MIB-1 (Ki-67) Immunostaining of Breast Cancer Cells in Cytologic Smears

1997 ◽  
Vol 41 (2) ◽  
pp. 229-237 ◽  
Author(s):  
Peter Dalquen ◽  
Betty Baschiera ◽  
Rosemarie Chaffard ◽  
Holger Dieterich ◽  
Georg E. Feichter ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Ki 67 ◽  
Mib 1

scholarly journals Tioconazole and Chloroquine Act Synergistically to Combat Doxorubicin-Induced Toxicity via Inactivation of PI3K/AKT/mTOR Signaling Mediated ROS-Dependent Apoptosis and Autophagic Flux Inhibition in MCF-7 Breast Cancer Cells

2021 ◽  
Vol 14 (3) ◽  
pp. 254
Author(s):  
Afnan H. El-Gowily ◽  
Samah A. Loutfy ◽  
Ehab M. M. Ali ◽  
Tarek M. Mohamed ◽  
Mohammed A. Mansour
Keyword(s):  
Breast Cancer ◽  
Combination Therapy ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Mtor Pathway ◽  
Tumor Growth Inhibition ◽  
Autophagic Flux ◽  
Ki 67 ◽  
Mcf 7

Cancer is a complex devastating disease with enormous treatment challenges, including chemo- and radiotherapeutic resistance. Combination therapy demonstrated a promising strategy to target hard-to-treat cancers and sensitize cancer cells to conventional anti-cancer drugs such as doxorubicin. This study aimed to establish molecular profiling and therapeutic efficacy assessment of chloroquine and/or tioconazole (TIC) combination with doxorubicin (DOX) as anew combination model in MCF-7 breast cancer. The drugs are tested against apoptotic/autophagic pathways and related redox status. Molecular docking revealed that chloroquine (CQ) and TIC could be potential PI3K and ATG4B pathway inhibitors. Combination therapy significantly inhibited cancer cell viability, PI3K/AkT/mTOR pathway, and tumor-supporting autophagic flux, however, induced apoptotic pathways and altered nuclear genotoxic feature. Our data revealed that the combination cocktail therapy markedly inhibited tumor proliferation marker (KI-67) and cell growth, along with the accumulation of autophagosomes and elevation of LC3-II and p62 levels indicated autophagic flux blockage and increased apoptosis. Additionally, CQ and/or TIC combination therapy with DOX exerts its activity on the redox balance of cancer cells mediated ROS-dependent apoptosis induction achieved by GPX3 suppression. Besides, Autophagy inhibition causes moderately upregulation in ATGs 5,7 redundant proteins strengthened combinations induced apoptosis, whereas inhibition of PI3K/AKT/mTOR pathway with Beclin-1 upregulation leading to cytodestructive autophagy with overcome drug resistance effectively in curing cancer. Notably, the tumor growth inhibition and various antioxidant effects were observed in vivo. These results suggest CQ and/or TIC combination with DOX could act as effective cocktail therapy targeting autophagy and PI3K/AKT/mTOR pathways in MCF-7 breast cancer cells and hence, sensitizes cancer cells to doxorubicin treatment and combat its toxicity.

Antisense Ki-67 cDNA Transfection Reverses the Tumorigenicity and Induces Apoptosis in Human Breast Cancer Cells

2008 ◽  
Vol 26 (8) ◽  
pp. 830-835 ◽  
Author(s):  
Rui Wang ◽  
Danfeng Luo ◽  
Xiangyi Ma ◽  
Wanhua Yang ◽  
Rui Chen ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Human Breast Cancer Cells ◽  
Human Breast ◽  
Ki 67

scholarly journals Overexpression of LncRNA BM466146 Predicts Better Prognosis of Breast Cancer

2021 ◽  
Vol 10 ◽  
Author(s):  
Yunxiang Zhang ◽  
Xiaotong Dong ◽  
Yang Wang ◽  
Liquan Wang ◽  
Guiyan Han ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Survival Analysis ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Target Genes ◽  
Ki 67 ◽  
Cd8 Cells ◽  
Kaplan Meier ◽  
Cancer Tissues ◽  
Breast Tissues

