MicroRNA hsa-miR-29b potentiates etoposide toxicity in HeLa cells via down-regulation of Mcl-1

2017 ◽  
Vol 40 ◽  
pp. 289-296 ◽  
Author(s):  
S. Kollinerová ◽  
Z. Dostál ◽  
M. Modrianský
Keyword(s):  
Hela Cells ◽  
Down Regulation

scholarly journals LAPTM4B Down Regulation Inhibits the Proliferation, Invasion and Angiogenesis of HeLa Cells In Vitro

2015 ◽  
Vol 37 (3) ◽  
pp. 890-900 ◽  
Author(s):  
Fanling Meng ◽  
Xiuwei Chen ◽  
Hongtao Song ◽  
Ge Lou
Keyword(s):  
Cervical Cancer ◽  
Hela Cells ◽  
Molecular Mechanisms ◽  
Tube Formation ◽  
Cell Counting ◽  
Migration And Invasion ◽  
Branch Points ◽  
Down Regulation ◽  
Migration Potential

Background/Aims: LAPTM4B (lysosome-associated protein transmembrane 4 beta) is a novel oncogene with important functions in aggressive human carcinomas, including cervical cancer. However, the specific functions and internal molecular mechanisms associated with this gene in the context of cervical cancer remain unclear. Methods: In this study, we explored the effects and mechanisms of LAPTM4B on tumor growth, metastasis and angiogenesis in vitro by depletion of LAPTM4B in Hela cell. RNA interference was used to induce down regulation of LAPTM4B gene expression in Hela cells. The motility, migration potential, and proliferation of the Hela cells were measured by flow cytometry, Transwell migration assays, wound healing assays, and Cell Counting Kit-8 assays. In addition, the cell cycle analysis utilized fluorescence-activated cell sorting. Results: In this study, RNAi-mediated LAPTM4B knockdown inhibited cell growth and angiogenesis. In vitro, HeLa cells with down regulated LAPTM4B also exhibited decreased migration and invasion activity as well as significantly reduced CDK12, HIF-1α, MMP-2, MMP-9 and VEGF expression. LAPTM4B blockade significantly decreased cord lengths and branch points in a tube formation assay. Conclusions: These results suggested that LAPTM4B inactivation could be a novel therapeutic target for cervical cancer.

scholarly journals Effect of mitochondrial ATP synthase subunit e and g (ATP5I and ATP5L) down-regulation in HeLa cells

2014 ◽  
Vol 1837 ◽  
pp. e18-e19 ◽  
Author(s):  
Patrick Paumard ◽  
Johann Habersetzer ◽  
Isabelle Larrieu ◽  
Muriel Priault ◽  
Bénédicte Salin ◽  
...  
Keyword(s):  
Atp Synthase ◽  
Hela Cells ◽  
Down Regulation ◽  
Mitochondrial Atp Synthase ◽  
Subunit E

Analysis of the biologic functions of H- and L-ferritins in HeLa cells by transfection with siRNAs and cDNAs: evidence for a proliferative role of L-ferritin

Blood ◽  
2004 ◽  
Vol 103 (6) ◽  
pp. 2377-2383 ◽  
Author(s):  
Anna Cozzi ◽  
Barbara Corsi ◽  
Sonia Levi ◽  
Paolo Santambrogio ◽  
Giorgio Biasiotto ◽  
...  
Keyword(s):  
Hela Cells ◽  
Iron Homeostasis ◽  
Background Level ◽  
Iron Availability ◽  
Small Interfering Rnas ◽  
Down Regulation ◽  
Independent Manner ◽  
Cellular Iron ◽  
Cell Clones ◽  
Cellular Iron Homeostasis

