scholarly journals Role and mechanism of Glut-1 and H+/K+-ATPase expression in pepsin-induced development of vocal cord leukoplakia

2021 ◽  
Author(s):  
Yin-Jie Ao ◽  
Ting-Ting Wu ◽  
Zai-Zai Cao ◽  
Shui-Hong Zhou ◽  
Yang-Yang Bao ◽  
...  
Keyword(s):  
Gastric Juice ◽  
Vocal Cord ◽  
Laryngeal Carcinoma ◽  
G1 Phase ◽  
Dependent Manner ◽  
Glut 1 ◽  
Laryngeal Mucosa ◽  
M Phase ◽  
Artificial Gastric Juice

Abstract Purpose We investigated the role of Glut-1 and H+/K+-ATPase expression in pepsin-induced development of human vocal cord leukoplakia cells (HVCLCs). Next, we analyzed the relationship between Glut-1 and H+/K+-ATPase expression with the clinicopathological features of laryngeal carcinoma. Methods Glut-1 and H+/K+-ATPase expression levels in HVCLCs were determined after treatment with artificial gastric juice containing pepsin and laryngeal carcinoma tissues. Results Exposure to pepsin-containing artificial gastric juice significantly enhanced the migration and proliferation of VSCLCs in a time-dependent manner. The apoptotic rate of VSCLCs decreased over time after exposure to pepsin and reached a nadir on day 7 (p < 0.01). With increasing duration of exposure to pepsin, the proportion of VSCLCs in G0/G1 phase decreased and the proportions in the S and G2/M phases significantly increased (p < 0.05). After treatment with pepsin-containing artificial gastric juice, RT-PCR and Western blotting showed that the expression of Glut-1 and H+/K+-ATPase α, β significantly increased in HVCLCs compared to in the absence of pepsin (p < 0.05). The expression of Glut-1 and H+/K+-ATPase α, β gradually increased from vocal cord leukoplakia (VLC) to laryngeal carcinoma (p < 0.05). Lentivirus-mediated inhibition of Glut-1 expression in VCL significantly inhibited the cells’ migration and proliferation (p < 0.05) but enhanced their apoptosis (p < 0.05). Also, inhibition of Glut-1 expression resulted in an increased proportion of cells in G0/G1 phase and a significantly decreased proportion in G2/M phase (p < 0.05). Conclusions Elevated Glut-1 expression may promote the development of VCL by upregulating laryngeal H+/K+-ATPase expression to reactivate absorbed pepsin, thus damaging the laryngeal mucosa.

Effects of removing heat and phlegm prescription on the proliferation and autoantigens expression of esophageal carcinoma cell.

2020 ◽  
Vol 38 (15_suppl) ◽  
pp. e16510-e16510
Author(s):  
Fuchun Si
Keyword(s):  
Esophageal Carcinoma ◽  
G1 Phase ◽  
Dependent Manner ◽  
Inhibitory Effects ◽  
Ethanol Extraction ◽  
Phase Arrest ◽  
G1 Phase Arrest ◽  
M Phase ◽  
Ic50 Values ◽  
Dose Dependent

e16510 Background: o explore the effects of removing heat and phlegm prescription (RHPP) on the proliferation and autoantigens expression of esophageal carcinoma(EC) cell, so as to provide basis for the molecular pathogenesis and clinical medication of EC. Methods: RHPP was developed by us for treating EC, EC autoantigens CK13, CK16, CaD, ACTG2 were identified in our previous studies. The effects of RHPP and and its ethanol extraction on the proliferation, cell cycle and autoantigen protein expression of Eca109 cell, EC9706 cell and TE-1 cell were investigated by MTT assay, flow cytometry and western blot analysis. Results: RHPP and its removing heat (RH) and removing phlegm (RP) separated prescriptions all have inhibitory effects on the proliferation of EC9706, EC109 and TE-1 cells in dose-dependent and time-dependent manner, changed morphology of four esophageal carcinoma cells, which appeared as round with rough edges, karyopyknosis, and karyorrhexis. Ic50 values of RHPP for Ec9706, Eca109 and TE1 cell were 33.31 ug·ml−1, 20.70 ug·ml−1, 21.93 ug·ml−1 respectively, while Ic50 values of RHPP’s ethanol extraction for Ec9706, Eca109, TE1 were 0.653 ug·ml−1, 0.082 ug·ml−1, 0.172 ug·ml−1 respectively. RHPP and RP induced G2/M phase arrest in EC109 and TE-1 cells, while RH induced G0/G1 phase arrest in EC109 and TE-1 cells; RHPP and RP induced G0/G1 phase arrest in EC9706 cells, while RH induced S phase arrest in EC9706 cells. RHPP and its two separated prescription could downregulate CK16, CaD, ACTG2 expression and upregulate CK13 expression. Conclusions: Autoantigens CK13, CK16, CaD and ACTG2 were expressed in EC cell, RHPP could regulate these four autoantigens expression. This study provides new basis for the EC mlecular mechanism and development of anti-esophageal carcinoma drugs in traditional Chinese medicine.

