scholarly journals Overexpression of Cell Cycle Progression Inhibitor Geminin is Associated with Tumor Stem-Like Phenotype of Triple-Negative Breast Cancer

2012 ◽  
Vol 15 (2) ◽  
pp. 162 ◽  
Author(s):  
Maurizio Di Bonito ◽  
Monica Cantile ◽  
Francesca Collina ◽  
Giosuè Scognamiglio ◽  
Margherita Cerrone ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Triple Negative Breast Cancer ◽  
Cell Cycle Progression ◽  
Triple Negative ◽  
Cycle Progression

scholarly journals FDI-6 inhibits the expression and function of FOXM1 to sensitize BRCA-proficient triple-negative breast cancer cells to Olaparib by regulating cell cycle progression and DNA damage repair

2021 ◽  
Vol 12 (12) ◽  
Author(s):  
Shu-Ping Wang ◽  
Shi-Qi Wu ◽  
Shi-Hui Huang ◽  
Yi-Xuan Tang ◽  
Liu-Qiong Meng ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Dna Damage ◽  
Triple Negative Breast Cancer ◽  
Cell Cycle Progression ◽  
Triple Negative ◽  
Parp Inhibitor ◽  
Dna Damage Repair ◽  
Cycle Progression ◽  
Damage Repair

AbstractInducing homologous-recombination (HR) deficiency is an effective strategy to broaden the indications of PARP inhibitors in the treatment of triple-negative breast cancer (TNBC). Herein, we find that repression of the oncogenic transcription factor FOXM1 using FOXM1 shRNA or FOXM1 inhibitor FDI-6 can sensitize BRCA-proficient TNBC to PARP inhibitor Olaparib in vitro and in vivo. Mechanistic studies show that Olaparib causes adaptive resistance by arresting the cell cycle at S and G2/M phases for HR repair, increasing the expression of CDK6, CCND1, CDK1, CCNA1, CCNB1, and CDC25B to promote cell cycle progression, and inducing the overexpression of FOXM1, PARP1/2, BRCA1/2, and Rad51 to activate precise repair of damaged DNA. FDI-6 inhibits the expression of FOXM1, PARP1/2, and genes involved in cell cycle control and DNA damage repair to sensitize TNBC cells to Olaparib by blocking cell cycle progression and DNA damage repair. Simultaneously targeting FOXM1 and PARP1/2 is an innovative therapy for more patients with TNBC.

scholarly journals The phosphatase PPM1A inhibits triple negative breast cancer growth by blocking cell cycle progression

2019 ◽  
Vol 5 (1) ◽  
Author(s):  
Abhijit Mazumdar ◽  
William M. Tahaney ◽  
Lakshmi Reddy Bollu ◽  
Graham Poage ◽  
Jamal Hill ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Triple Negative Breast Cancer ◽  
Cell Cycle Progression ◽  
Triple Negative ◽  
Cancer Growth ◽  
Cycle Progression ◽  
Breast Cancer Growth

Curcumin-like structure (CCA-1.1) induces permanent mitotic arrest (Senescence) on Triple-negative breast cancer (TNBC) cells, 4T1

2021 ◽  
pp. 4375-4382
Author(s):  
Dhania Novitasari ◽  
Riris Istighfari Jenie ◽  
Febri Wulandari ◽  
Rohmad Yudi Utomo ◽  
Dyaningtyas Dewi Pamungkas Putri ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Cell Death ◽  
Cytotoxic Activity ◽  
Triple Negative Breast Cancer ◽  
Cell Cycle Progression ◽  
Triple Negative ◽  
Apoptosis Induction ◽  
Cycle Progression ◽  
Intracellular Ros

Triple-negative breast cancer (TNBC) remains as the deadliest cancer type due to the lack of treatment options. Hence, several attempts have been made to develop new anticancer for TNBC therapy. This study intended to challenge curcumin analog (CCA)-1.1, which is derived from pentagamavunone-1 structure, against the 4T1 cell line and TNBC cell model, covering the cytotoxic activity in correlation with cell cycle progression, apoptosis induction, reactive oxygen species (ROS) generation, and senescence evidence. The cell viability, cell cycle profile, apoptosis induction, intracellular ROS level, and senescence induction were determined in vitro using trypan blue exclusion, propidium iodide (PI) staining, Annexin-PI staining, dichlorofluorescein diacetate staining, and senescence-associated-β-gal method. CCA-1.1 showed cytotoxic activity on 4T1 cells, giving half maximal inhibitory concentration value of 3M, but was less toxic on non-cancerous 3T3-L1 cells. CCA-1.1 induced rapid cell death and inhibited cell cycle progression at the mitotic phase. Instead, of causing apoptosis, CCA-1.1 induced mitotic catastrophe. Furthermore, CCA-1.1 itself increased the intracellular ROS level and induced senescence, possibly through catastrophic cell death. Altogether, our preliminary study strengthens the potency of CCA-1.1 for its anticancer activities against TNBC cells and prospective to be pharmaceutically developed as a novel candidate for cancer therapy.

scholarly journals Syndecan-1 Depletion Has a Differential Impact on Hyaluronic Acid Metabolism and Tumor Cell Behavior in Luminal and Triple-Negative Breast Cancer Cells

2021 ◽  
Vol 22 (11) ◽  
pp. 5874
Author(s):  
Sofía Valla ◽  
Nourhan Hassan ◽  
Daiana Luján Vitale ◽  
Daniela Madanes ◽  
Fiorella Mercedes Spinelli ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Hyaluronic Acid ◽  
Cell Lines ◽  
Cell Cycle Progression ◽  
Triple Negative ◽  
Cell Behavior ◽  
Cycle Progression ◽  
Tumor Cell Behavior ◽  
Mcf 7

