Nuclear scaffold protein p54nrb/NONO facilitates the hypoxia-enhanced progression of hepatocellular carcinoma

Shen, Mingxue; Zhang, Ruixue; Jia, Wenzhi; Zhu, Zongping; Zhao, Xiaoping; Zhao, Li; Huang, Gang; Li, Jianjun

doi:10.1038/s41388-021-01848-9

Cited by 19 publications

(13 citation statements)

References 41 publications

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“…52 In addition, NONO is involved ERK1/2, PI3K/AKT signaling pathways in cancer cells. 53,54 In the present study, we found that NONO deficiency impaired BCR-induced multiple signaling pathways in primary B cells, which include PI3K-AKT, ERK1/2 and NF-κB pathways. The mechanism on how NONO regulates BCR signaling is unclear.…”

Section: Discussionsupporting

confidence: 52%

“…For instance, NONO directly interacts with ERK1/2 and thus regulates PDGF‐induced ERK1/2 activation in vascular smooth muscle cells 35 ; NONO interacts with NF‐κB and thus enhances NF‐κB nuclear translocation and phosphorylation 52 . In addition, NONO is involved ERK1/2, PI3K/AKT signaling pathways in cancer cells 53,54 . In the present study, we found that NONO deficiency impaired BCR‐induced multiple signaling pathways in primary B cells, which include PI3K‐AKT, ERK1/2 and NF‐κB pathways.…”

Section: Discussionsupporting

confidence: 51%

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NONO regulates B‐cell development and B‐cell receptor signaling

et al. 2023

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B-cell development starts in the bone marrow (BM) and is completed in peripheral lymphoid tissues, such as spleen. Development in the BM progresses through pro-, pre-, and immature B-cell stages, and is accompanied by the sequential heavy (H) and light (L) chain immunoglobulin (Ig) gene rearrangement. 1,2 A successfully rearranged H chain and surrogate L chain form the pre-B-cell receptor (pre-BCR) which controls the pro-to pre-B-cell transition. The L-chain rearrangement occurs at pre-B-cell stage, and a successfully rearranged L-chain in combination of H-chain forms the B-cell receptor (BCR). B cells with a functional BCR rapidly process into immature B cells and migrate from BM into

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Section: Discussionsupporting

confidence: 52%

Section: Discussionsupporting

confidence: 51%

NONO regulates B‐cell development and B‐cell receptor signaling

et al. 2023

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“…Considering that the heart has a voracious requirement for energy 34 . Besides, Numerous studies have shown that NONO regulates energy metabolism in cancer cells 35 , 36 . We detected the total cellular ATP content, mitochondrial and glycolysis stress tests utilizing the Seahorse XF technology.…”

Section: Discussionmentioning

confidence: 99%

Nono deficiency impedes the proliferation and adhesion of H9c2 cardiomyocytes through Pi3k/Akt signaling pathway

Lei

Wei

et al. 2023

Sci Rep

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Congenital heart disease (CHD) is the most common type of birth defect and the main noninfectious cause of death during the neonatal stage. The non-POU domain containing, octamer-binding gene, NONO, performs a variety of roles involved in DNA repair, RNA synthesis, transcriptional and post-transcriptional regulation. Currently, hemizygous loss-of-function mutation of NONO have been described as the genetic origin of CHD. However, essential effects of NONO during cardiac development have not been fully elucidated. In this study, we aim to understand role of Nono in cardiomyocytes during development by utilizing the CRISPR/Cas9 gene editing system to deplete Nono in the rat cardiomyocytes H9c2. Functional comparison of H9c2 control and knockout cells showed that Nono deficiency suppressed cell proliferation and adhesion. Furthermore, Nono depletion significantly affected the mitochondrial oxidative phosphorylation (OXPHOS) and glycolysis, resulting in H9c2 overall metabolic deficits. Mechanistically we demonstrated that the Nono knockout impeded the cardiomyocyte function by attenuating phosphatidyl inositol 3 kinase-serine/threonine kinase (Pi3k/Akt) signaling via the assay for transposase-accessible chromatin using sequencing in combination with RNA sequencing. From these results we propose a novel molecular mechanism of Nono to influence cardiomyocytes differentiation and proliferation during the development of embryonic heart. We conclude that NONO may represent an emerging possible biomarkers and targets for the diagnosis and treatment of human cardiac development defects.

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“…33 NONO interacts with the hypoxia inducible factor-1/2 complex and its downstream transcripts to activate the transcription of hypoxia-induced genes, which facilitate HCC progression. 34 CENPI, a member of the centromere protein family, has an essential role in accurate chromosome segregation. 35 CENPI is upregulated in multiple cancers and serves as an oncogene to promote tumor cell proliferation, migration and invasion.…”

Section: Dovepressmentioning

confidence: 99%

CSTF2 Acts as a Prognostic Marker Correlated with Immune Infiltration in Hepatocellular Carcinoma

Zhang¹,

Wan²,

Zhang³

et al. 2022

CMAR

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Background: Cleavage stimulation factor 2 (CSTF2) encodes a nuclear protein that is implicated in the development of various cancers. However, the role of CSTF2 in hepatocellular carcinoma (HCC) has not been understood. This study aims to explore the function of CSTF2 in HCC. Methods: The expression, diagnostic capability, prognostic value, and immune cell effect of CSTF2 in HCC were explored using various databases. The expression level of CSTF2 were validated in our cell lines. The effect of CSTF2 on hepatocarcinogenesis was explored by CSTF2 silencing. Results: CSTF2 expression was significantly elevated in HCC and correlated with multiple clinicopathological characteristics. CSTF2 exhibited good diagnostic capability in discriminating HCC samples from nontumorous samples. High CSTF2 expression was significantly related to poor overall survival. Univariate and multivariate Cox regression analyses suggested that CSTF2 expression was an independent risk factor for HCC. These results were validated in ICGC cohorts. In addition, the nomogram based on CSTF2 showed better predictive performance than the AJCC staging system in TCGA and ICGC cohorts. Functional enrichment analysis revealed that CSTF2-related genes were involved in DNA/RNA processing and the cell cycle. In addition, we found that CSTF2 expression was closely related to the levels of various infiltrating immune cells, especially neutrophils. Moreover, some immune checkpoints had positive relationships with CSTF2 expression. CSTF2 silencing inhibited proliferation, invasion and migration, and promoted apoptosis in HepG2 cells. Western blotting analysis revealed that CSTF2 silencing inactivated the Wnt/β-catenin signaling pathway. Conclusion: High CSTF2 expression not only correlates with unfavorable outcomes but also affects immune cell infiltration and immune checkpoint expression in HCC. CSTF2 silencing can alleviate the malignant phenotypes of hepatic cancer cell by inactivating the Wnt/β-catenin signaling pathway. These results indicate that CSTF2 can serve as a promising prognostic marker and therapeutic target for HCC patients.

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Nuclear scaffold protein p54nrb/NONO facilitates the hypoxia-enhanced progression of hepatocellular carcinoma

Cited by 19 publications

References 41 publications

NONO regulates B‐cell development and B‐cell receptor signaling

NONO regulates B‐cell development and B‐cell receptor signaling

Nono deficiency impedes the proliferation and adhesion of H9c2 cardiomyocytes through Pi3k/Akt signaling pathway

CSTF2 Acts as a Prognostic Marker Correlated with Immune Infiltration in Hepatocellular Carcinoma

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