scholarly journals Laryngopharyngeal Reflux in Hypertrophic Laryngeal Diseases

2020 ◽  
pp. 014556132095323
Author(s):  
Honglei Han ◽  
Qiuping Lyu ◽  
Jianhui Zhao
Keyword(s):  
Vocal Cord ◽  
Laryngeal Carcinoma ◽  
Laryngopharyngeal Reflux ◽  
Laryngeal Diseases ◽  
Male Preponderance ◽  
Group 3 ◽  
Group 2 ◽  
The Relationship ◽  
Group 1

Objectives: To evaluate the characteristics of laryngopharyngeal reflux (LPR) in patients with different hypertrophic laryngeal diseases and to explore the relationship between LPR and these diseases. Methods: A retrospective analysis was performed. The clinical data of 154 patients were collected. According to their diagnoses, patients were divided into 3 groups. Group 1 included 49 patients with vocal cord polyps. Group 2 contained 52 patients with vocal cord leukoplakia. Group 3 included 53 patients with laryngeal carcinoma. The reflux symptom indexes (RSIs), reflux finding scores (RFSs), and Ryan scores of all patients were evaluated and compared. Results: Patients with vocal cord polyps were the youngest of the 3 groups, and those with laryngeal carcinoma were the oldest. A male preponderance emerged in each group. In total, 128 patients (83.12%) had positive RSI/RFS values and 60 (60/146, 41.1%) patients had positive Ryan scores. The positive RSI/RFS rates of both groups 1 and 2 (89.80% and 92.16%, respectively) were significantly higher than that of group 3 (69.81%). Moreover, the positive Ryan score rates in both groups 1 and 2 (39.58% and 53.85%, respectively) were significantly higher than that of group 3 (28.26%). Conclusions: Laryngopharyngeal reflux occurs in many patients with vocal cord polyps, vocal cord leukoplakia, and vocal cord carcinoma, indicating that LPR may be important in the pathogenesis of these diseases. Laryngopharyngeal reflux occurs more common in patients with vocal cord polyps and leukoplakia and less common in those with laryngeal carcinoma, suggesting the role of LPR on these diseases may be different.

Visfatin: a new player in mesangial cell physiology and diabetic nephropathy

2008 ◽  
Vol 295 (5) ◽  
pp. F1485-F1494 ◽  
Author(s):  
Hye Kyoung Song ◽  
Mi Hwa Lee ◽  
Bo Kyung Kim ◽  
Yun Gyu Park ◽  
Gang Jee Ko ◽  
...  
Keyword(s):  
Diabetic Nephropathy ◽  
Glucose Uptake ◽  
Cytochalasin B ◽  
Cell Physiology ◽  
Type I ◽  
Dependent Manner ◽  
Cellular Membranes ◽  
Nicotinamide Phosphoribosyltransferase ◽  
Glut 1

Visfatin is an adipocytokine that improves insulin resistance and has an antidiabetic effect. However, the role of visfatin in the kidney has not yet been reported. In this experiment, the synthesis and physiological action of visfatin in cultured mesangial cells (MCs) were studied to investigate the role of visfatin in diabetic nephropathy. Visfatin was found synthesized in MCs as well as adipocytes. Visfatin synthesis was markedly increased, not by angiotensin II, but by high glucose stimuli. In addition, visfatin treatment induced a rapid uptake of glucose, peaking at 20 min after visfatin treatment in a dose-dependent manner. A small inhibiting RNA against insulin receptor significantly blocked visfatin-mediated glucose uptake. Visfatin stimuli also enhanced intracellular NAD levels, and treatment with FK866, which is a specific inhibitor of nicotinamide phosphoribosyltransferase (Nampt), significantly inhibited visfatin-induced NAD synthesis and glucose uptake. Visfatin treatment increased glucose transporter-1 (GLUT-1) protein expression in isolated cellular membranes, and pretreatment with cytochalasin B completely inhibited visfatin-induced glucose uptake. Moreover, immunofluorescent microscopy showed the migration of cytosolic GLUT-1 into cellular membranes after visfatin treatment. In accordance with these results, the activation of protein kinase B was detected after visfatin treatment. Furthermore, visfatin treatment dramatically increased the synthesis of profibrotic molecules including transforming growth factor-β1, plasminogen activator inhibitor-1, and type I collagen, and pretreatment with cytochalasin B completely inhibited visfatin-induced upregulation of profibrotic molecules. These results suggest that visfatin is produced in MCs, which are a novel target for visfatin, and play an important role in the pathogenesis of diabetic nephropathy.

scholarly journals The role of cdc2 and other genes in meiosis in Schizosaccharomyces pombe.

