S-phase determination of immunoselected cytokeratin-containing breast cancer cells improves the prediction of recurrence

1994 ◽  
Vol 29 (2) ◽  
pp. 179-187 ◽  
Author(s):  
Sten Wingren ◽  
Olle St�l ◽  
John Carstensen ◽  
Xiao-Feng Sun ◽  
Bo Nordenskj�ld
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
S Phase ◽  
Phase Determination

scholarly journals Inhibition of MCF-7 breast cancer cell proliferation by 5alpha-dihydrotestosterone; a role for p21(Cip1/Waf1)

2004 ◽  
Vol 32 (3) ◽  
pp. 793-810 ◽  
Author(s):  
MA Greeve ◽  
RK Allan ◽  
JM Harvey ◽  
JM Bentel
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
S Phase ◽  
Cyclin D3 ◽  
P27 Kip1 ◽  
Mcf 7

Androgens inhibit the growth of breast cancer cells in vitro and in vivo by mechanisms that remain poorly defined. In this study, treatment of asynchronously growing MCF-7 breast cancer cells with the androgen, 5alpha-dihydrotestosterone (DHT), was shown to inhibit cell proliferation and induce moderate increases in the proportion of G1 phase cells. Consistent with targeting the G1-S phase transition, DHT pretreatment of MCF-7 cultures impeded the serum-induced progression of G1-arrested cells into S phase and reduced the kinase activities of cyclin-dependent kinase (Cdk)4 and Cdk2 to less than 50% of controls within 3 days. DHT treatment was associated with greater than twofold increases in the levels of the Cdk inhibitor, p27(Kip1), while p21(Cip1/Waf1) protein levels remained unchanged. During the first 24 h of DHT treatment, levels of Cdk4-associated p21(Cip1/Waf1) and p27(Kip1) were reduced coinciding with decreased levels of Cdk4-associated cyclin D3. In contrast, DHT treatment caused increased accumulation of Cdk2-associated p21(Cip1/Waf1), with no significant alterations in levels of p27(Kip1) bound to Cdk2 complexes. These findings suggest that DHT reverses the Cdk4-mediated titration of p21(Cip1/Waf1) and p27(Kip1) away from Cdk2 complexes, and that the increased association of p21(Cip1/Waf1) with Cdk2 complexes in part mediates the androgen-induced growth inhibition of breast cancer cells.

TK1 in Cancer Progression: elucidating its influence on cellular invasion and survival

2019 ◽  
Author(s):  
Eliza E. Bitter ◽  
Michelle H. Townsend ◽  
Kary Y.F. Tsai ◽  
Carolyn I. Allen ◽  
Rachel I. Erickson ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Survival ◽  
Cancer Cells ◽  
Cell Lines ◽  
Cancer Progression ◽  
Breast Cancer Cells ◽  
S Phase ◽  
Wild Type ◽  
Cellular Invasion ◽  
Cancer Pathogenesis

Abstract 1. Background: The salvage pathway enzyme thymidine kinase 1 (TK1) is elevated in the serum of several different cancer types and higher expression is associated with more aggressive tumor grade. As a result, it has potential as a biomarker for diagnosis and prognosis. Recent studies indicate that TK1 may be involved in cancer pathogenesis; however, its direct involvement has not been identified. We propose to evaluate the effects of TK1 on cancer progression in vitro through measuring cellular invasion and survival of breast cancer cells.2.Methods: Breast cancer cells MDA-MB-231, HCC 1806, and MCF7 were cultured according to standard techniques. We employed the use of TK1 target siRNA and a CRISPR-Cas9 TK1 knockout plasmid to compare transfected cell lines to wild type cell lines. Protein factors in survival and invasive pathways were also tested for correlations to TK1 in BRCA RNA-seq patient data (n=1095) using the TIMER program. Cellular invasion was quantified in cell index (factor of impedance) over a 24-hour period. Cell survival was measured by apoptosis under metabolic and DNA stress using flow cytometry. All results were statistically assessed using an ANOVA or t-test in GraphPad PRISM®.3.Results: Cellular invasion assays assessing wild type and TK1 knockdown/knockout (TK1-/-) cell types showed TK1-/- cell lines had increased invasion potential (p= 0.0001). Bioinformatically, we saw a strong overall negative correlation between apoptotic factors and TK1 (p ≤ 0.05). When testing TK1 effects on cell survival we saw a protective affect under DNA stress (p ≤ 0.05), but not under metabolic stress (p= 0.0001).4.Conclusion From cell cycle analysis, we observed a shift towards S phase in TK1-/- cells. This shift to S phase would promote growth and account for the increased cellular invasion and decrease in metabolic induced stress in TK1-/- cells. We propose that cancer cells still may elicit a cancer progressive phenotype based on effects of TK1, but that a system which isolates TK1 is not effective to understand the effects. Instead, identifying protein networks inclusive of TK1 will help to elucidate its effects on cancer progression.

