Inhibited MCF-7 Cell Proliferation Research Articles

Clinical Diagnostic Value of circ-ARHGER28 for Breast Cancer and its Effect on MCF 7 Cell Proliferation and Apoptosis.

Clinical diagnostic value of circ-ARHGER28 in breast cancer (BC), and the biological functions of circ-ARHGER28 on the proliferation and apoptosis of MCF-7 cells were investigated. Human circRNA microarray was performed to analyze the expression of circRNAs in BC patients. RT-qPCR combined with bioinformatics analysis was applied to verify the candidate circRNAs in BC tissues and peripheral blood samples. Circ-ARHGER28 was chosen as the candidate gene for further research. The clinical diagnostic value and biological functions of circ-ARHGER28 were analyzed. The overexpression and negative control vector of circ-ARHGER28 were constructed and transfected to MCF-7 cells. The CCK 8 assay and clone formation experiments were applied to detect the cell proliferative and migratory abilities. Flow cytometry was used to analyze cell apoptosis and cell cycle distribution. RT-qPCR and Western blot were performed to detect apoptosis and expression of PI3K/AKT/mTOR-associated genes and proteins. Overexpression of circ-ARHGER28 inhibited the proliferation, colony formation and migration of MCF-7 cells, while increasing the population of the cells in the G2/M phase and the apoptotic rate. Apoptosis associated genes and proteins were significantly increased, whereas gene and protein expression of PI3K, AKT and mTOR were decreased in the cells. Circular RNA ARHGER28 exhibits promising diagnostic value for BC. Circ-ARHGER28 inhibited MCF-7 cell proliferation and increased the apoptotic rate. The function of circ-ARHGER28 was associated with the PI3K/AKT/mTOR signaling pathway. Circ-ARHGER28 could be an ideal biomarker for BC diagnosis and a novel target for BC therapy.

MiR-450b-5p enhances the radiosensitivity of HR+ and HER2− breast cancer by targeting CDK6

Abstract Background The sensitivity of breast cancer cells to radiation is a key cause of locoregional recurrence after postoperative radiotherapy. Several studies have reported that microRNAs (miRNAs) are involved in the radiosensitivity of human breast cancer cells. One miRNA microarray study showed that miR-450b-5p was overexpressed 13.3-fold in patients with estrogen receptor–positive (ER+) and human epidermal growth factor receptor 2–negative (HER2−) breast cancer and no local relapse compared with local relapse patients. However, its underlying mechanism of action remains unknown. Methods The predicted target mRNAs of miR-450b-5p were screened using the TargetScan, miRDB, and miRWalk databases. Western blotting, quantitative polymerase chain reaction, and dual-luciferase reporter assays explored the association between cyclin-dependent kinase 6 (CDK6) and miR-450b-5p. The cell counting kit-8 assay and flow cytometry detected the proliferation of transfected MCF7 cells. Colony formation and xenograft tumors detected the radiosensitivity of the transfected MCF7 cells. Results Bioinformatics analysis, Western blotting, quantitative polymerase chain reaction, and dual-luciferase reporter assays demonstrated that CDK6 was the target gene of miR-450b-5p. Furthermore, in vitro and in vivo experiments showed that miR-450b-5p inhibited MCF7 cell proliferation and cell cycle progression, increased the sensitizer enhancement ratio, and decreased the volume of xenograft tumors after irradiation by regulating CDK6. Conclusions This study demonstrates that miR-450b-5p enhances the radiosensitivity of hormone receptor–positive (HR+) and HER2− breast cancer cells and elucidates its mechanism. miR-450b-5p may be considered a therapeutic target in HR+ and HER2− breast cancer treated with radiotherapy.