This study analyzes the expression and clinical significance of long non-coding RNA (lncRNA) BM466146 in breast cancer, and explores the role of BM466146 in immune regulation. The expression of BM466146 in 89 cases of breast cancer and their corresponding non-cancerous breast tissues was detected by quantitative real-time polymerase chain reaction (qRT-PCR). Kaplan-Meier survival analysis was applied to evaluate patient survival. EDU and CCK-8 experiments on breast cancer cells were performed to verify the function of BM466146 in vitro. The target genes of BM466146 were screened by informatics analysis to predict associated miRNAs and their corresponding mRNAs, immune genes associated with lncRNAs and chemokines associated with CD8. Immunohistochemistry was used to detect the expression of CD8, Ki-67, and CXCL-13 in the 89 breast cancer tissues. It was found that the expression of lncRNA BM466146 in breast cancer tissues was significantly lower than that in normal breast tissues (P < 0.001). In breast cancer, tissues that overexpressed BM466146 exhibited a lower Ki-67 index compared with that of low BM466146 expression (P = 0.048). Kaplan-Meier survival analysis showed that breast cancer patients with overexpression of BM466146 had longer overall survival. EDU and CCK8 experiments showed that overexpression of BM466146 inhibited the proliferation of breast cancer cells. The hsa-miR-224-3p is associated with BM466146, and its target gene might be CXCL-13. The positive CD8 cells in the BM466146 overexpression group was higher than that in the low BM466146 expression group (P=0.027), and the positive CD8 cells in the CXCL-13 positive group was higher (P=0.023) than that of the negative group. Our results indicate that the lncRNA BM466146 has the function of tumor suppressor gene. Overexpression of BM466146 is associated with better prognosis. BM466146 could regulate CXCL-13 by adsorbing hsa-miR-224-3p and inducing CD8+ T cells to accumulate in the tumor area which regulate immune response. Therefore, BM466146 could be a prognostic biomarker and a molecular immune target of breast cancer.

scholarly journals PEAK1 promotes invasion and metastasis and confers drug resistance in breast cancer

2021 ◽  
Author(s):  
Xingang Wang ◽  
Yan Zheng ◽  
Yu Wang
Keyword(s):  
Breast Cancer ◽  
Cell Growth ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Chemotherapy Resistance ◽  
Ki 67 ◽  
Cancer Tissues

AbstractPseudopodium-enriched atypical kinase 1 (PEAK1) has been reported to be upregulated in human malignancies and is correlated with a poor prognosis. Enhanced PEAK1 expression facilitates tumor cell survival, invasion, metastasis and chemoresistance. However, the role of PEAK1 in breast cancer is unclear. We investigated PEAK1 expression in breast cancer and analyzed the relationship with clinicopathological status and chemotherapy resistance. We also investigated the role of PEAK1 in breast cancer cells in vitro and in vivo. Immunohistochemistry for PEAK1 was performed in 112 surgically resected breast cancer tissues. The association between clinicopathological status, chemotherapy resistance and PEAK1 expression was determined. The effect of PEAK1 overexpression or downregulation on proliferation, colony formation, invasion, migration, metastasis and doxorubicin sensitivity in MCF-7 cells in vitro and in vivo was studied. PEAK1 was overexpressed in breast cancer tissues. High PEAK1 expression was correlated with tumor size, high tumor grade, tumor stage, lymph node metastasis, recurrence, Ki-67 expression, Her-2 expression and chemotherapy resistance. Inhibiting PEAK1 decreased cell growth, invasion, metastasis and reversed chemoresistance to doxorubicin in breast cancer cells both in vitro and in vivo. High PEAK1 expression was associated with the invasion, metastasis and chemoresistance of breast cancers. Furthermore, targeting PEAK1 inhibited cell growth and metastasis and reversed chemoresistance in breast cancer cells. Targeting PEAK1 could be an effective treatment strategy for breast cancer.

scholarly journals Targeting breast cancer cells with a CuInS2/ZnS quantum dot-labeled Ki-67 bioprobe

2017 ◽  
Author(s):  
Guang Sun ◽  
Wanying Xing ◽  
Ren Xing ◽  
Liu Cong ◽  
Sun Tong ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Quantum Dot ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Ki 67

scholarly journals Hsa_circ_0029693 (circ-LATS2) promotes cell proliferation and regulates WNT5A via miR-4686 in breast cancer cells.