Abstract We describe the use of small interfering RNAs (siRNAs) to down-regulate H- and L-ferritin levels in HeLa cells. siRNAs repressed H- and L-ferritin expression to about 20% to 25% of the background level in both stable and transient transfections. HeLa cells transfected with H- and L-ferritin cDNAs were analyzed in parallel to compare the effects of ferritin up- and down-regulation. We found that large modifications of L-ferritin levels did not affect iron availability in HeLa cells but positively affected cell proliferation rate in an iron-independent manner. The transient down-regulation of H-ferritin modified cellular iron availability and resistance to oxidative damage, as expected. In contrast, the stable suppression of H-ferritin in HeLa cell clones transfected with siRNAs did not increase cellular iron availability but made cells less resistant to iron supplementation and chelation. The results indicate that L-ferritin has no direct effects on cellular iron homeostasis in HeLa cells, while it has new, iron-unrelated functions. In addition, they suggest that H-ferritin function is to act as an iron buffer.

TNF Alpha-induced down regulation of the human KE4 gene in HeLa cells

2000 ◽  
Vol 28 (5) ◽  
pp. A286-A286
Author(s):  
I. Lana ◽  
A. Vergara ◽  
I. Encío
Keyword(s):  
Hela Cells ◽  
Tnf Alpha ◽  
Down Regulation

scholarly journals Antisense-induced down-regulation of thymidylate synthase and enhanced cytotoxicity of 5-FUdR in 5-FUdR-resistant HeLa cells

2001 ◽  
Vol 134 (7) ◽  
pp. 1437-1446 ◽  
Author(s):  
Peter J Ferguson ◽  
Janice M DeMoor ◽  
Mark D Vincent ◽  
James Koropatnick
Keyword(s):  
Thymidylate Synthase ◽  
Hela Cells ◽  
Down Regulation

scholarly journals Infarct-Induced Steroidogenic Acute Regulatory Protein: A Survival Role in Cardiac Fibroblasts

2013 ◽  
Vol 27 (9) ◽  
pp. 1502-1517 ◽  
Author(s):  
Eli Anuka ◽  
Natalie Yivgi-Ohana ◽  
Sarah Eimerl ◽  
Benjamin Garfinkel ◽  
Naomi Melamed-Book ◽  
...  
Keyword(s):  
Hela Cells ◽  
Cardiac Fibroblasts ◽  
Primary Cultures ◽  
Regulatory Protein ◽  
Steroidogenic Acute Regulatory Protein ◽  
Mouse Heart ◽  
Heart Cells ◽  
Down Regulation ◽  
Apparent Lack ◽  
Steroidogenic Acute Regulatory

Steroidogenic acute regulatory protein (StAR) is indispensable for steroid hormone synthesis in the adrenal cortex and the gonadal tissues. This study reveals that StAR is also expressed at high levels in nonsteroidogenic cardiac fibroblasts confined to the left ventricle of mouse heart examined 3 days after permanent ligation of the left anterior descending coronary artery. Unlike StAR, CYP11A1 and 3β-hydroxysteroid dehydrogenase proteins were not observed in the postinfarction heart, suggesting an apparent lack of de novo cardiac steroidogenesis. Work with primary cultures of rat heart cells revealed that StAR is induced in fibroblasts responding to proapoptotic treatments with hydrogen peroxide or the kinase inhibitor staurosporine (STS). Such induction of StAR in culture was noted before spontaneous differentiation of the fibroblasts to myofibroblasts. STS induction of StAR in the cardiac fibroblasts conferred a marked resistance to apoptotic cell death. Consistent with that finding, down-regulation of StAR by RNA interference proportionally increased the number of STS-treated apoptotic cells. StAR down-regulation also resulted in a marked increase of BAX activation in the mitochondria, an event known to associate with the onset of apoptosis. Last, STS treatment of HeLa cells showed that apoptotic demise characterized by mitochondrial fission, cytochrome c release, and nuclear fragmentation is arrested in individual HeLa cells overexpressing StAR. Collectively, our in vivo and ex vivo evidence suggests that postinfarction expression of nonsteroidogenic StAR in cardiac fibroblasts has novel antiapoptotic activity, allowing myofibroblast precursor cells to survive the traumatized event, probably to differentiate and function in tissue repair at the infarction site.

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