Carbonic anhydrase III is a new target of HIF1α in prostate cancer model

Okuyan, Derya; Türkoğlu, Sümeyye Aydoğan; Köçkar, Feray

doi:10.1016/j.gene.2020.145034

Cited by 11 publications

(8 citation statements)

References 41 publications

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“…Some of these genes were reported as upregulated, such as HSP90AB1, promoting cell adaptation to environmental changes [56]; SCARA3, the product of which depletes reactive oxygen species [57], and DNMT3A, encoding an enzyme involved in CpG or non-CpG motifs DNA methylation [58]. However, decreased expression of CA3 [48] and HPRT [40], both induced by hypoxiainducible factor 1α (HIF1-α), a transcription factor that adapts the cell during oxygen deprivation, might suggest an impaired adaptation to oxidative stress in airway remodeling pathology. Furthermore, downregulated HPRT might be related to the local overproduction of uric acid [40], likely stimulating cell proliferation and new blood vessel formation [41,42].…”

Section: Discussionmentioning

confidence: 99%

Reticular Basement Membrane Thickness Is Associated with Growth- and Fibrosis-Promoting Airway Transcriptome Profile-Study in Asthma Patients

Bazan-Socha

Buregwa-Czuma

Jakieła

et al. 2021

IJMS

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Airway remodeling in asthma is characterized by reticular basement membrane (RBM) thickening, likely related to epithelial structural and functional changes. Gene expression profiling of the airway epithelium might identify genes involved in bronchial structural alterations. We analyzed bronchial wall geometry (computed tomography (CT)), RBM thickness (histology), and the bronchial epithelium transcriptome profile (gene expression array) in moderate to severe persistent (n = 21) vs. no persistent (n = 19) airflow limitation asthmatics. RBM thickness was similar in the two studied subgroups. Among the genes associated with increased RBM thickness, the most essential were those engaged in cell activation, proliferation, and growth (e.g., CDK20, TACC2, ORC5, and NEK5) and inhibiting apoptosis (e.g., higher mRNA expression of RFN34, BIRC3, NAA16, and lower of RNF13, MRPL37, CACNA1G). Additionally, RBM thickness correlated with the expression of genes encoding extracellular matrix (ECM) components (LAMA3, USH2A), involved in ECM remodeling (LTBP1), neovascularization (FGD5, HPRT1), nerve functioning (TPH1, PCDHGC4), oxidative stress adaptation (RIT1, HSP90AB1), epigenetic modifications (OLMALINC, DNMT3A), and the innate immune response (STAP1, OAS2). Cluster analysis revealed that genes linked with RBM thickness were also related to thicker bronchial walls in CT. Our study suggests that the pro-fibrotic profile in the airway epithelial cell transcriptome is associated with a thicker RBM, and thus, may contribute to asthma airway remodeling.

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Section: Discussionmentioning

confidence: 99%

Reticular Basement Membrane Thickness Is Associated with Growth- and Fibrosis-Promoting Airway Transcriptome Profile-Study in Asthma Patients

Bazan-Socha

Buregwa-Czuma

Jakieła

et al. 2021

IJMS

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“…Some studies have revealed that diets low in protein might cause the loss of muscle volume [ 38 ]. However, our results showed that LPHF diets did not alter the corresponding muscle mass.…”

Section: Discussionmentioning

confidence: 99%

A Low-Protein High-Fat Diet Leads to Loss of Body Weight and White Adipose Tissue Weight via Enhancing Energy Expenditure in Mice

