Plasma Levels of Somatostatin and Gastrin in Sick Infants and Small for Gestational Age Infants

Marchini, Giovanna; Lagercrantz, Hugo; Milerad, Josef; Winberg, Jordan; Uvnäs‐Moberg, Kerstin

doi:10.1097/00005176-198809000-00003

Cited by 13 publications

(9 citation statements)

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“…Generally, DNA damage, nutrient depletion, and withdrawal of growth factors can all affect DNA replication, which in turn affects the cell cycle (Otto and Sicinski, 2017;Pietrzak et al, 2018). The G1 phase of cells is regulated by the interaction between cyclins and cyclin-dependent kinase (CDK), which in turn affects cell division (Hydbring et al, 2016;Swaffer et al, 2016), which are important for driving cells past checkpoints (Marchini et al, 1988). Importantly, obstacles to cell proliferation and differentiation are the two most important features of hematological malignancies.…”

Section: Discussionmentioning

confidence: 99%

LncRNA NR-104098 Inhibits AML Proliferation and Induces Differentiation Through Repressing EZH2 Transcription by Interacting With E2F1

Feng

et al. 2020

Front. Cell Dev. Biol.

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Abundant evidence has illustrated that long non-coding RNA (lncRNA) plays a vital role in the regulation of tumor development and progression. Most lncRNAs have been proven to have biological and clinical significance in acute myeloid leukemia (AML), but further investigation remains necessary. In this study, we investigated lncRNA NR-104098 in AML and its specific mechanism. The microarray analysis was performed on NB4 cells. Based on the related analysis results, we identified that lncRNA NR-104098 is a suppressor gene that is significantly upregulated in AML cells. LncRNA NR-104098 could inhibit proliferation and induce differentiation in AML cells in vitro and also play main role in the mouse xenografts. Mechanically, it was confirmed that lncRNA NR-104098 may effectively inhibit EZH2 transcription by directly binding to E2F1 and recruiting E2F1 to the EZH2 promoter. In addition, ATPR can significantly increase the expression of lncRNA NR-104098, whereas knocking down NR104098 can inhibit the inhibitory effect of ATPR on the proliferation and induction differentiation of AML cells. Taken together, these results lead to deeper insight into the mechanism of ATPR-induced AML differentiation and prevent proliferation by inhibiting EZH2 on the transcriptional level.

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Section: Discussionmentioning

confidence: 99%

LncRNA NR-104098 Inhibits AML Proliferation and Induces Differentiation Through Repressing EZH2 Transcription by Interacting With E2F1

Feng

et al. 2020

Front. Cell Dev. Biol.

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“…30,31 The interaction between cyclins and cyclin-dependent kinases (CDKs) regulates G1 phase and cell cycle progression as well as cell division, 32,33 which are important for driving cells past checkpoints. 34 The proliferation and differentiation abilities of cells are the two most important features of malignant cell behaviour. Targeting the cell cycle, proliferation and differentiation is a potential approach to treating leukaemia.…”

Section: Discussionmentioning

confidence: 99%

E2F4 functions as a tumour suppressor in acute myeloid leukaemia via inhibition of the MAPK signalling pathway by binding to EZH2

Feng

et al. 2020

J Cellular Molecular Medi

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Acute myeloid leukaemia (AML) is an aggressive and mostly incurable haematological malignancy with frequent relapse after an initial response to standard chemotherapy. Therefore, novel therapies are urgently required to improve AML clinical outcome. Here, we aim to study the dysregulation of a particular transcription factor, E2F4, and its role in the progression of AML. In this study, human clinical data from the Gene Expression Profiling Interactive Analysis (GEPIA) revealed that increased E2F4 expression was associated with poor prognosis in AML patients. Moreover, the experimental results showed that E2F4 was aberrantly overexpressed in human AML patients and cell lines. Depletion of E2F4 inhibited the proliferation, induced the differentiation and suppressed the growth of AML cells in a nude mouse model. By contrast, overexpression of E2F4 promoted the proliferation and inhibited the differentiation of AML cells in vitro. Additionally, E2F4 expression not only is positively correlated with EZH2 but also can bind to EZH2. RNA microarray results also showed that E2F4 can regulate MAPK signalling pathway. EZH2 can reverse the inhibitory effect of E2F4 silencing on MAPK signaling pathway. In summary, our data suggest that E2F4 may be a potential therapeutic target for AML therapy.

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“…Motilin, a stimu lant of motility [10], is supposed to be re leased in response to fetal distress [11] and in babies passing meconium prior to delivery [12]. Somatostatin on the other hand is inhibi tory to gut motility and its secretion is en hanced in sick newborns [13]. A study of the contribution of these hormones to first meco nium passage is however beyond the scope of this clinical study.…”

Section: Discussionmentioning

confidence: 99%

Effect of Mode of Delivery, Parity and Umbilical Blood Gas on First Meconium Passage in Full-Term Healthy Neonates

Tateishi

Yamauchi²,

Yamanouchi³

et al. 1994

Neonatology

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The various physiologic factors which might influence the time of first meconium passage were studied in 62 healthy full-term newborn infants. Thirty-two babies were born vaginally and 30 by elective cesarean section. Infants born vaginally were more acidotic and passed first stool earlier compared to those born by cesarean section. The same applies to vaginally delivered babies when comparing babies born to primipara and others. Acidosis is a presumed mechanism, and a role of gastrointestinal hormones is suggested to be the possible mediator of increased motility in these babies.

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Plasma Levels of Somatostatin and Gastrin in Sick Infants and Small for Gestational Age Infants

Cited by 13 publications

References 0 publications

LncRNA NR-104098 Inhibits AML Proliferation and Induces Differentiation Through Repressing EZH2 Transcription by Interacting With E2F1

LncRNA NR-104098 Inhibits AML Proliferation and Induces Differentiation Through Repressing EZH2 Transcription by Interacting With E2F1

E2F4 functions as a tumour suppressor in acute myeloid leukaemia via inhibition of the MAPK signalling pathway by binding to EZH2

Effect of Mode of Delivery, Parity and Umbilical Blood Gas on First Meconium Passage in Full-Term Healthy Neonates

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