Phytochemical profile, anti-inflammatory analysis and cytotoxic activity of SmE-SeNPs against breast (MCF-7) cancer cells

Plant extract is inexpensive and does not need special conditions to produce nanoparticles quickly; it is an eco-friendly approach. Selenium nanoparticles have attracted a lot of attention because of their various applications and benefits in medicine. This investigation studied a bio-synthesis of selenium nanoparticles using Sonchus maritimus leaves aqueous extract (SmE-SeNPs) to evaluate their anti-inflammatory and anti-cancer properties. The presence of SmE-SeNPs in the sample was confirmed by ultraviolet–visible (UV–vis) spectroscopy at different stage of synthesis, and transmission electron microscope. The S. maritimus extract was analyzed by LC-ESI-MS technique. The anti-inflammatory proprieties of the extract and SmE-SeNPs was estimated using protein denaturation and membrane stabilization assays, and the antiproliferative activity of the synthesized nanoparticles was assessed against breast cancer cell line (MCF-7). LC-ESI-MS results revealed the richness of S. maritimus extract by various phenolic compounds including protocachuic acid, trans frulic acid, o-coumaric acid and luteolin. Physical characterizations of nanoparticle demonstrated that the SeNPs have a spherical and regular circle shape with very small size reach to 7.154 ± 0.47 nm. Both of S. maritimus extract and SmE-SeNPs presented a potential anti-inflammatory activities compared to standard, each against denaturation of protein with IC50 value (334.369 ± 29 μg/mL) and (163.393 ± 14.1 μg/mL) respectively, or against the hemolysis of red blood cells through protecting and stabilizing their membrane with IC50 value (89.044 ± 4.11 μg/mL) for SmE-SeNPs and (53.539 ± 4.64 μg/mL) for S. maritimus extract. Moreover, this study showed that exposure of SmE-SeNPs can inhibited MCF-7 cell proliferation, which observed in breast cancer. As conclusion, our research suggested that Sonchus maritimus leaves aqueous extract can be used as reducer and stabilizer agents for green synthesis of SmE-SeNPs which provided their anti-inflammatory and anticancer effects.

The role of miR-133a in silibinin-mediated inhibition of the PI3K/AKT/mTOR pathway in MCF-7 breast carcinoma cells.

Breast cancer is particularly severe in women. Research highlights the crucial role of miRNAs in key cellular processes, showcasing their intricate interactions with the oncogenic PI3K/AKT/mTOR (PAM) signaling pathway and underscoring their significant role as tumor suppressors. The effect of silibinin on cell growth and survival was evaluated using an MTT assay. Bioinformatics analysis identified putative miR-133a targets inside the PAM pathway. After incubating MCF-7 cells with silibinin, we measured miR-133a, EGFR, PI3K, AKT, PTEN, and mTOR expression levels using qRT-PCR. Furthermore, protein expression levels of mTOR were assessed using Western blotting. The MTT experiment displayed that silibinin effectively inhibits MCF-7 cell proliferation in a time- and dose-dependent manner. Silibinin's IC50 value, determined at 370 μM after 48 hours, was established. qRT-PCR analysis at this IC50 concentration highlighted reduced expression of EGFR, PI3K, AKT, PTEN, and mTOR mRNAs, alongside increased miR-133a expression. Notably, miR-133a exhibited a negative correlation with both EGFR and PIK3C2A expression. Furthermore, western blotting confirmed silibinin's capacity to diminish p-mTOR protein levels, the ultimate element of the PAM signaling pathway. The findings enhance comprehension of silibinin's impact on PAM signaling and miR-133a expression, offering promise for targeted therapies in disrupting oncogenic pathways in MCF-7 breast cancer cells. This insight could advance breast cancer treatment strategies.