scholarly journals The synthetic antihyperlipidemic drug potassium piperate selectively kills breast cancer cells through inhibiting G1-S-phase transition and inducing apoptosis

Oncotarget ◽  
2017 ◽  
Vol 8 (29) ◽  
pp. 47250-47268 ◽  
Author(s):  
Lifei Fan ◽  
Xuemin Cao ◽  
Huijuan Yan ◽  
Qian Wang ◽  
Xiaoxia Tian ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Phase Transition ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
S Phase

Microarray determination of Bcl-2 family protein inhibition sensitivity in breast cancer cells

2013 ◽  
Vol 238 (2) ◽  
pp. 248-256 ◽  
Author(s):  
Sandra G Hudson ◽  
Devin R Halleran ◽  
Barbara Nevaldine ◽  
Anna Shapiro ◽  
Robert E Hutchison ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Protein Inhibition ◽  
Family Protein

Determination of HER2 amplification status in breast cancer cells using Raman spectroscopy

2010 ◽  
Author(s):  
Xiaohong Bi ◽  
Brent Rexer ◽  
Carlos L. Arteaga ◽  
Mingsheng Guo ◽  
Ming Li ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Raman Spectroscopy ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Her2 Amplification

scholarly journals Primary and Compensatory Roles for RB Family Members at Cell Cycle Gene Promoters That Are Deacetylated and Downregulated in Doxorubicin-Induced Senescence of Breast Cancer Cells

2006 ◽  
Vol 26 (7) ◽  
pp. 2501-2510 ◽  
Author(s):  
James G. Jackson ◽  
Olivia M. Pereira-Smith
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Drug Treatment ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Growth Arrest ◽  
S Phase ◽  
Cyclin B ◽  
Cell Cycle Gene ◽  
Gene Promoters

ABSTRACT When treated with DNA-damaging chemotherapy agents, many cancer cells, in vivo and in vitro, undergo a terminal growth arrest and acquire a senescence-like phenotype. We investigated the molecular basis for this in breast cancer cells following a 2-hour treatment with 1 μM doxorubicin. Treated cells arrested in G1 and G2 phases of the cell cycle, with concomitant reductions in S-phase and G2-M regulatory genes. p53 and p21 protein levels increased within hours after treatment and were maintained for 5 to 6 days but were reduced 8 days posttreatment, though the cells remained growth arrested. Levels of p130 rose after drug treatment, and it was the primary RB family member recruited to the S-phase promoters cyclin A and PCNA and G2-M promoters cyclin B and cdc2, remaining present for the entire 8-day time period. In contrast, p107 protein and promoter occupancy levels declined sharply after drug treatment. RB was recruited to only the PCNA promoter. In MCF-7 cells with p130 knockdown, p107 compensated for p130 loss at all cell cycle gene promoters examined, allowing cells to retain the growth arrest phenotype. Cells with p130 and p107 knockdown similarly arrested, while cells with knockdown of all three family members failed to downregulate cyclin A and cyclin B. These results demonstrate a mechanistic role for p130 and compensatory roles for p107 and RB in the long-term senescence-like growth arrest response of breast cancer cells to DNA damage.

scholarly journals 3P Determination of therapeutic effects of multifunctional micelle-based nanocarriers on breast cancer cells

2021 ◽  
Vol 32 ◽  
pp. S1
Author(s):  
G.T. Ulu ◽  
N.N. Bayram ◽  
N. Abdulhadi ◽  
S. Gürdap ◽  
A. İşoğlu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Therapeutic Effects
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