ChemInform Abstract: HIV-1 Neutralization and Tumor Cell Proliferation Inhibition in vitro by Simplified Analogues of Pyrido(4,3,2-mn)thiazolo(5,4-b)acridine Marine Alkaloids.

ChemInform ◽  
2010 ◽  
Vol 23 (52) ◽  
pp. no-no
Author(s):  
I. B. TARAPOREWALA ◽  
J. W. CESSAC ◽  
T. C. CHANH ◽  
A. V. DELGADO ◽  
R. F. SCHINAZI
Keyword(s):  
Cell Proliferation ◽  
Tumor Cell ◽  
Proliferation Inhibition ◽  
Tumor Cell Proliferation ◽  
Marine Alkaloids ◽  
Cell Proliferation Inhibition ◽  
Hiv 1

Evaluating the possible genotoxic, mutagenic and tumor cell proliferation-inhibition effects of a non-anticoagulant, but antithrombotic algal heterofucan

2010 ◽  
Vol 30 (7) ◽  
pp. 708-715 ◽  
Author(s):  
Jailma Almeida-Lima ◽  
Leandro Silva Costa ◽  
Naisandra Bezerra Silva ◽  
Raniere Fagundes Melo-Silveira ◽  
Fábio Vasconcelos Silva ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Tumor Cell ◽  
Proliferation Inhibition ◽  
Tumor Cell Proliferation ◽  
Cell Proliferation Inhibition

scholarly journals The human vault RNA enhances tumorigenesis and chemoresistance through the lysosome

2020 ◽  
Author(s):  
Iolanda Ferro ◽  
Jacopo Gavini ◽  
Lisamaria Bracher ◽  
Marc Landolfo ◽  
Daniel Candinas ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Tumor Cell ◽  
Chemotherapy Resistance ◽  
Autophagic Flux ◽  
Tumor Cell Proliferation ◽  
Apoptosis Resistance ◽  
Knock Out ◽  
Vault Rna

AbstractThe small non-coding vault RNA (vtRNA) 1-1 has been shown to confer apoptosis resistance in several malignant cell lines and also to modulate the autophagic flux in hepatocytes, thus highlighting its pro-survival role. Here we describe a new function of vtRNA1-1 in regulating in vitro and in vivo tumor cell proliferation, tumorigenesis and chemoresistance. By activating extracellular signal-regulated kinases (ERK 1/2), vtRNA1-1 knock-out (KO) inhibits transcription factor EB (TFEB), leading to a downregulation of the coordinated lysosomal expression and regulation (CLEAR) network genes and lysosomal compartment dysfunction. Pro-tumorigenic pathways dysregulation and decreased lysosome functionality potentiate the anticancer effect of conventional targeted cancer drugs in the absence of vtRNA1-1. Finally, vtRNA1-1 KO-reduced lysosomotropism, together with a higher intracellular compound availability, significantly reduced tumor cell proliferation in vitro and in vivo. These findings reveal the role of vtRNA1-1 in ensuring intracellular catabolic compartment stability and functionality, suggesting its importance in lysosome-mediated chemotherapy resistance.

scholarly journals PTP4A3, A Novel Target Gene of HIF-1alpha, Participates in Benzene-Induced Cell Proliferation Inhibition and Apoptosis through PI3K/AKT Pathway

2020 ◽  
Vol 17 (3) ◽  
pp. 910
Author(s):  
Yunqiu Pu ◽  
Fengxia Sun ◽  
Rongli Sun ◽  
Zhaodi Man ◽  
Shuangbin Ji ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Target Gene ◽  
Akt Pathway ◽  
Proliferation Inhibition ◽  
Cell Proliferation Inhibition ◽  
A Cell ◽  
Novel Target ◽  
In Cells