Characterization and efficiency of Ganoderma lucidum biomass as an antimicrobial and anticancer agent

The microconstituents of Ganoderma lucidum biomass (GLB) were evaluated, along with its antimicrobial and anticancer activities. Using gas chromatography-mass spectrometry analysis, 12-octadecadienoic acid (Z,Z)- and n-hexadecanoic acid with area% values of 21.0% and 11.0% were recognized in GLB. Uncooked biomass (UCB) and microwave-cooked (CE) biomass of G. lucidum caused a significant inhibition of human breast cancer (MCF-7) cell line proliferation in a dose-dependent manner. The inhibition of MCF-7 cell proliferation was 27.22 ± 1.64% using 16 µg/mL of CB while it was 52.29 ± 1.09% using 16 µg/mL of UCB. The cytotoxicity test recorded low IC50 (25.63 ± 0.52 µg/mL) of UCE compared to the IC50 value (49.99 ± 0.94 µg/mL) of CB. Highest antimicrobial activities were recorded via using UCE, compared to CE against Bacillus subtilis, Staphylococcus aureus, Escherichia coli, Klebsiella pneumoniae, Candida albicans, and Aspergillus niger. The 9,12-octadecadienoic acid (Z,Z)- and n-hexadecanoic acid were able to induce both anticancer and antibiotic-resistant properties. A key therapeutic target enzyme for evolving this resistant pathogenic activity on MCF-7 and K. pneumonia, was accessed thoroughly in silico study. The compounds described, therefore, might provide a great potential for the development of new therapeutics such as anticancer and antimicrobial agents.

Chemical synthesis and biochemical properties of cholestane-5α,6β-diol-3-sulfonate: A non-hydrolysable analogue of cholestane-5α,6β-diol-3β-sulfate

Cholestane-3β,5α,6β-triol (CT) is a primary metabolite of 5,6-epoxycholesterols (5,6-EC) that is catalyzed by the cholesterol-5,6-epoxide hydrolase (ChEH). CT is a well-known biomarker for Niemann-Pick disease type C (NP-C), a progressive inherited neurodegenerative disease. On the other hand, CT is known to be metabolized by the 11β-hydroxysteroid-dehydrogenase of type 2 (11β-HSD2) into a tumor promoter named oncosterone that stimulates the growth of breast cancer tumors. Sulfation is a major metabolic transformation leading to the production of sulfated oxysterols. The production of cholestane-5α,6β-diol-3β-O-sulfate (CDS) has been reported in breast cancer cells. However, no data related to CDS biological properties have been reported so far. These studies have been hampered because sulfate esters of sterols and steroids are rapidly hydrolyzed by steroid sulfatase to give free steroids and sterols. In order to get insight into the biological properties of CDS, we report herein the synthesis and the characterization of cholestane-5α,6β-diol-3β-sulfonate (CDSN), a non-hydrolysable analogue of CDS. We show that CDSN is a potent inhibitor of 11β-HSD2 that blocks oncosterone production on cell lysate. The inhibition of oncosterone biosynthesis of a whole cell assay was observed but results from the blockage by CDSN of the uptake of CT in MCF-7 cells. While CDSN inhibits MCF-7 cell proliferation, we found that it potentiates the cytotoxic activity of post-lanosterol cholesterol biosynthesis inhibitors such as tamoxifen and PBPE. This effect was associated with an increase of free sterols accumulation and the appearance of giant multilamellar bodies, a structural feature reminiscent of Type C Niemann-Pick disease cells and consistent with a possible inhibition by CDSN of NPC1. Altogether, our data showed that CDSN is biologically active and that it is a valuable tool to study the biological properties of CDS and more specifically its impact on immunity and viral infection.

Exploring the Pharmacological Action and Molecular Mechanism of Salidroside in Inhibiting MCF-7 Cell Proliferation and Migration.