Rang

Jiao

et al. 2021

Metabolites

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Obesity has become a worldwide health problem over the past three decades. During obesity, metabolic dysfunction of white adipose tissue (WAT) is a key factor increasing the risk of type 2 diabetes. A variety of diet approaches have been proposed for the prevention and treatment of obesity. The low-protein high-fat diet (LPHF) is a special kind of high-fat diet, characterized by the intake of a low amount of protein, while compared to typical high-fat diet, may induce weight loss and browning of WAT. Physical activity is another effective intervention to treat obesity by reducing WAT mass, inducing browning of WAT. In order to determine whether an LPHF, along with exercise enhanced body weight loss and body fat loss as well as the synergistic effect of an LPHF and exercise on energy expenditure in a mice model, we combined a 10-week LPHF with an 8-week forced treadmill training. Meanwhile, a traditional high-fat diet (HPHF) containing the same fat and relatively more protein was introduced as a comparison. In the current study, we further analyzed energy metabolism-related gene expression, plasma biomarkers, and related physiological changes. When comparing to HPHF, which induced a dramatic increase in body weight and WAT weight, the LPHF led to considerable loss of body weight and WAT, without muscle mass and strength decline, while it exhibited a risk of liver and pancreas damage. The mechanism underlying the LPHF-induced loss of body weight and WAT may be attributed to the synergistically upregulated expression of Ucp1 in WAT and Fgf21 in the liver, which may enhance energy expenditure. The 8-week training did not further enhance weight loss and increased plasma biomarkers of muscle damage when combined with LPHF. Furthermore, LPHF reduced the expression of fatty acid oxidation-related genes in adipose tissues, muscle tissues, and liver. Our results indicated that an LPHF has potential for obesity treatment, while the physiological condition should be monitored during application.

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“…In our previous study we found that CAIII is upregulated by hypoxia in prostate cancer cells. HIF1-α directly binds on to Hypoxia response elements in CAIII promoter [29]. Moreover, in our different study, in colon cancer cells, TGF-beta inhibited the CAIII gene via the phosphoinositide-3-kinase (PI3K) and mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) pathways [42].…”

Section: Sp1 Directly Binds On Multiple Putative Sp1 Sites Of Caiii P...mentioning

confidence: 76%

“…Although the expression of CAIII is mainly restricted in skeletal muscle, there is wide expression pattern in other tissues. CAIII expression was highly regulated by hypoxia [29]. In our previous study we found that CAIII is upregulated by hypoxia in prostate cancer cells.…”

Section: Sp1 Directly Binds On Multiple Putative Sp1 Sites Of Caiii P...mentioning

confidence: 85%

Transcriptional activation of Carbonic Anhydrase III (CAIII) mediated by SP1

Okuyan,

Köçkar

2024

Preprint

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Many physiological and pathological processes require the expression and control of CAIII. Although the CAIII promoter has not been fully characterized, promoters for other carbonic anhydrase genes in humans have. In this research, we for the first time located and described the human Carbonic anhydrase III gene promoter region. Progressive deletion analysis of the 5′-flanking region of the CAIII gene showed that the CAIII core promoter is mainly restricted to a minimum region of 129 bp. The CAIII gene promoter was discovered to include additional potential binding sites for transcriptional factors including C/EBP and NF-B despite lacking the standard TATA box, according to an investigation of transcriptional factor binding. Furthermore, site-directed mutagenesis assay showed that the proximal Sp1 binding site is required for the essential core promoter activity of the CAIII gene. It was also shown that the CAIII gene was up-regulated by SP1 at the mRNA and protein levels, and this effect was also observed in deletion promoter constructs. Our current study will shed light on further studies on the mechanism that regulates the expression of this important gene.

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Carbonic anhydrase III is a new target of HIF1α in prostate cancer model

Cited by 11 publications

References 41 publications

Reticular Basement Membrane Thickness Is Associated with Growth- and Fibrosis-Promoting Airway Transcriptome Profile-Study in Asthma Patients

Reticular Basement Membrane Thickness Is Associated with Growth- and Fibrosis-Promoting Airway Transcriptome Profile-Study in Asthma Patients

A Low-Protein High-Fat Diet Leads to Loss of Body Weight and White Adipose Tissue Weight via Enhancing Energy Expenditure in Mice

Transcriptional activation of Carbonic Anhydrase III (CAIII) mediated by SP1

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