scholarly journals Acute metabolic actions of the major polyphenols in chamomile: an in vitro mechanistic study on their potential to attenuate postprandial hyperglycaemia

2018 ◽  
Vol 8 (1) ◽  
Author(s):  
Jose A. Villa-Rodriguez ◽  
Asimina Kerimi ◽  
Laszlo Abranko ◽  
Sarka Tumova ◽  
Lauren Ford ◽  
...  
Keyword(s):  
Postprandial Hyperglycaemia ◽  
Mechanistic Study

scholarly journals High expression of PSMC2 promotes gallbladder cancer through regulation of GNG4 and predicts poor prognosis

Oncogenesis ◽  
2021 ◽  
Vol 10 (5) ◽  
Author(s):  
Dawei Zhu ◽  
Xing Gu ◽  
Zhengyu Lin ◽  
Dandan Yu ◽  
Jing Wang
Keyword(s):  
Gallbladder Cancer ◽  
Malignant Tumor ◽  
Xenograft Model ◽  
Tumor Grade ◽  
Significant Inhibition ◽  
Mechanistic Study ◽  
Downstream Target ◽  
Advanced Tumor

AbstractGallbladder cancer (GBC) is a common malignant tumor of the biliary tract, which accounts for 80–95% of biliary tumors worldwide, and is the leading cause of biliary malignant tumor-related death. This study identified PSMC2 as a potential regulator in the development of GBC. We showed that PSMC2 expression in GBC tissues is significantly higher than that in normal tissues, while high PSMC2 expression was correlated with more advanced tumor grade and poorer prognosis. The knockdown of PSMC2 in GBC cells induced significant inhibition of cell proliferation, colony formation and cell motility, while the promotion of cell apoptosis. The construction and observation of the mice xenograft model also confirmed the inhibitory effects of PSMC2 knockdown on GBC development. Moreover, our mechanistic study recognized GNG4 as a potential downstream target of PSMC2, knockdown of which could aggravate the tumor suppression induced by PSMC2 knockdown in vitro and in vivo. In conclusion, for the first time, PSMC2 was revealed as a tumor promotor in the development of GBC, which could regulate cell phenotypes of GBC cells through the interaction with GNG4, and maybe a promising therapeutic target in GBC treatment.

Carbamazepine pharmacokinetics are not affected by zonisamide: in vitro mechanistic study and in vivo clinical study in epileptic patients

2004 ◽  
Vol 62 (1) ◽  
pp. 1-11 ◽  
Author(s):  
Isabelle Ragueneau-Majlessi ◽  
Rene H. Levy ◽  
Donna Bergen ◽  
William Garnett ◽  
William Rosenfeld ◽  
...  
Keyword(s):  
Clinical Study ◽  
Mechanistic Study ◽  
Epileptic Patients

A mechanistic study of bulk contact lens dehydration in vitro

2015 ◽  
Vol 38 ◽  
pp. e20-e21
Author(s):  
Thomas Minchington ◽  
Brian Tighe
Keyword(s):  
Contact Lens ◽  
Mechanistic Study

In Vitro Mechanistic Study of the Anti-inflammatory Activity of a Quinoline Isolated fromSpondias pinnataBark

2018 ◽  
Vol 81 (9) ◽  
pp. 1956-1961 ◽  
Author(s):  
Nikhil B. Ghate ◽  
Dipankar Chaudhuri ◽  
Sourav Panja ◽  
Sudhir S. Singh ◽  
Gajendra Gupta ◽  
...  
Keyword(s):  
Inflammatory Activity ◽  
Mechanistic Study ◽  
Anti Inflammatory

scholarly journals Chromatin remodeling factor ARID2 suppresses hepatocellular carcinoma metastasis via DNMT1-Snail axis

2020 ◽  
Vol 117 (9) ◽  
pp. 4770-4780 ◽  
Author(s):  
Hao Jiang ◽  
Hui-Jun Cao ◽  
Ning Ma ◽  
Wen-Dai Bao ◽  
Jing-Jing Wang ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Chromatin Remodeling ◽  
Epithelial Mesenchymal Transition ◽  
Positive Association ◽  
Mechanistic Study ◽  
Migration And Invasion ◽  
Metastasis Suppressor ◽  
Mesenchymal Transition ◽  
Hcc Cells

