MicroRNA-9 restrains the sharp increase and boost apoptosis of human acute myeloid leukemia cells by adjusting the Hippo/YAP signaling pathway

Wang, Guoqing; Yu, Xiuwen; Xia, Jiajia; Sun, Jie; Huang, Haiyan; Liu, Yeqiong

doi:10.1080/21655979.2021.1915727

Cited by 12 publications

(5 citation statements)

References 31 publications

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“…It was reported that pyruvate kinase M1/2 (PKM) controlled the proteins level of cell apoptosis and proliferation-related genes by activating Hippo signaling pathway ( Luo et al, 2021 ). MiR-9 was found to promote apoptosis in human acute myeloid leukemia cells by regulating the Hippo-YAP signaling pathway ( Wang et al, 2021 ). P62/SQSTM1 co-located with the hippocampal signaling modulator Dachs and inactivated the Hippo signaling pathway, leading to excessive non-cellular proliferation of stem cells ( Nagai et al, 2021 ).…”

Section: Discussionmentioning

confidence: 99%

MiR-34a-5p promotes autophagy and apoptosis of ovarian granulosa cells via the Hippo-YAP signaling pathway by targeting LEF1 in chicken

Han¹,

Zhao²,

Zhang³

et al. 2023

Poultry Science

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Section: Discussionmentioning

confidence: 99%

MiR-34a-5p promotes autophagy and apoptosis of ovarian granulosa cells via the Hippo-YAP signaling pathway by targeting LEF1 in chicken

Han¹,

Zhao²,

Zhang³

et al. 2023

Poultry Science

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“…We have similarly demonstrated that the MAPK12 gene was upregulated at MDS diagnosis and downregulated in normal BM colonies after four cycles of treatment (25). The Hippo signaling pathway interacts with other growth control and cell proliferation pathways such as PI3-AKT, TGF-b, RAS-MAP kinase, JAK/ STAT, Notch, and Wnt signaling through YAP (Yes-associated protein) activation (28), and the downregulation of miR-9 and miR-550-1 is postulated to contribute to AML pathogenesis through inhibition of their tumor suppressor functions on the Hippo and YAP signaling pathways (29,30). In CML, the downregulation of miR-181a resulted in the decreased activation of YAP and restored sensitivity to the tyrosine kinase inhibitor imatinib (31).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA profiling in aplastic anemia reveals similarities between secondary myelodysplastic syndromes arising from clonal progression and de novo MDS

Chee,

Koldej,

Thio

et al. 2023

Front. Hematol.

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Aplastic anemia (AA) is a form of bone marrow failure (BMF) resulting in significant cytopenias and may progress with clonal evolution to myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML). MicroRNA expression is dysregulated in MDS/AML, but there are limited studies on its role in the pathogenesis of AA. Using stored bone marrow (BM) samples (n=81) from 52 patients collected between 2006 and 2019, we demonstrate key differences in miRNA expression between AA patients at diagnosis and de novo MDS patients (n=21). The five most significantly upregulated miRNAs in MDS patients (downregulated in AA) were miR-130a-3p, miR-221-3p, miR-126-3p, miR-27b-3p, and miR-196b-5p (adjusted p<0.001). However, at the time of AA clonal progression to secondary MDS/AML, no significant miRNA-based differences were identified, suggesting that the underlying mechanistic pathways between AA progression to MDS/AML and de novo MDS are similar. At diagnosis, miR-127-3p, miR-1271-5p, miR-301b-5p, miR-3934-5p, and miR-4531 (adjusted p=0.081) were upregulated in those whose AA eventually progressed in comparison with those without eventual clonal progression. Longitudinal molecular mutational analysis of myeloid genes in AA patients with disease progression revealed the acquisition of new mutations, mostly at the time of MDS/AML progression, with four patients developing mutations prior to morphological MDS progression. In contrast, no myeloid gene mutations were detected at diagnosis or follow-up in AA patients with no clonal progression. Using KEGG pathway analysis derived from miRPathDBv2.0, cytokine–cytokine receptor interaction, TGF-β, MAP kinase, prolactin, Hippo, neurotrophin, and FOXO signaling pathways were enriched in AA patients with clonal progression to MDS/AML; these pathways were similarly enriched in the de novo MDS cohort. These studies highlight the differing miRNA expression profiles in AA and MDS, in AA clonal evolution to MDS/AML, and the potential interplay with myeloid gene mutations acquired at the time of disease progression.

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“…The Hippo-YAP signalling pathway is an evolutionally conserved pathway that is associated with tumour development (50)(51)(52)(53)(54). YAP is a downstream effector of this pathway (55).…”

Section: Discussionmentioning

confidence: 99%

Hydroxyacyl-CoA dehydrogenase trifunctional multienzyme complex subunit beta gene as a tumour suppressor in stomach adenocarcinoma

Xiong

Zhang

et al. 2022

Front. Oncol.

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BackgroundStomach adenocarcinoma (STAD) is the most common type of gastric cancer. In this study, the functions and potential mechanisms of hydroxyacyl-CoA dehydrogenase trifunctional multienzyme complex subunit beta (HADHB) in STAD were explored.MethodsDifferent bioinformatics analyses were performed to confirm HADHB expression in STAD. HADHB expression in STAD tissues and cells was also evaluated using western blot, qRT-PCR, and immunohistochemistry. Further, the viability, proliferation, colony formation, cell cycle determination, migration, and wound healing capacity were assessed, and the effects of HADHB on tumour growth, cell apoptosis, and proliferation in nude mice were determined. The upstream effector of HADHB was examined using bioinformatics analysis and dual luciferase reporter assay. GSEA was also employed for pathway enrichment analysis and the expression of Hippo-YAP pathway-related proteins was detected.ResultsThe expression of HADHB was found to be low in STAD tissues and cells. The upregulation of HADHB distinctly repressed the viability, proliferation, colony formation, cell cycle progression, migration, invasion, and wound healing of HGC27 cells, while knockdown of HADHB led to opposite effects. HADHB upregulation impeded tumour growth and cell proliferation, and enhanced apoptosis in nude mice. KLF4, whose expression was low in STAD, was identified as an upstream regulator of HADHB. KLF4 upregulation abolished the HADHB knockdown-induced tumour promoting effects in AGS cells. Further, HADHB regulates the Hippo-YAP pathway, which was validated using a pathway rescue assay. Low expression of KLF4 led to HADHB downregulation in STAD.ConclusionHADHB might function as a tumour suppressor gene in STAD by regulation the Hippo-YAP pathway.

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MicroRNA-9 restrains the sharp increase and boost apoptosis of human acute myeloid leukemia cells by adjusting the Hippo/YAP signaling pathway

Cited by 12 publications

References 31 publications

MiR-34a-5p promotes autophagy and apoptosis of ovarian granulosa cells via the Hippo-YAP signaling pathway by targeting LEF1 in chicken

MiR-34a-5p promotes autophagy and apoptosis of ovarian granulosa cells via the Hippo-YAP signaling pathway by targeting LEF1 in chicken

MicroRNA profiling in aplastic anemia reveals similarities between secondary myelodysplastic syndromes arising from clonal progression and de novo MDS

Hydroxyacyl-CoA dehydrogenase trifunctional multienzyme complex subunit beta gene as a tumour suppressor in stomach adenocarcinoma

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