Proliferation Of Breast Cancer Cells MCF-7 Research Articles

MiR-622 Induces Breast Cancer Cell MCF-7 Proliferation, Migration, and Invasion by Directly Negatively Targeting EYA1

Breast cancer is the most common female cancer in the world. Breast cancer patients are currently treated with a combination of surgery, chemotherapy, radiotherapy, and targeted therapy, but the 5-year overall survival rate is still low. Therefore, we plan to explore the potential interaction mechanism between miR-622 and EYA1 in the breast cancer cells and their effect on proliferation, migration, and invasion of breast cancer, to lay a foundation for the gene therapy of breast cancer and improve the therapeutic effect. This study found that miR-622 was highly expressed in breast cancer cell lines, while EYA1 was poorly. In MCF-7 cell line, miR-622 had the highest expression level, while EYA1 had the lowest. Besides, the bioinformatics analysis showed that EYA1 possesses putative miR-622 binding sites within its 3 ′ UTR. The increased miR-622 significantly enhanced the proliferation, migration, and invasion of MCF-7 cell line and inhibited luciferase reporter activity in the 3 ′ UTR of EYA1-WT. When upregulating the expression of miR-622, the mRNA and protein expression levels of EYA1 were significantly decreased. We also found that the silencing of EYA1 promoted the proliferation, migration, and invasion of breast cancer MCF-7 cell line. These results indicate that miRNA-622 plays a tumor-promoting role in breast cancer through targeted negative regulation of EYA1, suggesting that miRNA-622 may become a potential target for breast cancer treatment.

The ion channel TRPM7 regulates zinc-depletion-induced MDMX degradation

Zinc deficiency has been linked to human diseases, including cancer. MDMX, a crucial zinc-containing negative regulator of p53, has been found to be amplified or overexpressed in various cancers and implicated in the cancer initiation and progression. We report here that zinc depletion by the ion chelator TPEN or Chelex resin results in MDMX protein degradation in a ubiquitination-independent and 20S proteasome-dependent manner. Restoration of zinc led to recovery of cellular levels of MDMX. Further, TPEN treatment inhibits growth of the MCF-7 breast cancer cell line, which is partially rescued by overexpression of MDMX. Moreover, in a mass-spectrometry-based proteomics analysis, we identified TRPM7, a zinc-permeable ion channel, as a novel MDMX-interacting protein. TRPM7 stabilizes and induces the appearance of faster migrating species of MDMX on SDS-PAGE. Depletion of TRPM7 attenuates, while TRPM7 overexpression facilitates, the recovery of MDMX levels upon adding back zinc to TPEN-treated cells. Importantly, we found that TRPM7 inhibition, like TPEN treatment, decreases breast cancer cell MCF-7 proliferation and migration. The inhibitory effect on cell migration upon TRPM7 inhibition is also partially rescued by overexpression of MDMX. Together, our data indicate that TRPM7 regulates cellular levels of MDMX in part by modulating the intracellular Zn2+ concentration to promote tumorigenesis.

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.

Ultrasound-mediated destruction of vascular endothelial growth factor (VEGF) targeted and paclitaxel loaded microbubbles for inhibition of human breast cancer cell MCF-7 proliferation

AimsVascular endothelial growth factor (VEGF) can promote cell division, proliferation and migration. In this study, we aimed to investigate roles of ultrasound-mediated destruction of VEGF-targeted and paclitaxel (PTX)-loaded lipid microbubbles (VTPLLM + US) in human breast cancer cells. MethodsThe activity of MCF-7 cells was determined by cell counting Kit-8. Flow cytometry was performed to detect the cells apoptosis and cell cycle. The expression of cell cycle-associated proteins, matrix metalloprotein-9 (MMP-9), VEGF and apoptosis-associated proteins were detected by qRT-PCR and Western blot. ResultsThe obtained data suggested that VTPLLM + US promoted the G1 phase cell cycle arrest and suppressed the viability of MCF-7 cells. We also found that VTPLLM + US accelerated cells apoptosis. Cell cycle-associated proteins and VEGF expression were modulated by VTPLLM + US. Moreover, VTPLLM + US was found to regulate the expression levels of apoptosis-associated proteins in MCF-7 cells. Our findings suggested that VTPLLM + US suppressed the proliferation and accelerated the apoptosis of MCF-7 cells through regulating VEGF expression. ConclusionsThe potential effects of VTPLLM + US on apoptosis of MCF-7 cells suggest that applying VTPLLM + US might be an effective strategy in breast cancer therapies.

