scholarly journals Effects of Ulinastatin on Proliferation and Apoptosis of Breast Cancer Cells by Inhibiting the ERK Signaling Pathway

2021 ◽  
Vol 2021 ◽  
pp. 1-6
Author(s):  
Zeyu Xing ◽  
Xin Wang ◽  
Jiaqi Liu ◽  
Gang Liu ◽  
Menglu Zhang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Mechanism Of Action ◽  
Breast Cancer Cells ◽  
Erk Signaling ◽  
Control Group ◽  
Hoechst 33258 ◽  
Protein Levels ◽  
Proliferation And Apoptosis ◽  
Positive Rate

Purpose. To explore the effects of ulinastatin on the proliferation and apoptosis of breast cancer cells and the relevant mechanism of action. Methods. Breast cancer cells (MCF-7) were cultured and randomly divided into three groups, namely, control group, ulinastatin group, and ulinastatin+extracellular-regulated protein kinase (ERK) inhibitor group. Then, the Cell Counting Kit-8 (CCK-8) assay was carried out to detect the effect of ulinastatin on the viability of breast cancer cells. The effects of ulinastatin on the proliferation and apoptosis of breast cancer cells were determined via EdU staining and Hoechst 33258 staining assays, respectively. The messenger ribonucleic acid (mRNA) and protein expression levels of ERK and forkhead box O3 (FOXO3) in breast cancer cells were measured through reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting. Results. In comparison with the control group, the ulinastatin group displayed decreased viability of breast cancer cells, a decreased positive rate of 5-ethynyl-2 ′ -deoxyuridine (EdU) staining, an increased positive rate of Hoechst 33258 staining, and reduced mRNA and protein levels of ERK and FOXO3 in breast cancer cells. Compared with those in the ulinastatin group, the viability of breast cancer cells was lowered, the positive rate of EdU staining was reduced, the positive rate of Hoechst 33258 staining was raised, and the mRNA and protein levels of ERK and FOXO3 in breast cancer cells clearly declined in the ulinastatin+ERK inhibitor group. Conclusion. Ulinastatin inhibits the proliferation and promotes the apoptosis of breast cancer cells. The possible mechanism of action is associated with the suppression of the ERK signaling pathway.

scholarly journals Ginsenoside induces cell death in breast cancer cells via ROS/PI3K/Akt signaling pathway

2020 ◽  
Vol 19 (8) ◽  
pp. 1631-1636
Author(s):  
Lihong He ◽  
Xiaorui Wang ◽  
Qing Ma ◽  
Weipeng Zhao ◽  
Yongsheng Jia ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Mechanism Of Action ◽  
Breast Cancer Cells ◽  
Akt Signaling ◽  
Control Group ◽  
Akt Signaling Pathway ◽  
Protein Expressions ◽  
Mcf 7

Purpose: To study the influence of ginsenoside on breast carcinoma, and the mechanism of action involved.Methods: Different concentrations of ginsenoside were used to treat MCF-7 breast cancer cell line. Cell viability was measured by MTT assay, while protein expressions of p-Akt and p-PI3K were determined using Western blotting. The concentrations of reactive oxidative reactants and reactive oxygen species (ROS) were assessed using fluorescence immunoassay and immunofluorescence assay. The mechanism of action involved in ginsenoside-mediated apoptosis was determined based on ROS/PI3K/Akt signaling pathway.Results: There was no change in the inhibition of MCF-7 cell proliferation in control cells with time (p > 0.05). However, inhibition of MCF-7 cell proliferation in ginsenoside group was significantly higher than that in the control group (p < 0.05); furthermore, it increased with time and ginsenoside concentration. Apoptosis was markedly and concentration-dependently higher in ginsenoside-treated MCF-7 cells than in controls (p > 0.05). There were lower protein levels of p-PI3K and p-Akt in ginsenoside-exposed MCF-7 cells than in control group; the protein expressions  decreased with increase in ginsenoside concentration (p < 0.05). The expressions of ROS in ginsenoside-treated MCF-7 cells declined, relative to the untreated group; in addition, the expressions decreased with increase in ginsenoside concentration (p < 0.05).Conclusion: Ginsenoside suppresses proliferation of MCF-7 cell line, and exerts apoptotic effect on the cells via inhibition of the ROS/PI3K/Akt signal pathway. This provides a new approach to treat breast cancer. Keywords: Breast cancer cells, Ginsenoside, Apoptosis, ROS/PI3K/Akt signaling pathway

scholarly journals WISP2/CCN5 gene knockdown in vitro and in vivo exhibits proliferation promotion of breast cancer through targeting Skp2 and p27Kip1