Genetics ◽  
1995 ◽  
Vol 140 (4) ◽  
pp. 1235-1245 ◽  
Author(s):  
Y Iino ◽  
Y Hiramine ◽  
M Yamamoto
Keyword(s):  
Dna Synthesis ◽  
Schizosaccharomyces Pombe ◽  
Nuclear Division ◽  
Large Subunit ◽  
S Phase ◽  
Dependent Manner ◽  
M Phase ◽  
Cdc2 Gene ◽  
Meiosis I

Abstract The requirement of the cdc2, cdc13 and cdc25 genes for meiosis in Schizosaccharomyces pombe was investigated using three different conditions to induce meiosis. These genes were known to be required for meiosis II. cdc13 and cdc25 are essential for meiosis I. The cdc2 gene, which is required for the initiation of both mitotic S-phase and M-phase, is essential for premeiotic DNA synthesis and meiosis II. The requirement of cdc2 for meiosis I was unclear. This contrasts with Saccharomyces cerevisiae, where CDC28, the homolog of cdc2, is required for meiosis I but not for premeiotic DNA synthesis. Expression of cdc13 and cdc25 was induced after premeiotic DNA synthesis, reaching a sharp peak before the first nuclear division. Expression of cdc22, encoding the large subunit of ribonucleotide reductase, was also induced but the peak was before premeiotic DNA synthesis. The induction of cdc13 and cdc25 was largely dependent on DNA synthesis and the function of the mei4 gene. The mei4 gene itself was also induced in a DNA synthesis-dependent manner. The chain of gene expression activating cdc25 may be important as part of the mechanism that ensures the dependency of nuclear division on DNA replication during meiosis.

scholarly journals shRNA Glut-1 inhibits cell viability, apoptosis and migration of laryngeal carcinoma HEp-2 cells through regulating Beclin-1-mediated autophagy

2020 ◽  
Author(s):  
Wen-Dong Wang ◽  
Jin-Long Zhu ◽  
Shui-Hong Zhou ◽  
Jun Fan ◽  
Yang-Yang Bao
Keyword(s):  
Cell Viability ◽  
Laryngeal Carcinoma ◽  
Migration Rate ◽  
Caspase 3 ◽  
Cell Model ◽  
Beclin 1 ◽  
Glut 1 ◽  
And Migration ◽  
Proliferation And Migration

AbstractObjectiveGlut-1 is a key regulator in the process of glucose uptake. Previous studies have shown that Glut-1 affects autophagy. However, it is unclear whether there is a correlation between Glut-1 and autophagy in the progression of laryngeal carcinoma. This study was performed to investigate the role of Glut-1 in the development of laryngeal carcinoma.MethodsA stable HEp-2 cell model was constructed by Glut-1 and Beclin-1 shRNA lentiviral infection. The autophagosome was measured by transmission electron microscopy. Protein levels of LC3, ATG5, CyclinD1, Bcl-2, Caspase-3, and c-Myc were determined by Western blotting. CCK8 assay and Transwell assays were used to determine cell viability and migration rate of HEp-2 cells, respectively. Flow cytometry was performed to analyze the rate of apoptosis. Immunofluorescence was performed to determine the expression distribution of LC3.ResultsGlut-1 knockdown significantly promoted autophagosome formation by upregulating the ratio of LC3-II/LC3-I as well as the role of rapamycin (RAP) and Beclin-1 overexpression on autophagy flux in HEp-2 cells. Glut-1 inhibition also reduced the viability of HEp-2 cells followed by the decreases in expression of cyclinD1 and c-Myc. In addition, Glut-1 depletion increased the number of apoptotic HEp-2 cells accompanied by activation of caspase-3 and downregulation of Bcl-2. Glut-1 knockdown also reduced the migration rate of HEp-2 cells by promoting the expression of N-cadherin and inhibiting the expression of E-cadherin. Beclin-1 consumption significantly reversed Gult-1 knockdown-mediated autophagy activation, resulting in promotion of both proliferation and migration and inhibition of apoptosis.ConclusionsGlut-1 knockdown-induced autophagy inhibits the proliferation and migration of HEp-2 cells, and promotes apoptosis of HEp-2 cells partly by regulating autophagy.

