scholarly journals Effects of estradiol and medroxyprogesterone acetate on expression of the cell cycle proteins cyclin D1, p21 and p27 in cultured human breast tissues

Cell Cycle ◽  
2008 ◽  
Vol 7 (1) ◽  
pp. 71-80 ◽  
Author(s):  
Natalija Eigeliene ◽  
Pirkko Härkönen ◽  
Risto Erkkola
Keyword(s):  
Cell Cycle ◽  
Cyclin D1 ◽  
Medroxyprogesterone Acetate ◽  
Human Breast ◽  
Cell Cycle Proteins ◽  
Breast Tissues

scholarly journals Everolimus induces G1 cell cycle arrest through autophagy-mediated protein degradation of cyclin D1 in breast cancer cells

2019 ◽  
Vol 317 (2) ◽  
pp. C244-C252 ◽  
Author(s):  
Guang Chen ◽  
Xiao-Fei Ding ◽  
Hakim Bouamar ◽  
Kyle Pressley ◽  
Lu-Zhe Sun
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Cyclin D1 ◽  
Cell Cycle Arrest ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Breast Tissue ◽  
Human Breast ◽  
Human Breast Tissue ◽  
Cycle Arrest

Everolimus inhibits mammalian target of rapamycin complex 1 (mTORC1) and is known to cause induction of autophagy and G1 cell cycle arrest. However, it remains unknown whether everolimus-induced autophagy plays a critical role in its regulation of the cell cycle. We, for the first time, suggested that everolimus could stimulate autophagy-mediated cyclin D1 degradation in breast cancer cells. Everolimus-induced cyclin D1 degradation through the autophagy pathway was investigated in MCF-10DCIS.COM and MCF-7 cell lines upon autophagy inhibitor treatment using Western blot assay. Everolimus-stimulated autophagy and decrease in cyclin D1 were also tested in explant human breast tissue. Inhibiting mTORC1 with everolimus rapidly increased cyclin D1 degradation, whereas 3-methyladenine, chloroquine, and bafilomycin A1, the classic autophagy inhibitors, could attenuate everolimus-induced cyclin D1 degradation. Similarly, knockdown of autophagy-related 7 (Atg-7) also repressed everolimus-triggered cyclin D1 degradation. In addition, everolimus-induced autophagy occurred earlier than everolimus-induced G1 arrest, and blockade of autophagy attenuated everolimus-induced G1 arrest. We also found that everolimus stimulated autophagy and decreased cyclin D1 levels in explant human breast tissue. These data support the conclusion that the autophagy induced by everolimus in human mammary epithelial cells appears to cause cyclin D1 degradation resulting in G1 cell cycle arrest. Our findings contribute to our knowledge of the interplay between autophagy and cell cycle regulation mediated by mTORC1 signaling and cyclin D1 regulation.

scholarly journals MiR-218-5p promotes breast cancer progression via LRIG1

2021 ◽  
Author(s):  
Mingping Qian ◽  
Hui Xu ◽  
Hongming Song ◽  
Hao Xi ◽  
Lin Fang
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Cancer Cells ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Luciferase Reporter ◽  
Human Breast ◽  
Egfr Expression ◽  
Breast Tissues ◽  
Mcf 7

Abstract Background : MiR-218-5p is a small non-coding RNA acting as either oncogenes or tumor suppressor genes in human cancer. The expression levels of some miRNAs in human breast cancer plays a potential role in disease pathogenesis. Methods : Thirty pairs of invasive ductal carcinoma and adjacent specimens were included in the study. Breast tissues cell lines MCF-7 and MDA-MB-231 were identified as a breast cancer research cell line. MiR-218-5p mimics, miR-218-5p inhibitor, or negative controls were transfected. Specific antibodies were probed with LRIG1, ErbB2, and EGFR. Proliferation, migration, cell cycle and apoptosis, dual-luciferase reporter assay and immunohistochemistry were used to analyze miR-218-5p、LRIG1 and so on. Results : It was shown that miR-218-5p expression was higher in 30 breast cancer specimens than adjacent normal breast tissues. In human breast cancer cells MCF-7 and MDA-MB-231, restoring miR-218-5p promoted cell proliferation and migration and inhibited cell apoptosis and cell cycle arrest in the G1 stage. Luciferase assays indicated miR-218-5p could bind with its putative target site in the 3'-untranslated region (3'-UTR) of LRIG1. RT-qPCR, western blot, and immunocytochemistry analyses all indicated miR-218-5p overexpression results in LRIG1 downregulation at the mRNA and protein levels. ErbB2 and EGFR were found to be downstream effectors of miR-218-5p. Conclusion : MiR-218-5p promotes ErbB2 and EGFR expression by inhibiting LRIG1 in breast cancer cells, which suggests miR-218-5p and LRIG1 may act as an oncogene in breast cancer and it could be used as a therapeutic target for breast cancer treatments. Keywords: Breast cancer; miR-218-5p; LRIG1; Oncogene

