scholarly journals Establishment of SHOX CNE9/10 knock-out osteosarcoma U2OS cell and its effects on cell growth and apoptosis

2020 ◽  
Vol 26 ◽  
Author(s):  
Xue-Jiao Xu ◽  
Shi-Jie Xin ◽  
Hui-Ying Mao ◽  
Hui-Jiao Zhang ◽  
Lan-Ni Chen ◽  
...  
Keyword(s):  
Cell Growth ◽  
U2os Cell ◽  
Knock Out

scholarly journals Primary effusion lymphoma enhancer connectome links super-enhancers to dependency factors

2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Chong Wang ◽  
Luyao Zhang ◽  
Liangru Ke ◽  
Weiyue Ding ◽  
Sizun Jiang ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Growth ◽  
Cell Line ◽  
Poor Prognosis ◽  
Target Gene ◽  
Primary Effusion Lymphoma ◽  
Knock Out ◽  
Growth And Survival ◽  
Super Enhancer ◽  
Genome Wide

AbstractPrimary effusion lymphoma (PEL) has a very poor prognosis. To evaluate the contributions of enhancers/promoters interactions to PEL cell growth and survival, here we produce H3K27ac HiChIP datasets in PEL cells. This allows us to generate the PEL enhancer connectome, which links enhancers and promoters in PEL genome-wide. We identify more than 8000 genomic interactions in each PEL cell line. By incorporating HiChIP data with H3K27ac ChIP-seq data, we identify interactions between enhancers/enhancers, enhancers/promoters, and promoters/promoters. HiChIP further links PEL super-enhancers to PEL dependency factors MYC, IRF4, MCL1, CCND2, MDM2, and CFLAR. CRISPR knock out of MEF2C and IRF4 significantly reduces MYC and IRF4 super-enhancer H3K27ac signal. Knock out also reduces MYC and IRF4 expression. CRISPRi perturbation of these super-enhancers by tethering transcription repressors to enhancers significantly reduces target gene expression and reduces PEL cell growth. These data provide insights into PEL molecular pathogenesis.

IL-2 and IL-4 double knock-out mice reject islet allografts: A role for novel T-cell growth factors?

1997 ◽  
Vol 29 (1-2) ◽  
pp. 1083-1084 ◽  
Author(s):  
P. Roy-Chaudhury ◽  
R.C. Manfro ◽  
J. Steiger ◽  
P.W. Nickerson ◽  
Y. Tian ◽  
...  
Keyword(s):  
Growth Factors ◽  
T Cell ◽  
Cell Growth ◽  
Knock Out ◽  
Islet Allografts ◽  
T Cell Growth ◽  
Knock Out Mice

scholarly journals gcFront: a tool for determining a Pareto front of growth-coupled cell factory designs

2021 ◽  
Author(s):  
Laurence Legon ◽  
Christophe Corre ◽  
Declan G. Bates ◽  
Ahmad A. Mannan
Keyword(s):  
Cell Growth ◽  
Coupling Strength ◽  
Rational Design ◽  
Pareto Front ◽  
Software Tool ◽  
Cell Factory ◽  
Knock Out ◽  
Cell Factories ◽  
Growth Product ◽  
Genome Scale

Motivation: A widely applicable strategy for developing evolutionarily robust cell factories is to knock out (KO) genes or reactions to couple chemical synthesis with cell growth. Genome-scale metabolic models enable their rational design, but KOs that provide growth-coupling (gc) are rare in the immense design space, making searching difficult and slow, and though several measures determine the utility of those strains, few drive the search. Results: To address these issues we developed a software tool named gcFront - using a genetic algorithm it explores KOs that maximise key performance objectives: cell growth, product synthesis, and coupling strength. Our measure of coupling strength facilitates the search, so gcFront not only finds a gc-design in minutes but also outputs many alternative Pareto optimal gc-designs from a single run - granting users freedom to select designs to take to the lab.

Tenascin C to regulate the function of sHER3, an endogenous inhibitor of neuregulin signaling.

2017 ◽  
Vol 35 (15_suppl) ◽  
pp. e23002-e23002
Author(s):  
Chunlin Cai ◽  
Mojun Zhu ◽  
Nita J. Maihle
Keyword(s):  
Cell Proliferation ◽  
Cell Migration ◽  
Cell Growth ◽  
Cell Lines ◽  
Melanoma Cell ◽  
Cell Growth And Migration ◽  
Knock Out ◽  
Tenascin C ◽  
And Migration