2020 ◽  
Author(s):  
Yan Lv ◽  
Chang Zhang ◽  
Xiao Jiang Li ◽  
Shan Gao ◽  
Xu Zheng ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Gene Knockdown ◽  
Control Group ◽  
Rt Pcr ◽  
Protein Levels ◽  
Mcf 7

AbstractBackgroundEmerging evidence has demonstrated that WISP2/CCN5 is critically involved in tumorigenesis. However, the function of WISP2/CCN5 in breast cancer carcinogenesis is largely unclear.Methodswe aim to explore the effects and potential mechanisms of WISP2/CCN5 on proliferation of breast cancer cells and carcinogenesis of breast cancer xenograft. Lentivirus vector with WISP2/CCN5shRNA was transfected into MCF-7, and breast cancer cells and xenograft were conducted. Effect of WISP2/CCN5 on growth and carcinogenesis of breast cancer cells and xenografts was evaluated by MTT assay and tumor volume. The relationship between WISP2/CCN5, Skp2 and p27Kip1 was detected in vitro and in vivo by RT-PCR at mRNA level and Western blotting at protein level.ResultsThe result of MTT assay indicated that MCF-7 cell growth viability in WISP2/CCN5 gene knockdown group was significantly higher than negative vector group(P<0.05) or control group (P<0.05). It suggested that knockdown of WISP2/CCN5 gene by shRNA lentivirus plasmid promoted proliferation of MCF-7 cells. The growth curves of breast cancer xenograft showed that xenografts in WISP2/CCN5 knockdown group grew more quickly than negative vector group(P< 0.05) or control group (P< 0.05). Subsequently, the results of RT-PCR and Western blotting revealed that WISP2/CCN5 gene knockdown led to increased Skp2 and decreased p27Kip1 at mRNA and protein levels. WISP2/CCN5 exerts its inhibition on proliferation of MCF-7 cell line and suppressive functions on growth of breast carcinoma via regulation of Skp2 and p27Kip1at mRNA and protein levels. However, WISP2/CCN5 gene knockdown resulted in loss of inhibition effect on MCF-7 and breast cancer.ConclusionsOur findings suggest that WISP2/CCN5 could be a useful therapeutic strategy for the treatment of breast cancer through targeting Skp2 and p27Kip1.

VITAMIN D DERIVATIVES IN COMBINATION WITH 9-cis RETINOIC ACID PROMOTE ACTIVE CELL DEATH IN BREAST CANCER CELLS

1995 ◽  
Vol 14 (3) ◽  
pp. 391-394 ◽  
Author(s):  
S Y James ◽  
A G Mackay ◽  
K W Colston
Keyword(s):  
Breast Cancer ◽  
Vitamin D ◽  
Retinoic Acid ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
P53 Protein ◽  
Protein A ◽  
Therapeutic Implications ◽  
Protein Levels ◽  
Mcf 7

ABSTRACT The effects of the novel vitamin D analogue, EB1089 alone, or in combination with the retinoid, 9-cis retinoic acid (9-cis RA) on indices of apoptosis in MCF-7 breast cancer cells have been examined. EB1089 was capable of reducing bcl-2 protein, a suppressor of apoptosis, and increasing p53 protein levels in MCF-7 cell cultures following 96h treatment. In the presence of 9-cis RA, EB1089 acted to further enhance the down-regulation and up-regulation of bcl-2 and p53 respectively. Furthermore, EB1089 induces DNA fragmentation in MCF-7 cells, a key feature of apoptosis, alone and in combination with 9-cis RA in situ. The observation that EB1089 and 9-cis RA act in a cooperative manner to enhance induction of apoptosis in these cells may have therapeutic implications.

scholarly journals Mummy Induces Apoptosis Through Inhibiting of Epithelial-Mesenchymal Transition (EMT) in Human Breast Cancer Cells