Distribution and prognostic significance of cell cycle proteins in squamous carcinoma of the larynx, hypopharynx and adjacent epithelial hyperplastic lesions

2003 ◽  
Vol 117 (4) ◽  
pp. 286-293 ◽  
Author(s):  
Metka Volavšek ◽  
Matej Bračko ◽  
Nina Gale
Keyword(s):  
Cell Cycle ◽  
Protein Expression ◽  
Cyclin D1 ◽  
Prognostic Significance ◽  
Squamous Carcinoma ◽  
Malignant Tumours ◽  
Tumour Grade ◽  
Cancer Specific Survival ◽  
Biological Behaviour ◽  
Cell Cycle Proteins

Alterations of cell cycle proteins contribute to the development and biological behaviour of malignant tumours. We evaluated the distribution and prognostic significance of immunohistochemically detected proteins p53, p21, Rb, and cyclin D1 in 101 laryngeal and hypopharyngeal squamous cell carcinomas (SCC) and adjacent epithelial hyperplastic lesions (EHL). Protein expression was correlated with tumour grade and stage.Varying patterns of protein expression were found in SCC. A significant correlation (p <0.05) was found between Rb expression and tumour grade. Different grades of EHL exhibited randomly distributed p53 and cyclin D1 positive cell clusters with no association to the pattern of their expression in SCC.Our study demonstrated derailment of cell cycle regulation in almost all cases of SCC of the larynx and hypopharynx. However, only cyclin D1 expression had an independent prognostic value for cancer-specific survival. The results also suggest that Rb gene inactivation, although rare, might be more important in the development of SCC than previously thought.

Antiandrogenic actions of medroxyprogesterone acetate on epithelial cells within normal human breast tissues cultured ex vivo

2014 ◽  
Vol 21 (1) ◽  
pp. 79-88 ◽  
Author(s):  
Aleksandra M. Ochnik ◽  
Nicole L. Moore ◽  
Tanja Jankovic-Karasoulos ◽  
Tina Bianco-Miotto ◽  
Natalie K. Ryan ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Medroxyprogesterone Acetate ◽  
Ex Vivo ◽  
Human Breast ◽  
Normal Human Breast ◽  
Normal Human ◽  
Breast Tissues

scholarly journals Effects of Auraptene on IGF-1 Stimulated Cell Cycle Progression in the Human Breast Cancer Cell Line, MCF-7

2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Prasad Krishnan ◽  
Heather Kleiner-Hancock
Keyword(s):  
Cell Cycle ◽  
Cyclin D1 ◽  
Cell Cycle Progression ◽  
D1 Protein ◽  
Cancer Cell Line ◽  
S Phase ◽  
Human Breast ◽  
Cycle Progression ◽  
Cyclin D1 Protein ◽  
Mcf 7

Auraptene is being investigated for its chemopreventive effects in many models of cancer including skin, colon, prostate, and breast. Many mechanisms of action including anti-inflammatory, antiproliferative, and antiapoptotic effects are being suggested for the chemopreventive properties of auraptene. We have previously shown in theN-methylnitrosourea induced mammary carcinogenesis model that dietary auraptene (500 ppm) significantly delayed tumor latency. The delay in time to tumor corresponded with a significant reduction in cyclin D1 protein expression in the tumors. Since cyclin D1 is a major regulator of cell cycle, we further studied the effects of auraptene on cell cycle and the genes related to cell cycle in MCF-7 cells. Here we show that auraptene significantly inhibited IGF-1 stimulated S phase of cell cycle in MCF-7 cells and significantly changed the transcription of many genes involved in cell cycle.

Expression of Cell Cycle Proteins (Cyclin D1 and cdk4) After Controlled Cortical Impact in Rat Brain

1999 ◽  
Vol 16 (12) ◽  
pp. 1187-1196 ◽  
Author(s):  
SENOL SAHIN KAYA ◽  
ASIM MAHMOOD ◽  
YI LI ◽  
EKREM YAVUZ ◽  
MICHAEL CHOPP
Keyword(s):  
Cell Cycle ◽  
Cyclin D1 ◽  
Rat Brain ◽  
Cell Cycle Proteins ◽  
Controlled Cortical Impact ◽  
Cortical Impact
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