Meiotic CENP-C is a shepherd: bridging the space between the centromere and the kinetochore in time and space

2020 ◽  
Vol 64 (2) ◽  
pp. 251-261
Author(s):  
Jessica E. Fellmeth ◽  
Kim S. McKim
Keyword(s):  
Chromosome Segregation ◽  
New Technologies ◽  
Early Prophase ◽  
Unique Role ◽  
Kinetochore Assembly ◽  
M Phase ◽  
In Vivo Analysis ◽  
Meiosis I

Abstract While many of the proteins involved in the mitotic centromere and kinetochore are conserved in meiosis, they often gain a novel function due to the unique needs of homolog segregation during meiosis I (MI). CENP-C is a critical component of the centromere for kinetochore assembly in mitosis. Recent work, however, has highlighted the unique features of meiotic CENP-C. Centromere establishment and stability require CENP-C loading at the centromere for CENP-A function. Pre-meiotic loading of proteins necessary for homolog recombination as well as cohesion also rely on CENP-C, as do the main scaffolding components of the kinetochore. Much of this work relies on new technologies that enable in vivo analysis of meiosis like never before. Here, we strive to highlight the unique role of this highly conserved centromere protein that loads on to centromeres prior to M-phase onset, but continues to perform critical functions through chromosome segregation. CENP-C is not merely a structural link between the centromere and the kinetochore, but also a functional one joining the processes of early prophase homolog synapsis to late metaphase kinetochore assembly and signaling.

Role of vitamin C in gastric cancer

2018 ◽  
Vol 01 (1) ◽  
Author(s):  
Takalkar U Vidyadhar
Keyword(s):  
Gastric Cancer ◽  
Vitamin C ◽  
Gastric Juice ◽  
Oxidative Dna Damage ◽  
Preventive Measure ◽  
Dietary Factors ◽  
Preventive Strategy ◽  
H Pylori

Gastric cancer is a multifactorial disease with complex interplay of environmental and genetic factors. Helicobacter pylori (H. pylori) infestation has been identified as the most important etiological agent in the pathogenesis of gastric cancer. Also, the role of dietary factors that is low consumption of fruits and vegetables have been found to be associated with gastric cancer. Among the dietary factors, antioxidants especially vitamin C has been found to confer the strongest protection against gastric cancer. Its anti-proliferative and pro-apoptotic action has been suggested in vitro. Because of its antioxidant activity, it protects cells against oxidative DNA damage caused by toxic effects of reactive oxygen species. It also inhibits production of carcinogenic N-nitroso compound in the stomach. The person with H. pylori infection has low levels of vitamin C in their gastric juice and levels of vitamin C normalizes on eradication of H. pylori. Vitamin C levels are high in gastric mucosa and gastric juice, sometimes more than that of in plasma. But gastric pathological conditions cause lowered secretion of vitamin C into gastric juice. Effect of H. pylori on vitamin C in gastric juice is reversible and on eradication of H. pylori, it returns to normal level. Hence, eradication of H. pylori and chemoprevention with antioxidant supplementation will be an effective preventive strategy to reduce the incidence of gastric cancer and related mortality. Vitamin C and gastric cancer is an area of potential interest for researchers as a preventive measure. Keywords: Vitamin C, H. pylori, gastric cancer.

Amelioration of Carbon Tetrachloride-Induced Liver Injury by Citrus Leaf Extract

2019 ◽  
Vol 17 (4) ◽  
pp. 426-431
Author(s):  
Jin Xuezhu ◽  
Li Jitong ◽  
Nie Leigang ◽  
Xue Junlai
Keyword(s):  
Carbon Tetrachloride ◽  
Leaf Extract ◽  
Hepatic Injury ◽  
The Body ◽  
Dependent Manner ◽  
Weight Changes ◽  
Citrus Leaf ◽  
Dose Dependent ◽  
And Oxidative Stress

The main purpose of this study is to investigate the role of citrus leaf extract in carbon tetrachloride-induced hepatic injury and its potential molecular mechanism. Carbon tetrachloride was used to construct hepatic injury animal model. To this end, rats were randomly divided into 4 groups: control, carbon tetrachloride-treated, and two carbon tetrachloride + citrus leaf extract-treated groups. The results show that citrus leaf extract treatment significantly reversed the effects of carbon tetrachloride on the body weight changes and liver index. Besides, treatment with citrus leaf extract also reduced the levels of serum liver enzymes and oxidative stress in a dose-dependent manner. H&E staining and western blotting suggested that citrus leaf extract could repair liver histological damage by regulating AMPK and Nrf-2.

Role of Ultrasound in Analysis of Vocal Cord Movements in Comparison with Laryngoscopy

2019 ◽  
Vol 7 (2) ◽  
pp. 32-35
Author(s):  
Nagaraj Murthy ◽  
◽  
Dimple Bhatia ◽  
Keyword(s):  
Vocal Cord
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