2020 ◽  
Vol 9 ◽  
pp. 1812
Author(s):  
Solmaz Rahmani Barouji ◽  
Arman Shahabi ◽  
Mohammadali Torbati ◽  
Seyyed Mohammad Bagher Fazljou ◽  
Ahmad Yari Khosroushahi
Keyword(s):  
Breast Cancer ◽  
Gene Expression ◽  
Anticancer Activity ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Epithelial Mesenchymal Transition ◽  
Control Group ◽  
Mrna Levels ◽  
Mesenchymal Transition ◽  
Mcf 7

Background: Mummy (Iranian pure shilajit) is a remedy with possessing anti-inflammatory, antioxidant and anticancer activities. This study aimed to examine mummy effects on epithelial-mesenchymal transition (EMT) and invasiveness of MCF-7 and MDA-MB-231 breast cancer (BC) cell lines with underlying its mechanism. Materials and Methods: The dose-dependent inhibitory effect of the mummy on cell proliferation in vitro was determined using the MTT assay.  Flow cytometry and 4’,6-diamidino-2-phenylindole dihydrochloride staining were respectively used for quantitative and qualitative analysis of cellular apoptosis, and gene expression analysis was conducted using real-time PCR. Results: MDA-MB-231 showed more sensitivity than the MCF-7 cell line to the anticancer activity of mummy, while mummy did not exhibit significant cell cytotoxicity against human normal cells (MCF-10A). The gene expression profile demonstrated a significant decrease in TGF-β1, TGF-βR1, TWIST1, NOTCH1, CTNNB1, SRC along with an increase in E-cadherin mRNA levels in mummy treated cells compared to the untreated control group (P≤0.05). Conclusion: Mummy triggers inhibition of EMT and metastasis in breast cancer cells mainly through the downregulation of TGFβ1 activity, and more studies required to find its specific anticancer activity with details. [GMJ.2020;9:e1812]

Luteolin-Loading Her-2 Nanospheres Enhances Targeting and Therapeutic Effects of Breast Cancer

2021 ◽  
Vol 17 (8) ◽  
pp. 1545-1553
Author(s):  
Chuanguang Xiao ◽  
Xiaohong Wang ◽  
Jiacheng Shen ◽  
Yanjie Xia ◽  
Shusheng Qiu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Water Solubility ◽  
Ultrasonic Method ◽  
Mrna Level ◽  
Therapeutic Effects ◽  
Treatment Benefit ◽  
Protein Levels ◽  
Her 2

Despite the broad anticancer activity, whereas the clinical application of luteolin is hindered by unsatisfactory water solubility and non-targeting. Herein, targeted inhibitory effects of luteolin-loading HER2 nanospheres (Her-2-NPs) were successfully prepared by thin film ultrasonic method. In comparison with the non-targeted nanospheres, Her-2 nanospheres could significantly boost the intake of luteolin in SK-BR-3 cells. The proliferation and apoptosis of breast cancer cells were detected by MTT testing and flow cytometry examination, respectively. Consequently, the expressions of FOXO1 mRNA level was detected using qPCR assay and protein level was detected using Westernblot. We discovered that Luteolin-loading Her-2 nanospheres could significantly hinder the proliferation of breast cancer cells, down-regulation their migration, and up-regulation FOXO1 expression at mRNA and protein levels, reveal a mechanism whereby luteolin interferes with breast cancer. Collectively, these results suggest Her-2-modified nanospheres increases the efficiency of luteolin uptake and thus improves the treatment benefit of breast cancer.

SIK2 Promotes Cisplatin Resistance Induced by Aerobic Glycolysis in Breast Cancer Cells through PI3K/AKT/mTOR Signaling Pathway

2020 ◽  
Author(s):  
Shoukai Zong ◽  
Wei Dai ◽  
Wencheng Fang ◽  
Xiangting Guo ◽  
Kai Wang
Keyword(s):  
Breast Cancer ◽  
Western Blot ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Breast Cancer Cells ◽  
Cisplatin Resistance ◽  
Aerobic Glycolysis ◽  
Mtor Signaling ◽  
Mtor Signaling Pathway ◽  
Protein Levels