Salidroside (Sal) contains anti-carcinogenic, anti-hypoxic, and anti-inflammatory pharmacological activities. However, its underlying anti-breast cancer mechanisms have been only incompletely elucidated. Hence, this protocol intended to decode the potential of Sal in regulating the PI3K-AKT-HIF-1α-FoxO1 pathway in the malignant proliferation of human breast cancer MCF-7 cells. First, the pharmacological activity of Sal against MCF-7 was evaluated by CCK-8 and cell scratch assays. Moreover, the resistance of MCF-7 cells was measured by migration and Matrigel invasion assays. For cell apoptosis and cycle assays, MCF-7 cells were processed in steps with annexin V-FITC/PI and cell cycle-staining detection kits for flow cytometry analyses, respectively. The levels of reactive oxygen species (ROS) and Ca2+ were examined by DCFH-DA and Fluo-4 AM immunofluorescence staining. The activities of Na+-K+-ATPase and Ca2+-ATPase were determined using the corresponding commercial kits. The protein and gene expression levels in apoptosis and the PI3K-AKT-HIF-1α-FoxO1 pathway were further determined using western blot and qRT-PCR analyses, respectively. We found that Sal treatment significantly restricted the proliferation, migration, and invasion of MCF-7 cells with dose-dependent effects. Meanwhile, Sal administration also dramatically forced MCF-7 cells to undergo apoptosis and cell cycle arrest. The immunofluorescence tests showed that Sal observably stimulated ROS and Ca2+ production in MCF-7 cells. Further data confirmed that Sal promoted the expression levels of pro-apoptotic proteins, Bax, Bim, cleaved caspase-9/7/3, and their corresponding genes. Consistently, Sal intervention prominently reduced the expression of the Bcl-2, p-PI3K/PI3K, p-AKT/AKT, mTOR, HIF-1α, and FoxO1 proteins and their corresponding genes. In conclusion, Sal can be used as a potential herb-derived compound for treating breast cancer, as it may reduce the malignant proliferation, migration, and invasion of MCF-7 cells by inhibiting the PI3K-AKT-HIF-1α-FoxO1 pathway.

Apoptosis Induction Activity and Inhibition of MCF-7 Cell Proliferation in Active Isolate of Butterfly Pea Flower (Clitoria ternatea L.)

Clitoria ternatea L. is one of the plants whose all parts have functional benefits for the human body. The flower petals are reported to be useful as anticancer. This study aims to determine the activity of inhibiting cell proliferation, and apoptotic induction activity and identify the chemical content of isolates from Clitoria ternatea L. Analysis of the results of the MTT assay test ethanol extract of butterfly pea flower has an IC50 value of 17.46 g/mL, CTEE has an IC50 value of 13, 19 g/mL, isolate 1 and isolate 2 of EAFCT had IC50 values of 6.79 and 7.12 g/mL. The results obtained were categorized as potent cytotoxic. Isolation of EAFCT compounds using radial system chromatography then analyzed GC-MS EAFCT isolates containing pyridine hydrochloride (51.42 %) and pentanal (2.79 %) and identified compounds using UV-Vis spectrophotometry and FTIR. The results of the cell proliferation inhibition test used a series of concentrations of IC50, ⅟2 IC50, ⅟4 IC50 and ⅟8 IC50, the CTEE obtained a doubling time of 178.47; 160.86; 151.18; 150.09, EAFCT is 188.53; 164.37; 156.82; 154.79, isolate 1 EAFCT is 212.96; 174.64; 148.53; 145.82 and isolates 2 EAFCT were 190.62; 168.23; 150.24; 148.94. Analysis of the apoptotic potential test results can be concluded from CTEE, EAFCT, isolates 1 and 2 EAFCT have apoptotic potential. HIGHLIGHTS The Clitoria ternatea 1 and 2 ethyl acetate fractions had a cytotoxic effect on MCF-7 cells with IC50 values of 6.79 and 7.12 μg/mL and inhibited the growth rate of MCF-7 cells with doubling times of 212.96 and 190.62 hours Clitoria ternatea 1 and 2 isolates' ethyl acetate fraction induced apoptosis in MCF-7 cells, as indicated by the presence of orange fluorescent cells, indicating that the cells had died The Ethyl acetate fraction of Clitoria ternatea isolate contains compounds with anticancer potential, including Pyridine hydrochloride and Pentanal GRAPHICAL ABSTRACT

Absolute Stereochemistry and Cytotoxic Effects of Vismione E from Marine Sponge-Derived Fungus Aspergillus sp. 1901NT-1.2.2.