e23002 Background: HER3 expression is associated with poor prognosis in melanoma patients but the mechanistic basis has not been determined. An endogenous secreted isoform of HER3, p85-sHER3, has been shown by us to inhibit neuregulin-1 mediated, Akt-dependent breast and ovarian cancer cell growth in vitro. Here we demonstrate that p85-sHER3 also regulates neuregulin-dependent melanoma cell migration via an Akt- independent, tenascin C-dependent mechanism. Methods: Immunoblot analysis and RT-PCR were used to study HER3 and p85-sHER expression. Cell proliferation and chamber assays were conducted to determine the effect of p85-sHER3 on melanoma cell growth and migration. Mass spectrometry (MS) was performed to identify sHER3-interacting proteins. CRSPR in vitro editing methods were used to knock out tenascin C (TNC) expression. Results: HER3 and p85-sHER3 were expressed in 5 of 6 human melanoma-derived cell lines tested, with exception of SK-MEL-103 which did not express either gene product. Exogenous addition of 10 nM p85-sHER3 inhibited growth in 3 cells lines, although Akt phosphorylation was not reduced. Protein extracts from M14-MEL cell conditioned media were characterized by MS, and identified p85-sHER3 and TNC. Their association was confirmed by co-immunoprecipitation. sHER3 was further shown to inhibit neuregulin stimulated cell migration in 2 cell lines which exhibited high levels of TNC. CRSPR knockout of TNC in these cell lines (but not in control lines) eliminated sHER3 inhibition of neuregulin stimulated melanoma cell migration. Conclusions: Our results suggest that p85-sHER3, predominantly secreted by HER3-expressing melanoma cells, inhibits melanoma cell proliferation and migration via an Akt-independent mechanism, which is likely achieved through interaction(s) with TNC. TNC promotes an intermediate adhesive state favoring cell migration and this state appears to be mediated by Rho-associated kinase signaling. The Rho inhibitor, CCG-203971 has been shown to inhibit melanoma cell migration. Together, these results suggest the existence of a TNC and HER3-dependent signaling pathway in melanoma that regulates cell migration, and therefore may be correlated with poor patient survival.

Electron Microscopic Study of the Epithelium of the Seminal Vesicle of Aging Rats

1974 ◽  
Vol 32 ◽  
pp. 138-139
Author(s):  
V. F. Allison ◽  
G. C. Fink ◽  
G. W. Cearley
Keyword(s):  
Cell Growth ◽  
Epithelial Cell ◽  
Epithelial Cells ◽  
Seminal Vesicle ◽  
Seminal Vesicles ◽  
Epithelial Layer ◽  
Epithelial Hyperplasia ◽  
Electron Microscopic ◽  
Aging Rats ◽  
Pseudostratified Epithelium

It is well known that epithelial hyperplasia (benign hypertrophy) is common in the aging prostate of dogs and man. In contrast, little evidence is available for abnormal epithelial cell growth in seminal vesicles of aging animals. Recently, enlarged seminal vesicles were reported in senescent mice, however, that enlargement resulted from increased storage of secretion in the lumen and occurred concomitant to epithelial hypoplasia in that species.The present study is concerned with electron microscopic observations of changes occurring in the pseudostratified epithelium of the seminal vescles of aging rats. Special attention is given to certain non-epithelial cells which have entered the epithelial layer.

Rotary Beveling for In Situ Thin-Section Microscopy of Cell Cultures

1981 ◽  
Vol 39 ◽  
pp. 550-551
Author(s):  
Dean A. Handley ◽  
Jack T. Alexander ◽  
Shu Chien
Keyword(s):  
Cell Growth ◽  
Cell Cultures ◽  
Molecular Interactions ◽  
Convenient Method ◽  
Petri Dish ◽  
Simple Method ◽  
Thin Section Microscopy ◽  
Thin Sectioning ◽  
Organic Fluids

In situ preparation of cell cultures for ultrastructural investigations is a convenient method by which fixation, dehydration and embedment are carried out in the culture petri dish. The in situ method offers the advantage of preserving the native orientation of cell-cell interactions, junctional regions and overlapping configurations. In order to section after embedment, the petri dish is usually separated from the polymerized resin by either differential cryo-contraction or solvation in organic fluids. The remaining resin block must be re-embedded before sectioning. Although removal of the petri dish may not disrupt the native cellular geometry, it does sacrifice what is now recognized as an important characteristic of cell growth: cell-substratum molecular interactions. To preserve the topographic cell-substratum relationship, we developed a simple method of tapered rotary beveling to reduce the petri dish thickness to a dimension suitable for direct thin sectioning.

414: Induction of LNCAP Cell Growth, Androgen-Independence and Bone Metastasis by Human Prostate Fibroblasts of Different Zonal Origin

2006 ◽  
Vol 175 (4S) ◽  
pp. 135-135
Author(s):  
George N. Thalmann ◽  
H. Rhee Atlanta ◽  
R.A. Sikes ◽  
S. Pathak ◽  
Haiyen E. Zhau ◽  
...  
Keyword(s):  
Bone Metastasis ◽  
Cell Growth ◽  
Lncap Cell ◽  
Human Prostate ◽  
Androgen Independence
Sign in / Sign up

Export Citation Format

Share Document