Abstract Objective This study aimed to investigate the effect of SIK2 on cisplatin resistance induced by aerobic glycolysis in breast cancer cells and its potential mechanism. Methods qRT-PCR and Western blot were used to detect SIK2 mRNA and protein levels. Cisplatin (DDP) resistant cell lines of breast cancer cells were established, CCK-8 was used to measure and evaluate the viability, and Transwell was used to evaluate the cell invasion capability. Flow cytometry was adopted to evaluate the apoptosis rate. The glycolysis level was evaluated by measuring glucose consumption and lactic acid production. The protein levels of p-PI3K, p- protein kinase B (Akt) and p-mTOR were determined by western blot. Results SIK2 is highly expressed in breast cancer tissues and cells compared with adjacent tissues and normal human breast epithelial cells, and has higher diagnostic value for breast cancer. Silencing SIK2 expression can inhibit proliferation and invasion of breast cancer cells and induce their apoptosis. In addition, SIK2 knockdown inhibits glycolysis, reverses the resistance of drug-resistant cells to cisplatin, and inhibits PI3K/AKT/mTOR signaling pathway. When LY294002 is used to inhibit PI3K/AKT/mTOR signaling pathway, the effect of Sh-SIK2 on aerobic glycolysis of breast cancer cells can be reversed. Conclusion SIK2 can promote cisplatin resistance caused by aerobic glycolysis of breast cancer cells through PI3K/AKT/mTOR signaling pathway, which may be a new target to improve cisplatin resistance of breast cancer cells.

scholarly journals Screening antiproliferative drug for breast cancer from bisbenzylisoquinoline alkaloid tetrandrine and fangchinoline derivatives by targeting BLM helicase

BMC Cancer ◽  
2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Wangming Zhang ◽  
Shuang Yang ◽  
Jinhe Liu ◽  
Linchun Bao ◽  
He Lu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Dna Binding ◽  
Small Molecules ◽  
Cancer Cells ◽  
Small Molecule ◽  
Breast Cancer Cells ◽  
Dna Unwinding ◽  
Protein Levels ◽  
Blm Helicase ◽  
Bisbenzylisoquinoline Alkaloids

Abstract Background The high expression of BLM (Bloom syndrome) helicase in tumors involves its strong association with cell expansion. Bisbenzylisoquinoline alkaloids own an antitumor property and have developed as candidates for anticancer drugs. This paper aimed to screen potential antiproliferative small molecules from 12 small molecules (the derivatives of bisbenzylisoquinoline alkaloids tetrandrine and fangchinoline) by targeting BLM642–1290 helicase. Then we explore the inhibitory mechanism of those small molecules on proliferation of MDA-MB-435 breast cancer cells. Methods Fluorescence polarization technique was used to screen small molecules which inhibited the DNA binding and unwinding of BLM642–1290 helicase. The effects of positive small molecules on the ATPase and conformation of BLM642–1290 helicase were studied by the malachite green-phosphate ammonium molybdate colorimetry and ultraviolet spectral scanning, respectively. The effects of positive small molecules on growth of MDA-MB-435 cells were studied by MTT method, colony formation and cell counting method. The mRNA and protein levels of BLM helicase in the MDA-MB-435 cells after positive small molecule treatments were examined by RT-PCR and ELISA, respectively. Results The compound HJNO (a tetrandrine derivative) was screened out which inhibited the DNA binding, unwinding and ATPase of BLM642–1290 helicase. That HJNO could bind BLM642–1290helicase to change its conformationcontribute to inhibiting the DNA binding, ATPase and DNA unwinding of BLM642–1290 helicase. In addition, HJNO showed its inhibiting the growth of MDA-MB-435 cells. The values of IC50 after drug treatments for 24 h, 48 h and 72 h were 19.9 μmol/L, 4.1 μmol/L and 10.9 μmol/L, respectively. The mRNA and protein levels of BLM helicase in MDA-MB-435 cells increased after HJNO treatment. Those showed a significant difference (P < 0.05) compared with negative control when the concentrations of HJNO were 5 μmol/L and 10 μmol/L, which might contribute to HJNO inhibiting the DNA binding, ATPase and DNA unwinding of BLM helicase. Conclusion The small molecule HJNO was screened out by targeting BLM642–1290 helicase. And it showed an inhibition on MDA-MB-435 breast cancer cells expansion.

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