The metabolic profile of the Aspergillus sp. 1901NT-1.2.2 sponge-associated fungal strain was investigated using the HPLC MS technique, and more than 23 peaks in the HPLC MS chromatogram were detected. Only two minor peaks were identified as endocrocin and terpene derivative MS data from the GNPS database. The main compound was isolated and identified as known anthraquinone derivative vismione E. The absolute stereochemistry of vismione E was established for the first time using ECD and quantum chemical methods. Vismione E showed high cytotoxic activity against human breast cancer MCF-7 cells, with an IC50 of 9.0 µM, in comparison with low toxicity for normal human breast MCF-10A cells, with an IC50 of 65.3 µM. It was found that vismione E inhibits MCF-7 cell proliferation and arrests the cell cycle in the G1 phase. Moreover, the negative influence of vismione E on MCF-7 cell migration was detected. Molecular docking of vismione E suggested the IMPDH2 enzyme as one of the molecular targets for this anthraquinone derivative.

An in vitro investigation of the apoptosis-inducing activity of corosolic acid in breast cancer cells.

Breast cancer is the most prevalent cancer among females with different molecular subtypes. Corosolic acid is a pentacyclic triterpenoid with anti-cancer properties. The MTT assay was used to assess the cytotoxic activity of corosolic acid on MDA-MB-231 and MCF7 cell lines. To determine the apoptotic cells, the flow cytometry technique was utilized. The expression levels of apoptosis-related genes and proteins were quantified using quantitative real time-PCR (qRT-PCR) and Western blotting methods. The activity of caspase enzymes was measured by spectrophotometry. Corosolic acid significantly inhibited the proliferation of both cell lines compared with controls. This agent markedly induced apoptosis in MDA-MB-231 cells but did not affect MCF7 cells compared with controls. Treating the MADA-MB-231 and MCF7 cell lines with corosolic acid showed an inducing effect on apoptosis-associated caspases, including Caspase-8, 9, and -3, in MADA-MB-231 cells with no effect on apoptotic markers in MCF7 cells. Further experiments uncovered corosolic acid-induced apoptosis in MADA-MB-231 cells by decreasing the expression of the phosphorylated form of JAK2 and STAT3 proteins. The present data suggested that corosolic acid is an apoptosis-inducing phytochemical in triple-negative breast cancer MADA-MB-231 cells. Also, corosolic acid triggered apoptosis in these cells by stimulating both pathways of apoptosis and inhibiting the JAK/STAT signaling. Furthermore, corosolic acid was found to inhibit MCF7 cell proliferation by a non-apoptotic mechanism.

New Mn(III)/Fe(III) complexes with thiohydantoin-supported imidazolium ionic liquids for breast cancer therapy

This study offers, for the first time, the design and synthesis of hybrids integrating imidazolium ionic liquids (IMILs) and thiohydantoins (THs) motifs and their Mn/Fe(III) complexes for cancer therapeutic applications. The molecular structures of thiohydantoin-supported imidazolium ionic liquids (THIMILs) (4a-c) and their complexes were proposed based on microanalytical and spectroscopic investigations. On the other hand, the UV–Vis spectroscopic and magnetic measurements, as well as comparisons with previously reported comparable complexes, led to the postulation of square pyramidal and octahedral geometries for Mn(III)THIMIL and Fe(III)THIMIL complexes, respectively. According to the MTT cytotoxicity assay results, the new hybrids inhibited MCF-7 cell proliferation more effectively than HepG2 and selectively as well. The anti-breast cancer performance varies depending on the hybrid structure, dose, and treatment duration. Among the compounds tested, Fe(III)THIMIL analog (6b) was the most active and selective anti-MCF-7 agent (IC50 1.98±0.56 μM, SI 34.92). It was found that 6b has the capacity to trigger G2/M cell cycle arrest and apoptosis in MCF-7 cells, presumably through a p50 route. Meanwhile, the molecular docking of 6b with Bcl-2 and p50 proteins showed great promise in the field of cancer treatment by modulating the levels of expression in these proteins.

