Downregulation of ALDOB is associated with poor prognosis of patients with gastric cancer

He, Jun; Yi, Jing; Yuan, Chen; Yao, Huang; Xia, Yingjie; Ma, Yingyu; Wang, Wei; Shao, Qin-shu

doi:10.2147/ott.s110203

Cited by 77 publications

(67 citation statements)

References 32 publications

(43 reference statements)

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“…Specifically, the two aldolase isoforms A and C, which foster glycolysis were unchanged, but the aldolase isoform B, necessary for gluconeogenesis was greatly diminished in pRCC. This again indicates a critical metabolic change, as previously observed in chRCC (27) and in gastric cancer (35). Conversely, an over-expression of gluconeogenic genes and proteins is frequently found in other tumor species, such as the over-expression of ALDOB in ccRCC (36) and colon cancer (37)(38)(39), which was also associated with tumor progression and poor prognosis.…”

Section: Discussionsupporting

confidence: 74%

Papillary renal cell carcinomas rewire glutathione metabolism and are deficient in anabolic glucose synthesis

Alahmad

Paffrath

Clima

et al. 2019

Preprint

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Papillary renal cell carcinoma (pRCC) is a malignant kidney cancer with a prevalence of 7-20% of all renal tumors. Proteome and metabolome profiles of 19 pRCC and patient-matched healthy kidney controls were used to elucidate the regulation of metabolic pathways and the underlying molecular mechanisms. Glutathione (GSH), a main reactive oxygen species (ROS) scavenger, was highly increased and can be regarded as a new hallmark in this malignancy. Isotope tracing of pRCC derived cell lines revealed an increased de novo synthesis rate of GSH, based on glutamine consumption. Furthermore, rewiring of the main pathways involved in ATP and glucose synthesis was observed at the protein level. In contrast, transcripts encoding for the respiratory chain were not regulated, which prompts for non-genetic profiling. The molecular characteristics of pRCC are increased GSH synthesis to cope with ROS stress, deficient anabolic glucose synthesis, and compromised oxidative phosphorylation, which could potentially be exploited in innovative anti-cancer strategies.

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Section: Discussionsupporting

confidence: 74%

Papillary renal cell carcinomas rewire glutathione metabolism and are deficient in anabolic glucose synthesis

Alahmad

Paffrath

Clima

et al. 2019

Preprint

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“…A TCGA gene dataset named TCGA‐STAD/Xena_Matrices/TCGA‐STAD.htseq_fpkm‐uq.tsv (including 372 GC tissues and 35 normal tissues) with version number 09‐14‐2017 was downloaded from the UCSC cancer browser (https://xenabrowser.net/datapages/). We obtained the normalized expression values of NUSAP1 from “TCGA‐STAD.htseq_fpkm‐uq.tsv.” Additionally, we used the GSE51575 dataset (containing 26 paired GC tissues and adjacent normal tissues) and GSE79973 dataset (including 10 paired tissues) in NCBI GEO (https://www.ncbi.nlm.nih.gov/gds/) to evaluate NUSAP1 expression levels. The normalized data were extracted from “MINiML formatted family file.” The data employed for gene set enrichment analysis (GSEA) were also acquired from TCGA and GSE51575 dataset using the GSEA v3.0 software (http://software.broadinstitute.org/gsea/downloads.jsp).…”

Section: Methodsmentioning

confidence: 99%

Downregulation of NUSAP1 suppresses cell proliferation, migration, and invasion via inhibiting mTORC1 signalling pathway in gastric cancer