Glycosaminoglycans (GAGs) and proteoglycans (PGs) are major components of the glycocalyx. The secreted GAG and CD44 ligand hyaluronic acid (HA), and the cell surface PG syndecan-1 (Sdc-1) modulate the expression and activity of cytokines, chemokines, growth factors, and adhesion molecules, acting as critical regulators of tumor cell behavior. Here, we studied the effect of Sdc-1 siRNA depletion and HA treatment on hallmark processes of cancer in breast cancer cell lines of different levels of aggressiveness. We analyzed HA synthesis, and parameters relevant to tumor progression, including the stem cell phenotype, Wnt signaling constituents, cell cycle progression and apoptosis, and angiogenic markers in luminal MCF-7 and triple-negative MDA-MB-231 cells. Sdc-1 knockdown enhanced HAS-2 synthesis and HA binding in MCF-7, but not in MDA-MB-231 cells. Sdc-1-depleted MDA-MB-231 cells showed a reduced CD24-/CD44+ population. Furthermore, Sdc-1 depletion was associated with survival signals in both cell lines, affecting cell cycle progression and apoptosis evasion. These changes were linked to the altered expression of KLF4, MSI2, and miR-10b and differential changes in Erk, Akt, and PTEN signaling. We conclude that Sdc-1 knockdown differentially affects HA metabolism in luminal and triple-negative breast cancer model cell lines and impacts the stem phenotype, cell survival, and angiogenic factors.

scholarly journals LncRNA LUCAT1 facilitates tumorigenesis and metastasis of triple-negative breast cancer through modulating miR-5702

2019 ◽  
Vol 39 (9) ◽  
Author(s):  
Exian Mou ◽  
Hao Wang
Keyword(s):  
Breast Cancer ◽  
Triple Negative Breast Cancer ◽  
Cell Cycle Progression ◽  
Triple Negative ◽  
Cycle Progression ◽  
Tumor Promotor ◽  
Advanced Stages ◽  
Non Coding Rnas ◽  
Shed Light ◽  
Aggressive Breast Cancer

Abstract Triple-negative breast cancer (TNBC) is a subtype of aggressive breast cancer with high recurrence and poor survival. Emerging evidence has indicated that long non-coding RNAs (lncRNAs) play pivotal roles in the development and progression of multiple cancers. Although there are substantial studies revealing that lung cancer-associated transcript 1 (LUCAT1) functions as a tumor promotor in various human cancers, the molecular mechanism of LUCAT1 in TNBC remains largely to be explored. In our study, we identified that LUCAT1 expression was dramatically enhanced in TNBC samples and cells. High LUCAT1 expression was strongly associated with advanced stages and poor prognosis of TNBC. LUCAT1 contributed to TNBC development through accelerating cell proliferation, cell cycle progression and metastasis as well as attenuating cell apoptosis. Moreover, miR-5702 was proved to directly bind to LUCAT1 and be negatively modulated by LUCAT1. Knockdown of miR-5702 reversed the suppressing influences of LUCAT1 depletion on TNBC progression. In conclusion, it was the first investigation to shed light on the significant function and underlying regulatory mechanism of LUCAT1 in TNBC tumorigenesis. We validated that LUCAT1 induced tumorigenesis and metastasis of TNBC via miR-5702, which provided clues for improving the treatment of TNBC.

scholarly journals The Anticancer Effects of Flavonoids through miRNAs Modulations in Triple-Negative Breast Cancer

Nutrients ◽  
2021 ◽  
Vol 13 (4) ◽  
pp. 1212
Author(s):  
Getinet M. Adinew ◽  
Equar Taka ◽  
Patricia Mendonca ◽  
Samia S. Messeha ◽  
Karam F. A. Soliman
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Cancer Progression ◽  
Triple Negative Breast Cancer ◽  
Triple Negative ◽  
Therapeutic Potential ◽  
Biological Activities ◽  
Therapeutic Option ◽  
Mesenchymal Transition ◽  
Anticancer Effects

Triple- negative breast cancer (TNBC) incidence rate has regularly risen over the last decades and is expected to increase in the future. Finding novel treatment options with minimum or no toxicity is of great importance in treating or preventing TNBC. Flavonoids are new attractive molecules that might fulfill this promising therapeutic option. Flavonoids have shown many biological activities, including antioxidant, anti-inflammatory, and anticancer effects. In addition to their anticancer effects by arresting the cell cycle, inducing apoptosis, and suppressing cancer cell proliferation, flavonoids can modulate non-coding microRNAs (miRNAs) function. Several preclinical and epidemiological studies indicate the possible therapeutic potential of these compounds. Flavonoids display a unique ability to change miRNAs’ levels via different mechanisms, either by suppressing oncogenic miRNAs or activating oncosuppressor miRNAs or affecting transcriptional, epigenetic miRNA processing in TNBC. Flavonoids are not only involved in the regulation of miRNA-mediated cancer initiation, growth, proliferation, differentiation, invasion, metastasis, and epithelial-to-mesenchymal transition (EMT), but also control miRNAs-mediated biological processes that significantly impact TNBC, such as cell cycle, immune system, mitochondrial dysregulation, modulating signaling pathways, inflammation, and angiogenesis. In this review, we highlighted the role of miRNAs in TNBC cancer progression and the effect of flavonoids on miRNA regulation, emphasizing their anticipated role in the prevention and treatment of TNBC.

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