Mitochondria-Targeted Ergosterol Peroxide Derivatives: Synthesis, Anticancer Properties and Their Preliminary Mechanism of Inhibiting MCF-7 Cell Proliferation

Ergosterol peroxide (EP) has been extensively studied for its antitumor activities. However, its further development has been restricted due to its limited intracellular accumulation and poor aqueous solubility. In this study, a novel triphenylphosphonium cation (TPP+) moiety was coupled to ergosterol peroxide to precisely target it at tumor cell mitochondria. The synthesized Mito-EP derivatives Mito-EP-3a-3d displayed stronger cytotoxicity than the EP parent and exhibited selectively cytotoxic effects between cancer cells and normal gastric epithelial (GES-1) cells. The most potent compound, Mito-EP-3b, was 9.7-fold more efficacious than ergosterol peroxide in the MCF-7 (breast cancer) cell line and showed good selectivity (SI = IC50GES-1/IC50MCF-7 = 4.04, IC50: concentrations to inhibit 50% of cell growth). Furthermore, Mito-EP-3b was able to decrease the mitochondrial membrane potential and induced reactive oxygen species production, accompanied by activating the expression of cytochrome c and Bax, while Bcl-2 expression was suppressed. The molecular mechanism may refer to the mitochondrial apoptotic pathway. Overall, the above results incentivize the further study of Mito-EP-3b derivatives as potent anticancer agents.

Organic fluorescent probe for concurrent imaging and apoptosis induction in cancer cells in vivo and in vitro by utilizing endogenous hydrogen sulfide

The organic fluorescent probe XZH1-H2S was successfully designed and synthesized to recognize exo- and endogenous hydrogen sulfide in cancer cells both in vivo and in vitro. The probe has low toxicity and shown favorable anti-interference performance, accompanying a detection limit of 180 nM due to H2S-induced effective thiolysis of dinitrophenyl ether. The fluorescent probe XZH1-H2S reacted with H2S to release a fluorophore that could inhibit MCF-7 cell proliferation with an IC50 of 10.12 μM. In view of its favorable biocompatibility, this fluorescence probe is also successfully used in vivo imaging and treatment of tumor-bearing nude mouse with good tumor inhibition rate of 69 %. Therefore, we successfully engineered an easy-to-synthesize bifunctional organic fluorescent probe for concurrent imaging and apoptosis induction in cancer cells in vitro and in vivo. The study is expected to be a valuable resource for breast cancer theranostics.

Serine O-acetyltransferase derived NV14 peptide reduces cytotoxicity in H2O2 induced MDCK cells and inhibits MCF-7 cell proliferation through caspase gene expression.

Most of the bioactive peptides exhibit antioxidant effect and do elicit inhibitory effect on proliferation of cancer cells. This study investigates the in-vitro antioxidant and anti-cancer properties of NV14 peptide, derived from serine O-acetyltransferase (SAT) of spirulina, Arthrospira platensis. The anti-cancer effect of the peptide was evaluated using human adenocarcinoma epithelial cells (MCF-7), while the anti-oxidant potential, as in reduction in ROS concentration, has been established using the H2O2-exposed, Madin-Darby canine kidney (MDCK) cells. The outcome of the in vitro analyses has been evaluated by in silico molecular docking analyses. The peptide, dose-dependently, reduced oxidative stress as well as cell proliferation. Besides, based on the binding scores between NV14 peptide and the important proteins associated with apoptosis and antioxidant defense, it is evident that the peptide has antioxidant and anti-cancer effect, in vitro. Together, this study demonstrates that NV14 has a potent antioxidant and anti-cancer capability; however, further direction needs to be focused on clinical or pharmacodynamics aspects.