Lin

et al. 2019

Cell Biochemistry & Function

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Gastric cancer (GC) is one of the most common causes of cancer-related death worldwide, and outstanding biomarkers for therapeutic targets or predicting GC survival are still lacking. Increasing evidence indicated that nucleolar and spindle associated protein 1 (NUSAP1) involved in regulating the progression of various cancers; however, its specific role in GC remained unclear. In this study, we found that NUSAP1 was upregulated in the GC tissues and cell lines via analysing data from The Cancer Genome Atlas (TCGA), gene expression omnibus (GEO), qRT-PCR, and western blot assays. Patients with high NUSAP1 expression levels showed shorter freeprogression survival (FPS), larger tumour size, and higher lymphatic metastasis rate compared with those with low NUSAP1 expression. Further functional experiments revealed knockdown of NUSAP1 could inhibit the growth, migration, and invasion of GC cells in vitro and vivo. Additionally, silencing NUSAP1 induced G0/G1 phase arrest, apoptosis, and suppressed the epithelial-mesenchymal transition (EMT) process. Finally, we performed gene set enrichment analysis (GSEA) and observed NUSAP1 was positive with mTORC1 signalling pathway, which was verified by the subsequent immunoblotting. In conclusion, our findings suggested that NUSAP1 contributed to GC progression and may act as a potential therapeutic target for GC.Significance of the study: Our results firstly illuminated that NUSAP1 expression was significantly upregulated in GC tissues and predicted poor FPS. Silencing it could attenuate GC progression via inhibiting mTORC1 signalling pathway. Hence, NUSAP1 may act as a promising therapy target for GC.

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“…To verify the microarray results from the Cu‐NP exposure experiments, qRT‐PCR was performed as described previously . Ten genes ( VEGFα , Mmp12 , Mt2A , Mt3 , TIMP1 , Cebpb Mmp11, Lpl, Ntn4, and Pdgfrl) associated with apoptosis, stress, and inflammation were analyzed.…”

Section: Methodsmentioning

confidence: 99%

Copper nanoparticle‐induced uterine injury in female rats

Yang

Rao

et al. 2018

Environmental Toxicology

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Copper nanoparticles (Cu-NPs) have been used increasingly in various products and applications.Although recent studies have reported that exposure to Cu-NPs leads to organ accumulation and obvious toxicity, it remains unclear whether Cu-NPs can be translocated to and cause damage in the uterus. In this study, we investigated the potential for uterine injury and gene expression patterns in female rats exposed to 3.12, 6.25, or 12.5 mg/kg/d Cu-NPs via intraperitoneal injection for 14 consecutive days. The results indicated that exposure to Cu-NPs led to significant decreases in the relative uterine weight coefficients and increases in inflammatory cell infiltration, mitochondrial swelling and vacuolization, shortened and reduced endometrial epithelial cell microvilli, and apoptosis. Furthermore, exposure to Cu-NPs increased malondialdehyde (MDA) accumulation and decreased superoxide dismutase (SOD) levels. Signal transduction mechanism studies indicated that exposure to Cu-NPs activated caspases 3, 8, and 9 and BH3 interacting domain death agonist (tBid), reduced B cell leukemia/lymphoma 2 (Bcl-2) expression, and increased the expression of apoptotic peptidase activating factor 1 (Apaf-1), BCL2-associated X, apoptosis regulator (Bax), and cytochrome c. A microarray analysis revealed significant alterations in the expression of 963 genes; of these, 622 were upregulated and 341 were downregulated. The results of further evaluations of some altered genes, including matrix metallopeptidase 12 (Mmp12), using quantitative RT-PCR agreed with the microarray findings. These results provide strong evidence that Cu-NPs can trigger both intrinsic and extrinsic apoptotic pathways to mediate uterine injury, resulting in oxidative stressrelated changes in gene expression. K E Y W O R D Sapoptosis, Cu-NPs, microarray, rat, uterus

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Downregulation of ALDOB is associated with poor prognosis of patients with gastric cancer

Cited by 77 publications

References 32 publications

Papillary renal cell carcinomas rewire glutathione metabolism and are deficient in anabolic glucose synthesis

Papillary renal cell carcinomas rewire glutathione metabolism and are deficient in anabolic glucose synthesis

Downregulation of NUSAP1 suppresses cell proliferation, migration, and invasion via inhibiting mTORC1 signalling pathway in gastric cancer

Copper nanoparticle‐induced uterine injury in female rats

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