2020 ◽  
Author(s):  
Jiashu Hu ◽  
Kaiyao Hua ◽  
Changle Ji ◽  
Xuehui Wang ◽  
Hongming Song ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Western Blot ◽  
Cancer Cells ◽  
Immunohistochemical Staining ◽  
Breast Cancer Cells ◽  
Hippo Pathway ◽  
Luciferase Reporter ◽  
Ki 67 ◽  
Reporter Assays

Abstract Background: Breast cancer (BC) is the most malignant form of tumor in women, which threatens females’ health. Circular RNAs (circRNAs), a class of non-coding RNAs, can act as a disease biomarker and endogenous “sponge” molecules for microRNAs (miRNAs). circRNAs may also influence the expression of their parent gene. LATS2 is a vital suppressor gene in Hippo pathway, which is a signaling cascade composed of a group of conserved kinases. The Hippo pathway plays an important role in almost all cancer types. Methods: Colony formation assays, MTT assays, wound healing assays, xenografts mice experiment, qRT-PCR, western blot assays, immunohistochemical staining assays, dual-luciferase reporter assays and Fluorescence in situ hybridization. Student’s t-test was used to analyse the results.Results: We discovered that circular RNA hsa_circ_0029693 (circ-LATS2), an exonic circRNA, are highly expressed in breast cancer cells. Furthermore, in BC patients’ samples, higher expression of circ-LATS2 was significantly related to higher percentage of Ki-67 expression; however the expression of circ-LATS2 was higher in HER2 negative BC patients compared to HER2 positive ones. We investigated the potential function and mechanism of circ-LATS2 action in BC. The results suggested that circ-LATS2 promoted cell proliferation, growth and migration. Through western blot and immunohistochemical staining assays, we found that circ-LATS2 could influence LATS2 expression. We also discovered that there was an inverse expression relationship between miR-4686 and circ-LATS2, suggesting that circ-LATS2 might act as an endogenous “sponge” for miR-4686. Using dual-luciferase reporter assays, we confirmed that circ-LATS2 can bind miR-4686. Increased miR-4686 expression caused a reduction in the protein levels of WNT5A, which is a putative target of miR-4686. We confirm this using dual-luciferase reporter assays that revealed that miR-4686 targets WNT5A by binding its 3’-untranslated region (3’UTR). Conclusions: Our results showed that circ-LATS2 expression in BC patients’ samples were significantly related to Ki-67 expression. In addition, circ-LATS2 acted as a promoter of proliferation and growth of breast cancer cells. These indicated that circ-LATS2 is a proliferative factor, similar to Ki-67; it also acts as a co-biomarker with Ki-67 in clinical treatment.

scholarly journals Increasing of malignancy of breast cancer cells after cryopreservation: molecular detection and activation of angiogenesis after CAM-Xenotransplantation.

2020 ◽  
Author(s):  
Xin Du ◽  
P. Todorov ◽  
Evgenia Isachenko ◽  
G Rahimi ◽  
P. Mallmann ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Cell Lines ◽  
Breast Cancer Cells ◽  
Immunofluorescent Staining ◽  
Ovarian Tissue Cryopreservation ◽  
Ki 67 ◽  
Wide Range ◽  
E Cadherin