Melittin-Induced Cell Death Through p53 and 8-OHdG in Breast Cell Cancer MCF-7

Melittin, one of the cytolytic peptides derived from bee venom, is a broad-spectrum efficacy candidate as an antibacterial, antifungal, and antitumor agent. This study demonstrates the cytotoxic effect of melittin isolated from Apis mellifera through the induction of p53 and 8-OHdG. The antiproliferative effect was evaluated against breast cell cancer MCF-7 via MTT assay, while the molecular mechanism of melittin on MCF-7 was assayed by p53 and 8-OHdG ELISA. With an IC50 value of 5.86 µg/mL ((very toxic)), the cytotoxic impact inhibits MCF-7 cell proliferation in a dose-dependent manner. Significant (p < 0.05) elevations in the level of p53 and 8-OHdG were evident in the IC50-treated cells compared to control. In conclusion, melittin may have considerable potential as a novel natural product-based for breast cancer.

Synthesis of Xylan-Click-Quaternized Chitosan via Click Chemistry and Its Application in the Preparation of Nanometal Materials.

For the high-valued utilization of hemicelluloses and for realizing the controllable synthesis of NPs, this paper’s aim is to combine xylan, chitosan and nanometal materials at the same time. In this research study, firstly, propargyl xylan was synthesized via nucleophilic substitution reaction between xylan and propargyl bromide in NaOH solution. On the other hand, a tosyl group was introduced onto the 6th position of synthesized quaternized chitosan (QCS), and the azide group replaced the tosyl group to obtain 6-amido-QCS (QCS-N3). The synthesis conditions of the above reactions were optimized. Subsequently, the novel xylan-click-QCS polymer was obtained via click reaction between terminal alkyne groups on the xylan chains and azide groups on QCS. Then, AgNPs and AuNPs were synthesized by adopting the xylan-click-QCS polymer as the reducing and stabilizing agent, and the reaction conditions were optimized to obtain well-dispersed and highly stable nanoparticles. There were two kinds of Ag nanomaterials, with diameters of 10~20 nm and 2~5 nm, respectively, indicating the formation of Ag nanoclusters, except for Ag nanoparticles, in this reaction. The diameter of the synthesized AuNPs was 20~30 nm, which possessed a more uniform size distribution. The Ag nanoclusters with a smaller size (2~5 nm) could inhibit MCF-7 cell proliferation effectively, indicating their application potential in cancer therapy. The study gives a new approach to the high-value utilization of biopolymers.

Phytoestrogens on the Proliferation of Breast Cancer Cell MCF-7

A cell is an organic whole containing biological macromolecules such as nucleic acid and protein. Human cells contain about 15,000 proteins, which play an important role in the development of cell life. This article aims to study the effect of phytoestrogens on the proliferation of breast cancer cells MCF-7. The estrogen-dependent MCF-7 cells described in this article are grown on average DMEM (containing calf serum 10) and connected to single cell culture. Five days before adding the test product, the cells were washed with PBS and converted into red-free phenol. High-sugar DMEM containing 5 parts of bovine embryo serum was cultured and treated with activated charcoal glucan glycosides. In the experiment, four dose groups of solvent control, estrogen control, anti-estrogens and two test substances were used for control, and the proliferation of MCF-7 cells was analyzed by integration method and flow cytometry. The experimental results in this article show that compared with the solvent control group, GS can significantly inhibit MCF-7 cell proliferation and cell DNA synthesis, and G/M can block the cell cycle and produce a similar inhibitory effect. 96mol/L zein treatment for 24 hours can significantly promote MCF-7 cell proliferation and cell DNA composition, promote cell cycle, and increase cell separation and proliferation index.

Knockout of Calcyclin Binding Protein Impedes the Growth of Breast Cancer Cells by Regulating Cell Apoptosis and β-Catenin Signaling.

Breast invasive carcinoma (BRCA) is becoming the most common malignant disease worldwide, and there is intense interest in identifying diagnostic biomarkers that can be targeted for treatment of BRCA. Recent evidence has shown that calcyclin binding protein (CacyBP) can function as either a tumor promoter or suppressor during carcinogenesis. Data in The Cancer Genome Atlas (TCGA) database show that CacyBP is overexpressed in human BRCA tissues, and high levels of CacyBP are associated with shorter overall survival. Immunohistochemical staining has shown that CacyBP levels are high in cancer tissue samples and associated with a higher likelihood of disease progression. We, therefore, conducted a knockout assay to determine the role of CacyBP in the development of BRCA. Knockout of CacyBP significantly inhibited MCF7 cell proliferation and colony formation. Apoptosis was higher in CacyBP knockout cells compared with control cells. Microarray analysis showed that the CacyBP knockout caused dysregulation of numerous genes closely related to β-catenin signaling, whereas quantitative reverse-transcription PCR and immunoblotting showed that it to be inactivated. In summary, we conclude that when overexpressed, CacyBP acts as a potential oncogene for BRCA by regulating β-catenin signaling.