HIF-1α Promotes Breast Cancer Cell MCF-7 Proliferation and Invasion Through Regulating miR-210

Many malignant tumors grow in hypoxic condition, which is associated with tumor growth, invasion, and metastasis. MicroRNAs are of great significance in the development of multiple malignant tumors. This study cultured breast cancer cell MCF-7 under the condition of different concentrations of oxygen, to test cell proliferation and invasion, and detect miR-210 expression, aiming to analyze the influence of hypoxia on breast cancer cell behaviors as well as miR-210 expressions. Breast cancer cell MCF-7 was cultured under normoxia, hypoxia, or anaerobic conditions for 12, 24, or 48 hours. Cell proliferation was detected by MTT assay. Cell invasion and migration were tested by transwell assay. HIF-1α mRNA and miR-210 expressions were determined by real-time polymerase chain reaction. MCF-7 cell proliferation was gradually increased following time extension (p < 0.05). MCF-7 cell exhibited higher proliferation, invasion, and migration activities in hypoxic and anaerobic groups compared with those in normoxic group during the same time period. HIF-1α mRNA and miR-210 were significantly upregulated in anaerobic group compared with those in other groups (p < 0.05). HIF-1α mRNA and miR-210 were obviously elevated at 12, 24, and 48 hours (p < 0.05). MCF-7 cell proliferation was increased, invasion and migration were enhanced, with upregulated expression of HIF-1α mRNA and miR-210 in the hypoxic and anaerobic group following time extension.

The research of As4S4 inhibit the growth of breast cancer cell by regulating phosphatidylinositol 3 kinase/protein kinase B/mammalian target of rapamycin signal pathway

Objective To investigate the effect of As4S4 inhibit the growth of breast cancer cell by regulating phosphatidylinositol 3 kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) signal pathway. Methods Methyl thiazol tetrazolium (MTT) assay was used to detect breast cancer cell MCF-7 proliferation after 0, 20, 40, 60, 80 μmol/L As4S4 treatment for 24, 48, 72 h, and 10 μmol/L LY294002 treatment 48 h. Wound healing and transwell were used to detect the distance of MCF-7 cell migration and invasion after As4S4 dealing with 48 h. Flow cytometry was used to detect MCF-7 cell apoptosis after and 10 μmol/L LY294002 treatment 48 h. Western blotting was used to detect PI3K, p-Akt, mTOR expression levels in MCF-7 cell after As4S4 and 10 μmol/L LY294002 dealing with 48 h. Results Compared with 0 μmol/L treatment, 20 μmol/L As4S4 had no significant inhibition of cell proliferation at 24 h (P=0.065), it had a significant inhibition of cell proliferation at 48 h and 72 h (P=0.033) with the inhibition ratio of 11.1% and14.3%, respectively.40, 60, 80 μmol/L As4S4 treatment had the most obvious inhibitory effect at 72 h (P=0.002) the inhibition ratio of 47.9%, 58.8%, 67.1%, respectively. After60 As4S4 treatment for 48 h, the migration rate and invasion ability of MCF-7 cell were lower than the control group (with decrease of 42.4%), the difference was significant (P=0.005), the apptosis rate was significant increased to (19.56±1.12)% (P=0.009), the expression of PI3K in MCF-7 cell had no significantly change and p-Akt, mTOR were significantly decreased than control group (P=0.008) with the decrease of 64.3% and 58.7%, respectively. The results of proliferation and apoptosis was consistent with the LY294002 treatment. Conclusion As4S4 may inhibit breast cancer MCF-7 cell proliferation and metastasis and promote apoptosis by inhibiting PI3K/Akt/mTOR signaling pathway. Key words: As4S4; Breast cancer; Proliferation; Transfer; Apoptosis

Antioxidization and antiproliferation of extract from leaves of Toona sinensis.

To determine the antioxidization and antiproliferation of extract from leaves of Toona sinensis (LTS). The total phenolic extract of LTS was obtained by solvent and polyamide resin to determine the content. The antioxidization of the LTS extract was measured by TOSC assay. Antiproliferation was studied in vitro with different human cancer cells. The total phenolic content in the LTS was (427.53±4.31) mg/g and antioxidization was 807.64 μmoL vitamin C equivalents/g in the sample. The extract significantly inhibited the colon cancer cell Caco-2, human liver cancer cell HepG(2) and breast cancer cell MCF-7 proliferation with EC(50) (4.00±0.39), (153.16±13.49) and (193.46±14.68) μg/mL, respectively. The bioactivity index (BI) of the LTS extract was nearly 283. Caco-2 was more sensitive than MCF-7 and HepG(2). Extract from LTS has anticancer properties useful for preventing chronic diseases.

Assessment of styrene oligomers eluted from polystyrene-made food containers for estrogenic effects in in vitro assays

Recently, several substances from among the huge numbers of chemicals used by mankind have been implicated as instigators of disrupted endocrine function and related human health problems. Polystyrene (PS) is one of the most frequently used resins in the world, and the styrene oligomer dissolved out from PS has been designated as a potential trigger of estrogen-like activity in the Wingspread Declaration and the Japan Environment Agency's SPEED98 [JEA (Japan Environment Agency) Strategic Problem on Environmental Endocrine Disruptors '98 (SPEED) '98), http://www.env.go.jp/en/pol/speed98/sp98.html]. In order to assess the endocrine disrupting effect of styrene oligomers, we tested one styrene monomer (SM), three styrene dimers (SDs) and seven styrene trimers (STs), newly isolated from optical isomers, known to dissolve in small amounts from cup noodle containers made of polystyrene by the estrogen receptor binding assay, luciferase reporter gene assay, and human breast cancer cell MCF-7 proliferation assay. In all three tests, none of the SM, SDs and STs showed any significant activity. Accordingly, we concluded that these substances have no estrogenic activity.