Abstract Background: Ovarian tissue cryopreservation has a wide range of cancerous indications. Avoiding relapse becomes a specific area of concern that clinicians frequently encounter. The data about the comparative viability of cancer cells after cryopreservation are limited. This study aimed to evaluate the effect of cryopreservation on breast cancer cells.Methods: Samples were prepared using ZR-75-1 and MDA-MB-231 cell lines and divided into cryopreserved and non-intervened groups, respectively. Biological properties and the related protein markers were investigated. Cell morphology was monitored under the microscope. Cell proliferation, migration, and invasion were characterized by CCK-8, wound-healing, and transmembrane assay, respectively. The expression of Ki-67, P53, GATA-3, E-cadherin, Vimentin, and F-Actin was measured by immunofluorescent staining and western blotting. Xenotransplantation was established on the chorioallantoic membrane (CAM) culture system to explore angiogenesis close to the grafts.Results: Lamellipodia and filopodia were observed in cryopreserved ZR-75-1 cells. Both cell lines demonstrated increased cell motility and invasive ability after cryopreservation. However, cell proliferation was invariable in accordance with a regular expression of Ki-67 and P53. In ZR-75-1 cells, data exhibited a downregulation of E-cadherin after the decreased expression of GATA3, indicating the loss of intercellular adhesion after cryopreservation. Vimentin and F-actin were both upregulated in cryopreserved sample cells. Angiogenesis in CAM was significantly activated by cryopreserved MDA-MB-231 cells.Conclusions: Cryopreservation causes an increasing malignancy of ZR-75-1 and MDA-MB-231 cells and thus raises the risk of metastasis.

scholarly journals Chemopreventive Potential of DSC Anthocyanins and Total Phenolics Extracted from Dark Sweet Cherry (DSC) Through Modulation of MDA-MB-453 Breast Tumor Proteomic Profile

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 305-305
Author(s):  
Shirley Arbizu ◽  
Giuliana Noratto ◽  
Marjorie Layosa ◽  
Nara N Lage ◽  
Liezl Atienza ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Nude Mice ◽  
Breast Cancer Cells ◽  
Sweet Cherry ◽  
Total Phenolics ◽  
Volume Growth ◽  
Cancer Prognosis ◽  
Ki 67 ◽  
Athymic Nude Mice

Abstract Objectives To investigate in vivo the chemopreventive activity of dark sweet cherry (DSC) extracted total phenolics (WE) or fractions enriched in anthocyanins (ACN) or proanthocyanidins (PCN) in athymic nude mice xenografted with MDA-MB-453 breast cancer cells. Methods MDA-MB-453 breast cancer cells (1 × 106 cells) were xenografted into athymic nude mice. Mice were gavaged with WE, ACN, or PCN extracts (150 mg/kg body weight/day) for 36 days followed by animal termination. Main organs and tumors were dissected for protein analyses following standard molecular biology techniques and high-resolution nano-HPLC tandem mass spectrometry. Results Tumor volume growth was suppressed at similar levels by WE, ACN, and PCN compared to controls (C) without signs of toxicity in main organs. Tumor protein analysis revealed ERK1/2 phosphorylation induced by WE, ACN, and PCN at similar levels, which may be linked to apoptosis induction by stress regulated ERK1/2 activation. Immunohistochemistry analysis showed decreased tumor cell proliferation and Ki-67 H-scores with potency WE ≥ ACN ≥ PCN. Differential quantitative proteomic analysis of tumor tissues from ACN and C groups revealed the identity of 71 proteins associated with poor breast cancer prognosis that were expressed only in C group (66 proteins), or upregulated in C group (5 proteins) compared to ACN group (p < 0.05). Conclusions These findings revealed the potential of DSC phenolics for breast cancer invasion and metastasis chemoprevention. Funding Sources This work was supported by the Northwest Cherry Growers, Washington State Fruit Commission.

scholarly journals Can transforming growth factor-beta1 and retinoids modify the activity of estradiol and antiestrogens in MCF-7 breast cancer cells?.

2004 ◽  
Vol 51 (3) ◽  
pp. 733-745 ◽  
Author(s):  
Ewa Czeczuga-Semeniuk ◽  
Tomasz Anchim ◽  
Janusz Dziecioł ◽  
Milena Dabrowska ◽  
Sławomir Wołczyński
Keyword(s):  
Breast Cancer ◽  
Growth Factor ◽  
Cancer Cells ◽  
Transforming Growth Factor Beta ◽  
Breast Cancer Cells ◽  
Transforming Growth Factor ◽  
Proliferating Cells ◽  
Ki 67 ◽  
Stimulatory Action ◽  
Mcf 7

