scholarly journals The role of the molecular chaperone CCT in protein folding and mediation of cytoskeleton-associated processes: implications for cancer cell biology

2018 ◽  
Vol 24 (1) ◽  
pp. 17-27 ◽  
Author(s):  
Josefine Vallin ◽  
Julie Grantham
Keyword(s):  
Protein Folding ◽  
Cancer Cell ◽  
Molecular Chaperone ◽  
Cell Biology

scholarly journals The autophagy protein Ambra1 regulates gene expression by supporting novel transcriptional complexes

2020 ◽  
Vol 295 (34) ◽  
pp. 12045-12057
Author(s):  
Christina Schoenherr ◽  
Adam Byron ◽  
Billie Griffith ◽  
Alexander Loftus ◽  
Jimi C. Wills ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cancer Cell ◽  
Cell Invasion ◽  
Cell Biology ◽  
Protein Complexes ◽  
Transcriptional Regulators ◽  
Adaptor Proteins ◽  
Nuclear Pore ◽  
Biochemical Fractionation

Ambra1 is considered an autophagy and trafficking protein with roles in neurogenesis and cancer cell invasion. Here, we report that Ambra1 also localizes to the nucleus of cancer cells, where it has a novel nuclear scaffolding function that controls gene expression. Using biochemical fractionation and proteomics, we found that Ambra1 binds to multiple classes of proteins in the nucleus, including nuclear pore proteins, adaptor proteins such as FAK and Akap8, chromatin-modifying proteins, and transcriptional regulators like Brg1 and Atf2. We identified biologically important genes, such as Angpt1, Tgfb2, Tgfb3, Itga8, and Itgb7, whose transcription is regulated by Ambra1-scaffolded complexes, likely by altering histone modifications and Atf2 activity. Therefore, in addition to its recognized roles in autophagy and trafficking, Ambra1 scaffolds protein complexes at chromatin, regulating transcriptional signaling in the nucleus. This novel function for Ambra1, and the specific genes impacted, may help to explain the wider role of Ambra1 in cancer cell biology.

scholarly journals PRMT5 promotes cancer cell migration and invasion through the E2F pathway

2020 ◽  
Vol 11 (7) ◽  
Author(s):  
Wojciech Barczak ◽  
Li Jin ◽  
Simon Mark Carr ◽  
Shonagh Munro ◽  
Samuel Ward ◽  
...  
Keyword(s):  
Cell Migration ◽  
Cancer Cell ◽  
Cell Biology ◽  
Arginine Methylation ◽  
Migration And Invasion ◽  
Genome Wide ◽  
A Genome ◽  
Important Pathway ◽  
Major Target

Abstract The pRb-E2F pathway is a critical point of regulation in the cell cycle and loss of control of the pathway is a hallmark of cancer. E2F1 is the major target through which pRb exerts its effects and arginine methylation by PRMT5 plays a key role in dictating E2F1 activity. Here we have explored the functional role of the PRMT5-E2F1 axis and highlight its influence on different aspects of cancer cell biology including viability, migration, invasion and adherence. Through a genome-wide expression analysis, we identified a distinct set of genes under the control of PRMT5 and E2F1, including some highly regulated genes, which influence cell migration, invasio and adherence through a PRMT5-dependent mechanism. Most significantly, a coincidence was apparent between the expression of PRMT5 and E2F1 in human tumours, and elevated levels of PRMT5 and E2F1 correlated with poor prognosis disease. Our results suggest a causal relationship between PRMT5 and E2F1 in driving the malignant phenotype and thereby highlight an important pathway for therapeutic intervention.

The role of Sp1 and Sp3 in normal and cancer cell biology

2010 ◽  
Vol 192 (5) ◽  
pp. 275-283 ◽  
Author(s):  
Lin Li ◽  
James R. Davie
Keyword(s):  
Cancer Cell ◽  
Cell Biology

APPLICATIONS OF NUCLEAR MICROPROBE ANALYSIS IN CANCER CELL BIOLOGY AND PHARMACOLOGY

1999 ◽  
Vol 09 (03n04) ◽  
pp. 235-244 ◽  
Author(s):  
RICHARD ORTEGA
Keyword(s):  
Cancer Cell ◽  
Anticancer Agents ◽  
Cell Biology ◽  
Microprobe Analysis ◽  
Nuclear Microprobe ◽  
Cellular Pharmacology ◽  
Metal Carcinogenesis ◽  
In Trans ◽  
Particle Backscattering

