scholarly journals Epigenetic silencing of miR-296 and miR-512 ensures hTERT dependent apoptosis protection and telomere maintenance in basal-type breast cancer cells

Oncotarget ◽  
2017 ◽  
Vol 8 (56) ◽  
pp. 95674-95691 ◽  
Author(s):  
Roberto Dinami ◽  
Valentina Buemi ◽  
Rosanna Sestito ◽  
Antonina Zappone ◽  
Yari Ciani ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Epigenetic Silencing ◽  
Telomere Maintenance ◽  
Basal Type

scholarly journals Control of MYC-dependent apoptotic threshold by a co-amplified ubiquitin E3 ligase UBR5

2019 ◽  
Author(s):  
Xi Qiao ◽  
Ying Liu ◽  
Maria Llamazares Prada ◽  
Abhishekh Gupta ◽  
Alok Jaiswal ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Protein Expression ◽  
Cancer Cells ◽  
Ubiquitin Ligase ◽  
Breast Cancer Cells ◽  
Human Cancer ◽  
Cancer Therapeutics ◽  
Cancer Tissue ◽  
Basal Type

AbstractMYC protein expression has to be tightly controlled to allow for maximal cell proliferation without inducing apoptosis. Here we discover UBR5 as a novel MYC ubiquitin ligase and demonstrate how it functions as a molecular rheostat to prevent excess accumulation of MYC protein. UBR5 effects on MYC protein stability are independent on N-terminal FBW7 degron of MYC. Endogenous UBR5 inhibition induces MYC protein expression and activates MYC target genes. Moreover, UBR5 governs MYC-dependent phenotypes in vivo in Drosophila. In cancer cells, UBR5-mediated MYC protein suppression diminishes cell killing activity of cancer therapeutics. Further, we demonstrate that UBR5 dominates MYC protein expression at the single-cell level in human basal-type breast cancer tissue. Myc and Ubr5 are co-amplified in MYC-driven human cancer types, and UBR5 controls MYC-mediated apoptotic threshold in co-amplified basal type breast cancer cells. In summary, UBR5 is a novel MYC ubiquitin ligase and an endogenous rheostat for MYC protein expression in vivo. Clinically, expression of UBR5 may be important for protection of breast cancer cells from drug-induced, and MYC-dependent, apoptosis.

scholarly journals Resveratrol Prevents Epigenetic Silencing of BRCA-1 by the Aromatic Hydrocarbon Receptor in Human Breast Cancer Cells

2010 ◽  
Vol 140 (9) ◽  
pp. 1607-1614 ◽  
Author(s):  
Andreas J. Papoutsis ◽  
Sarah D. Lamore ◽  
Georg T. Wondrak ◽  
Ornella I. Selmin ◽  
Donato F. Romagnolo
Keyword(s):  
Breast Cancer ◽  
Aromatic Hydrocarbon ◽  
Cancer Cells ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Epigenetic Silencing ◽  
Human Breast Cancer Cells ◽  
Human Breast ◽  
Aromatic Hydrocarbon Receptor ◽  
Brca 1

scholarly journals Epigenetic silencing of RNF144A expression in breast cancer cells through promoter hypermethylation and MBD4

2018 ◽  
Vol 7 (4) ◽  
pp. 1317-1325 ◽  
Author(s):  
Ye Zhang ◽  
Yin-Long Yang ◽  
Fang-Lin Zhang ◽  
Xiao-Hong Liao ◽  
Zhi-Min Shao ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Promoter Hypermethylation ◽  
Epigenetic Silencing

scholarly journals Epigenetic Silencing of miR-203 Upregulates SNAI2 and Contributes to the Invasiveness of Malignant Breast Cancer Cells

2011 ◽  
Vol 2 (8) ◽  
pp. 782-791 ◽  
Author(s):  
Z. Zhang ◽  
B. Zhang ◽  
W. Li ◽  
L. Fu ◽  
L. Fu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Epigenetic Silencing ◽  
Malignant Breast

scholarly journals hTERT Downregulation Attenuates Resistance to DOX, Impairs FAK-Mediated Adhesion, and Leads to Autophagy Induction in Breast Cancer Cells

Cells ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 867
Author(s):  
Aleksandra Romaniuk-Drapała ◽  
Ewa Totoń ◽  
Natalia Konieczna ◽  
Marta Machnik ◽  
Wojciech Barczak ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Therapeutic Potential ◽  
Telomerase Activity ◽  
Telomere Maintenance ◽  
Population Doubling ◽  
Cell Cycle Distribution ◽  
Human Telomerase Reverse Transcriptase ◽  
Human Telomerase

Telomerase is known to contribute to telomere maintenance and to provide cancer cell immortality. However, numerous reports are showing that the function of the enzyme goes far beyond chromosome ends. The study aimed to explore how telomerase downregulation in MCF7 and MDA-MB-231 breast cancer cells affects their ability to survive. Consequently, sensitivity to drug resistance, proliferation, and adhesion were assessed. The lentiviral-mediated human telomerase reverse transcriptase (hTERT) downregulation efficiency was performed at gene expression and protein level using qPCR and Western blot, respectively. Telomerase activity was evaluated using the Telomeric Repeat Amplification Protocol (TRAP) assay. The study revealed that hTERT downregulation led to an increased sensitivity of breast cancer cells to doxorubicin which was demonstrated in MTT and clonogenic assays. During a long-term doubling time assessment, a decreased population doubling level was observed. Interestingly, it did not dramatically affect cell cycle distribution. hTERT downregulation was accompanied by an alteration in β1-integrin- and by focal adhesion kinase (FAK)-driven pathways together with the reduction of target proteins phosphorylation, i.e., paxillin and c-Src. Additionally, autophagy activation was observed in MDA-MB-231 cells manifested by alternations in Atg5, Beclin 1, LC3II/I ratio, and p62. These results provide new evidence supporting the possible therapeutic potential of telomerase downregulation leading to induction of autophagy and cancer cells elimination.

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