Benzene, a commonly used chemical, has been confirmed to specifically affect the hematopoietic system as well as overall human health. PTP4A3 is overexpressed in leukemia cells and is related to cell proliferation. We previously found that HIF-1alpha was involved in benzene toxicity and PTP4A3 may be the target gene of HIF-1alpha via ChIP-seq. The aim of this study is to confirm the relationship between HIF-1alpha and PTP4A3 in benzene toxicity, as well as the function of PTP4A3 on cell toxicity induced by 1,4-benzoquinone (1,4-BQ). Our results indicate that HIF-1alpha could regulate PTP4A3 with in vivo and in vitro experiments. A cell line with suppressed PTP4A3 was established to investigate the function of PTP4A3 in 1,4-BQ toxicity in vitro. The results revealed that cell proliferation inhibition was more aggravated in PTP4A3 low-expression cells than in the control cells after 1,4-BQ treatment. The relative oxygen species (ROS) significantly increased in cells with inhibited PTP4A3, while the rise was inferior to the control cells at the 20 μM 1,4-BQ group. An increase in DNA damage was seen in PTP4A3 down-regulated cells at the 10 μM 1,4-BQ group, whereas the results reversed at the concentration of 20 μM. Moreover, the apoptosis rate increased higher in down-regulated PTP4A3 cells after 1,4-BQ exposure. In addition, PI3K/AKT pathway was significantly restrained in cells with inhibited PTP4A3 after 1,4-BQ treatment. Our results indicate that HIF-1alpha may regulate PTP4A3 to be involved in benzene toxicity. Inhibition of PTP4A3 could aggravate cell proliferation suppression and apoptosis by regulating PI3K/AKT pathway after 1,4-BQ treatment.

scholarly journals Assessment of Tracer 99mTc(V)-DMSA Uptake as a Measure of Tumor Cell Proliferation In Vitro

PLoS ONE ◽  
2013 ◽  
Vol 8 (1) ◽  
pp. e54361 ◽  
Author(s):  
Fatma J. Al-Saeedi ◽  
Princy M. Mathew ◽  
Yunus A. Luqmani
Keyword(s):  
Cell Proliferation ◽  
Tumor Cell ◽  
Tumor Cell Proliferation ◽  
Proliferation In Vitro

In Vitro Effects of Glycosphingolipids on Human Tumor Cell Proliferation

1981 ◽  
Vol 166 (1) ◽  
pp. 107-112 ◽  
Author(s):  
P. M. Kimball ◽  
L. Hammonds ◽  
J. M. McKibbin ◽  
M. G. Brattain ◽  
G. Glover ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Tumor Cell ◽  
Human Tumor ◽  
Tumor Cell Proliferation ◽  
Human Tumor Cell ◽  
In Vitro Effects

scholarly journals NLRR1 Is a Potential Therapeutic Target in Neuroblastoma and MYCN-Driven Malignant Cancers

2021 ◽  
Vol 11 ◽  
Author(s):  
Atsushi Takatori ◽  
Shamim Hossain ◽  
Atsushi Ogura ◽  
Jesmin Akter ◽  
Yohko Nakamura ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Tumor Cell ◽  
Inhibitory Effect ◽  
Tumor Cell Proliferation ◽  
Growth Inhibitory Effect ◽  
Extracellular Domains ◽  
Growth Inhibitory ◽  
Fniii Domain

Receptor tyrosine kinases (RTKs) receive different modulation before transmitting proliferative signals. We previously identified neuronal leucine-rich repeat 1 (NLRR1) as a positive regulator of EGF and IGF-1 signals in high-risk neuroblastoma cells. Here, we show that NLRR1 is up-regulated in various adult cancers and acts as a key regulator of tumor cell proliferation. In the extracellular domains of NLRR1, fibronectin type III (FNIII) domain is responsible for its function to promote cell proliferation. We generated monoclonal antibodies against the extracellular domains of NLRR1 (N1mAb) and screened the positive N1mAbs for growth inhibitory effect. The treatment of N1mAbs reduces tumor cell proliferation in vitro and in vivo, and sensitizes the cells to EGFR inhibitor, suggesting that NLRR1 is a novel regulatory molecule of RTK function. Importantly, epitope mapping analysis has revealed that N1mAbs with growth inhibitory effect recognize immunoglobulin-like and FNIII domains of NLRR1, which also indicates the importance of FNIII domain in the function of NLRR1. Thus, the present study provides a new insight into the development of a cancer therapy by targeting NLRR1 as a modulator of proliferative signals on cellular membrane of tumor cells.

Sign in / Sign up

Export Citation Format

Share Document