Nuclear microprobe analysis studies in cancer cell pharmacology and biology carried out at Bordeaux-Gradignan are reported. The cellular pharmacology of two anticancer agents, cis-diammine-dichloroplatinum(II), and 4′-iodo-4′-deoxy-doxorubicin, were investigated, as well as the role of iron in neuroblastoma carcinogenesis, and chromium(III) in trans-generation carcinogenesis. Nuclear microprobe analysis, using PIXE and particle backscattering microanalysis, was able to reveal intracellular and tissue distributions of the elements under investigation. Moreover, the fully quantitative and multi-elemental character of nuclear microprobe analysis offered information on possible mechanisms of drug action, metal carcinogenesis, and interactions with endogenous trace elements in cancer cells.

scholarly journals KH-type splicing regulatory protein controls colorectal cancer cell growth and modulates the tumor microenvironment

2018 ◽  
Author(s):  
Francesco Caiazza ◽  
Katarzyna Oficjalska ◽  
Miriam Tosetto ◽  
James J. Phelan ◽  
Sinéad Noonan ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Fate ◽  
Cancer Cell ◽  
In Silico ◽  
Cell Biology ◽  
Ex Vivo ◽  
Regulatory Protein ◽  
Nucleic Acid Binding ◽  
Metastatic Setting

ABSTRACTKH-type splicing regulatory protein (KHSRP) is a multifunctional nucleic acid binding protein implicated in key aspects of cancer cell biology: inflammation and cell-fate determination. However, the role KHSRP plays in colorectal cancer (CRC) tumorigenesis remains largely unknown. Using a combination ofin silicoanalysis of large datasets,ex vivoanalysis of protein expression in patients, and mechanistic studies usingin vitromodels of CRC, we investigated the oncogenic role of KHSRP. We demonstrated KHSRP expression in the epithelial and stromal compartments of both primary and metastatic tumors. Elevated expression was found in tumor versus matched normal tissue, and we validated these findings in larger independent cohortsin silico.KHSRP expression was a prognostic indicator of worse overall survival (HR=3.74, 95% CI = 1.43-22.97, p=0.0138). Mechanistic data in CRC cell line models supported a role of KHSRP in driving epithelial cell proliferation in both a primary and metastatic setting, through control of the G1/S transition. Additionally, KHSRP promoted a pro-angiogenic extracellular environment by regulating the secretion of oncogenic proteins involved in diverse cellular processes such as migration and response to cellular stress. Our study provides novel mechanistic insight into the tumor-promoting effects of KHSRP in CRC.

Chemokines: Brief review and its Role in Cancer Cell Biology

2012 ◽  
Vol 2 (12) ◽  
pp. 415-416
Author(s):  
Dr. Priyanka R Prasad ◽  
◽  
Dr. Anju N Duttargi ◽  
Dr. Sreeshyla H.S Dr. Sreeshyla H.S ◽  
Dr. Usha Hegde ◽  
...  
Keyword(s):  
Cancer Cell ◽  
Cell Biology

ARFGAP3 an androgen target gene promotes prostate cancer cell proliferation and migration.

2020 ◽  
Author(s):  
Lungwani Muungo
Keyword(s):  
Cell Proliferation ◽  
Cancer Cell ◽  
Cell Biology ◽  
Adaptor Protein ◽  
Cancer Cell Proliferation ◽  
Lncap Cells ◽  
Gtpase Activating Protein ◽  
Cell Proliferation And Migration ◽  
And Migration ◽  
Proliferation And Migration

ADP ribosylation factor GTPase-activating protein 3 (ARFGAP3) is a GTPase-activating protein that associates with the Golgiapparatus and regulates the vesicular trafficking pathway. In the present study, we examined the contribution of ARFGAP3 toprostate cancer cell biology. We showed that ARFGAP3 expression was induced by 100 nM of dihydrotestosterone (DHT) atboth the mRNA and protein levels in androgen-sensitive LNCaP cells. We generated stable transfectants of LNCaP cells withFLAG-tagged ARFGAP3 or a control empty vector and showed that ARFGAP3 overexpression promoted cell proliferation andmigration compared with control cells. We found that ARFGAP3 interacted with paxillin, a focal adhesion adaptor protein thatis important for cell mobility and migration. Small interfering RNA (siRNA)-mediated knockdown of ARFGAP3 showed thatARFGAP3 siRNA markedly reduced LNCaP cell growth. Androgen receptor (AR)-dependent transactivation activity on prostatespecificantigen (PSA) enhancer was synergistically promoted by exogenous ARFGAP3 and paxillin expression, as shown byluciferase assay in LNCaP cells. Thus, our results suggest that ARFGAP3 is a novel androgen-regulated gene that can promoteprostate cancer cell proliferation and migration in collaboration with paxillin.

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