Recurrence and metastasis remain the major obstacles to successful treatment of hepatocellular carcinoma (HCC). Chromatin remodeling factor ARID2 is commonly mutated in HCC, indicating its important role in cancer development. However, its role in HCC metastasis is largely elusive. In this study, we find that ARID2 expression is significantly decreased in metastatic HCC tissues, showing negative correlation with pathological grade, organ metastasis and positive association with survival of HCC patients. ARID2 inhibits migration and invasion of HCC cells in vitro and metastasis in vivo. Moreover, ARID2 knockout promotes pulmonary metastasis in different HCC mouse models. Mechanistic study reveals that ARID2 represses epithelial–mesenchymal transition (EMT) of HCC cells by recruiting DNMT1 to Snail promoter, which increases promoter methylation and inhibits Snail transcription. In addition, we discover that ARID2 mutants with disrupted C2H2 domain lose the metastasis suppressor function, exhibiting a positive association with HCC metastasis and poor prognosis. In conclusion, our study reveals the metastasis suppressor role as well as the underlying mechanism of ARID2 in HCC and provides a potential therapeutic target for ARID2-deficient HCC.

scholarly journals DEPDC1B is a tumor promotor in development of bladder cancer through targeting SHC1

2020 ◽  
Vol 11 (11) ◽  
Author(s):  
Chin-Hui Lai ◽  
Kexin Xu ◽  
Jianhua Zhou ◽  
Mingrui Wang ◽  
Weiyu Zhang ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Cancer Cells ◽  
Malignant Tumors ◽  
Tumor Grade ◽  
In Vivo Studies ◽  
Mechanistic Study ◽  
Tumor Promotor ◽  
Bladder Cancer Cells

AbstractBladder cancer is one of the most commonly diagnosed malignant tumors in the urinary system and causes a massive cancer-related death. DEPDC1B is a DEP domain-containing protein that has been found to be associated with a variety of human cancers. This study aimed to explore the role and mechanism of DEPDC1B in the development of bladder cancer. The analysis of clinical specimens revealed the upregulated expression of DEPDC1B in bladder cancer, which was positively related to tumor grade. In vitro and in vivo studies showed that DEPDC1B knockdown could inhibit the growth of bladder cancer cells or xenografts in mice. The suppression of bladder cancer by DEPDC1B was executed through inhibiting cell proliferation, cell migration, and promoting cell apoptosis. Moreover, a mechanistic study found that SHC1 may be an important route through which DEPDC1B regulates the development of bladder cancer. Knockdown of SHC1 in DEPDC1B-overexpressed cancer cells could abolish the promotion effects induced by DEPDC1B. In conclusion, DEPDC1B was identified as a key regulator in the development of bladder cancer, which may be used as a potential therapeutic target in the treatment of bladder cancer.

In vitro and in vivo mechanistic study of a novel proanthocyanidin, GC-(4→8)-GCG from cocoa tea (Camellia ptilophylla) in antiangiogenesis

2014 ◽  
Vol 25 (3) ◽  
pp. 319-328 ◽  
Author(s):  
Kai-kai Li ◽  
Cheuk-lun Liu ◽  
Jacqueline Chor-wing Tam ◽  
Hin-fai Kwok ◽  
Ching-po Lau ◽  
...  
Keyword(s):  
Mechanistic Study ◽  
Cocoa Tea

scholarly journals Vanadium pentoxide (V2O5) induced mucin production by airway epithelium

2011 ◽  
Vol 301 (1) ◽  
pp. L31-L39 ◽  
Author(s):  
Dongfang Yu ◽  
Dianne M. Walters ◽  
Lingxiang Zhu ◽  
Pak-Kei Lee ◽  
Yin Chen
Keyword(s):  
Vanadium Pentoxide ◽  
Mapk Pathway ◽  
Mechanistic Study ◽  
Chronic Obstructive ◽  
In Vivo Models ◽  
Mucin Production ◽  
Airway Diseases ◽  
Chronic Airway

Exposure to environmental pollutants has been linked to various airway diseases and disease exacerbations. Almost all chronic airway diseases such as chronic obstructive pulmonary disease and asthma are caused by complicated interactions between gene and environment. One of the major hallmarks of those diseases is airway mucus overproduction (MO). Excessive mucus causes airway obstruction and significantly increases morbidity and mortality. Metals are major components of environmental particulate matters (PM). Among them, vanadium has been suggested to play an important role in PM-induced mucin production. Vanadium pentoxide (V2O5) is the most common commercial source of vanadium, and it has been associated with occupational chronic bronchitis and asthma, both of which are MO diseases. However, the underlying mechanism is not entirely clear. In this study, we used both in vitro and in vivo models to demonstrate the robust inductions of mucin production by V2O5. Furthermore, the follow-up mechanistic study revealed a novel v-raf-1 murine leukemia viral oncogene homolog 1-IKK-NF-κB pathway that mediated V2O5-induced mucin production. Most interestingly, the reactive oxygen species and the classical mucin-inducing epidermal growth factor receptor (EGFR)-MAPK pathway appeared not to be involved in this process. Thus the V2O5-induced mucin production may represent a novel EGFR-MAPK-independent and environmental toxicant-associated MO model. Complete elucidation of the signaling pathway in this model will not only facilitate the development of the treatment for V2O5-associated occupational diseases but also advance our understanding on the EGFR-independent mucin production in other chronic airway diseases.

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