicine

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“…The rats were randomly allocated to experimental groups. The left anterior descending (LAD) coronary artery was ligated to reproduce myocardial I/R model, as described before [9].…”

Section: Animals and Groupsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Protective effect of FBXL10 in myocardial ischemia reperfusion injury via inhibiting endoplasmic reticulum stress

Gao

Guo

Liu

et al. 2020

Respiratory Medicine

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“…Autophagy is an evolutionarily conserved catabolic process that provides pro-survival advantages to cells under stressful conditions, such as nutrient inadequacy, hypoxia and microbial infection [ 18 , 19 ]. The most famous regulator of autophagy is the mammalian target of rapamycin, a serine/threonine kinase that activated by metabolic stimuli, including amino acids, growth factors, and energy sufficiency [ 20 – 23 ]. Typically, the classic mTOR signaling pathway is considered to be crucial negative regulator for the formation of autophagosomes, where mTOR activation by nutrients and growth factors leads to inhibition of autophagy through the phosphorylation of multiple autophagy-related proteins that promote autophagy initiation and autophagosomes nucleation [ 24 – 26 ].…”

Section: Introductionmentioning

confidence: 99%

NUCKS promotes cell proliferation and suppresses autophagy through the mTOR-Beclin1 pathway in gastric cancer

Zhao

Feng

Bai

et al. 2020

J Exp Clin Cancer Res

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Background Nuclear casein kinase and cyclin-dependent kinase substrate (NUCKS), a novel gene first reported in 2001, is a member of the high mobility group (HMG) family. Although very little is known regarding the biological roles of NUCKS, emerging clinical evidence suggests that the NUCKS protein can be used as a biomarker and therapeutic target in various human ailments, including several types of cancer. Methods We first assessed the potential correlation between NUCKS expression and gastric cancer prognosis. Then functional experiments were conducted to evaluate the effects of NUCKS in cell proliferation, cell cycle, apoptosis and autophagy. Finally, the roles of NUCKS on gastric cancer were examined in vivo. Results We found that NUCKS was overexpressed in gastric cancer patients with poor prognosis. Through manipulating NUCKS expression, it was observed to be positively associated with cell proliferation in vitro and in vivo. NUCKS knockdown could induce cell cycle arrest and apoptosis. Then further investigation indicated that NUCKS knockdown could also significantly induce a marked increase in autophagy though the mTOR-Beclin1 pathway, which could be was rescued by NUCKS restoration. Moreover, silencing Beclin1 in NUCKS knockdown cells or adding rapamycin in NUCKS-overexpressed cells also confirmed these results. Conclusions Our findings revealed that NUCKS functions as an oncogene and an inhibitor of autophagy in gastric cancer. Thus, the downregulation or inhibition of NUCKS may be a potential therapeutic strategy for gastric cancer.

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“…On the other hand, in close support with our view that autophagy is decreased during CG, we have detected three genes ( KDM2B, MKL1 and PFKFB3 ) that inhibit autophagy and are upregulated in RE pigs (Additional file 3 : Table S3). The downregulation of KDM2B (Lysine-specific demethylase 2B) in gastric cancer cells immediately induces autophagy followed by an inhibition of cell proliferation [ 48 ], and the inactivation of Megakaryoblastic Leukemia (Translocation) 1 ( MKL1 ) gene in mouse embryos causes myocardial cell necrosis that could be the consequence of a decreased ability of the myocardium to cope with environmental stresses [ 49 ]. The case of the PFKFB3 gene, the most upregulated gene in RE vs AL animals, is even more enlightening.…”

Section: Discussionmentioning

confidence: 99%

Role of AMPK signalling pathway during compensatory growth in pigs

et al. 2018

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BackgroundThe molecular basis of compensatory growth in monogastric animals has not yet been fully explored. Herewith, in this study we aim to determine changes in the pig skeletal muscle transcriptome profile during compensatory growth following a feed restriction period. A RNA-Seq experiment was performed with a total of 24 females belonging to a Duroc commercial line. Half of the animals received either a restricted (RE) or ad libitum (AL) diet during the first fattening period (60–125 d of age). After that, all gilts were fed ad libitum for a further ~30 d until the age of ~155 d, when animals were slaughtered and samples of gluteus medius muscle were harvested to perform RNA-Seq analyses and intramuscular fat content determination.ResultsDuring the period following food restriction, RE animals re-fed ad libitum displayed compensatory growth, showed better feed conversion rate and tended to deposit more subcutaneous fat than AL fed animals. Animals were slaughtered in the phase of accelerated growth, when RE animals had not completely compensated the performance of AL group, showing lower live and carcass weights. At intramuscular level, RE gilts showed a higher content of polyunsaturated fatty acids during the compensatory growth phase. The comparison of RE and AL expression profiles allowed the identification of 86 (ǀlog2Fold-Changeǀ > 1, padj < 0.05) differentially expressed (DE) genes. A functional categorization of these DE genes identified AMPK Signaling as the most significantly enriched canonical pathway. This kinase plays a key role in the maintenance of energy homeostasis as well as in the activation of autophagy. Among the DE genes identified as components of AMPK Signaling pathway, five out of six genes were downregulated in RE pigs.ConclusionsAnimals re-fed after a restriction period exhibited a less oxidative metabolic profile and catabolic processes in muscle than animals fed ad libitum. The downregulation of autophagy observed in the skeletal muscle of pigs undergoing compensatory growth may constitute a mechanism to increase muscle mass thus ensuring an accelerated growth rate. These results reveal that the downregulation of AMPK Signaling plays an important role in compensatory growth in pigs.Electronic supplementary materialThe online version of this article (10.1186/s12864-018-5071-5) contains supplementary material, which is available to authorized users.

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Inhibition of cell proliferation and induction of autophagy by KDM2B/FBXL10 knockdown in gastric cancer cells

Cited by 32 publications

References 39 publications

Protective effect of FBXL10 in myocardial ischemia reperfusion injury via inhibiting endoplasmic reticulum stress

Protective effect of FBXL10 in myocardial ischemia reperfusion injury via inhibiting endoplasmic reticulum stress

NUCKS promotes cell proliferation and suppresses autophagy through the mTOR-Beclin1 pathway in gastric cancer

Role of AMPK signalling pathway during compensatory growth in pigs

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