Retinoic acid and transforming growth factor-beta (TGF-beta) affect differentiation, proliferation and carcinogenesis of epithelial cells. The effect of both compounds on the proliferation of cells of the hormone sensitive human breast cancer cell line (ER+) MCF-7 was assessed in the presence of estradiol and tamoxifen. The assay was based on [3H]thymidine incorporation and the proliferative activity of PCNA- and Ki 67-positive cells. The apoptotic index and expression of the Bcl-2 and p53 antigens in MCF-7 cells were also determined. Exogenous TGF-beta1 added to the cell culture showed antiproliferative activity within the concentration range of 0.003-30 ng/ml. Irrespective of TGF-beta1 concentrations, a marked reduction in the stimulatory action of estradiol (10(-9) and 10(-8) M) was observed whereas in combination with tamoxifen (10(-7) and 10(-6) M) only 30 ng/ml TGF-beta1 caused a statistically significant reduction to approximately 30% of the proliferative cells. In further experiments we examined the effect of exposure of breast cancer cells to retinoids in combination with TGF-beta1. The incorporation of [3H]thymidine into MCF-7 cells was inhibited to 52 +/- 19% (control =100%) by 3 ng/ml TGF-beta1, and this dose was used throughout. It was found that addition of TGF-beta1 and isotretinoin to the culture did not decrease proliferation, while TGF-beta1 and tretinoin at low concentrations (3 x 10(-8) and 3 x 10(-7) M) reduced the percentage of proliferating cells by approximately 30% (67+/-8% and 67+/-5%, P

scholarly journals Increasing of malignancy of breast cancer cells after cryopreservation: molecular detection and activation of angiogenesis after CAM-Xenotransplantation.

2020 ◽  
Author(s):  
Xin Du ◽  
P. Todorov ◽  
Evgenia Isachenko ◽  
G Rahimi ◽  
P. Mallmann ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Cell Lines ◽  
Breast Cancer Cells ◽  
Immunofluorescent Staining ◽  
Ovarian Tissue Cryopreservation ◽  
Ki 67 ◽  
Wide Range ◽  
E Cadherin

Abstract Background: Ovarian tissue cryopreservation has a wide range of cancerous indications. Avoiding relapse becomes a specific concern that clinicians frequently encounter. The data about the comparative viability of cancer cells after cryopreservation are limited. This study aimed to evaluate the effect of cryopreservation on breast cancer cells. Methods: We used in-vitro cultured ZR-75-1 and MDA-MB-231 cell lines. Cell samples of each lineage were distributed into the non-intervened and cryopreserved groups. The cryopreservation procedures comprised programmed slow freezing followed by thawing at 100°C, 60 s. Biological phenotypes and the related protein markers were compared between the two groups. The EVOS FL Auto 2 Cell Image System was used to monitor cell morphology. Cell proliferation, motility, and penetration were characterized by CCK-8, wound-healing, and transmembrane assay, respectively. The expression of Ki-67, P53, GATA-3, E-cadherin, Vimentin, and F-Actin was captured by immunofluorescent staining and western blotting as the proxy measurements of the related properties. The chorioallantoic membrane (CAM) xenotransplantation was conducted to explore angiogenesis induced by cancer cells. Results: After 5-days in vitro culture, the cell concentration of cryopreserved and non-intervened groups was 15.7×104 vs. 14.4×104cells/ml, (ZR-75-1, p>0.05), and 25.1 ×104 vs. 26.6×104 cells/ml (MDA-MB-231, p>0.05). Some cryopreserved ZR-75-1 cells presented spindle shape with filopodia and lamellipodia and dissociated from the cell cluster after cryopreservation. Both cell lines demonstrated increased cell migrating capability and invasion after cryopreservation. The expression of Ki-67 and P53 did not differ between the cryopreserved and control groups. E-cadherin and GATA3 expression downregulated in the cryopreserved ZR-75-1 cells. Vimentin and F-actin exhibited upregulated level in cryopreserved ZR-75-1 and MDA-MB-231 cells. The cryopreserved MDA-MB-231 cells induced significant angiogenesis around the grafts on CAM with the vascular density 0.313±0.03 and 0.342±0.04, compared with that of fresh cells of 0.238±0.05 and 0.244±0.03, p<0.0001.Conclusions: Cryopreservation promotes breast cancer cells in terms of epithelial-mesenchymal transition and angiogenesis induction, thus increasing metastasis risk.

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