A new cytotoxic sesquiterpene lactone from Euphorbia microsphaera Boiss against human breast cancer (MCF-7) and human fibrosarcoma (HT1080) cells

A new guaianolide sesquiterpene lactone with cytotoxic properties was isolated from Euphorbia microsphaera Boiss. To determine the highest active fraction and isolate bioactive compounds, a bioassay guided fractionation approach was used. The general toxicity properties of the plant's extracts and fractions (fr1-10) were assessed against Artemia salina, Oryzeaphilus mercator, and Tribolium castaneum. Cytotoxic activities were investigated against normal human foreskin fibroblasts and two malignant cell lines, including human breast cancer (MCF-7) and human fibrosarcoma cells (HT1080) using the MTT assay at different time points of 24, 48, and 72 h. Single crystal X-ray diffraction (SC-XRD) and mass spectrometry data were used to determine the structure of the active guaianolide sesquiterpene lactone (3aR,4S,4aS,5R,7aS,9aS)-5-hydroxy-5,8-dimethyl-3-methylene-2-oxo-2,3,3a,4,4a,5,6,7,7a, 9a decahydroazuleno [6,5-b] furan-4-yl acetate (named aryanin). Chloroformic fraction 7 (fr7, LC50 = 93.50 μg/mL for general toxicity) had the highest toxicity result, with a mortality rate of more than 50% for both insect species after 12 h at 15 mg/mL. The highest cytotoxicity of aryanin was observed on 24 h treated MCF-7 with an IC50 of 13.81 μg/mL. After 24 h, the inhibition of MCF-7 cell proliferation was 92%–94% at concentrations of 25–50 μg/mL, respectively. On MCF-7, the IC50 was found to be 49.35 μg/mL after 72 h. This compound had a considerable cytotoxicity (IC50 ≤ 12.5 μg/mL, 24 h) on human foreskin fibroblasts. In contrast to the MCF-7 cell line, the proliferation of human foreskin fibroblasts was increased after 72 h.

Antioxidant and Antiproliferative Potential of Acacia auriculiformis Methanol Leaves Extract Against Breast Cancer Cell Model

Acacia auriculiformis is a plant which often found in Indonesia. Acacia leaves have been known to have high antioxidant content. The phenolic compound of A. auriculiformis is the largest of these plants and phenolic compound have potential as anticancer protective agents. The aims of this study were to determine the phenolic compound, antioxidant activity, cytotoxic and antiproliferative activity of acacia leaves extract against T47D and MCF-7 breast cancer cell lines. Extraction was carried out by maceration method using methanol as a solvent. Phenolic compounds were examined by Thin Layer Chromatography (TLC) and antioxidant activity was measured using DPPH assay, followed by cytotoxicity and antiproliferation test measured by MTT Assay to obtain the IC50 value and percent of antiproliferation. Based on TLC, A. auriculiformis methanol leaves extract contain a phenolic compound with Rf value of 0.85 compared to gallic acid.  Antioxidant activity A. auriculiformis with IC50 value of 9 ppm is classified as high antioxidant activity and MTT assay results for cytotoxicity with IC50 value of 273.8 and 31.26 ppm for T47D and MCF-7 cells, respectively. Antiproliferative analysis also showed high values for MCF-7 cells. These data have shown that methanol leaves extract of A. auriculiformis has high antioxidant activity and inhibited MCF-7 cell proliferation but not T47D breast cancer cell lines.ÂÂ