SOX4 Serves an Oncogenic Role in the Tumourigenesis of Human Breast Adenocarcinoma by Promoting Cell Proliferation, Migration and Inhibiting Apoptosis

2020 ◽  
Vol 15 (1) ◽  
pp. 49-58
Author(s):  
Junhe Zhang ◽  
Shujie Chai ◽  
Xinyu Ruan
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Caspase 3 ◽  
Breast Adenocarcinoma ◽  
Migration Ability ◽  
Expression Levels ◽  
Apoptosis Rate ◽  
And Migration ◽  
Mcf 7 ◽  
Proliferation And Migration

Background: Breast cancer is among the most common malignant cancers worldwide, and breast adenocarcinoma in glandular tissue cells has excessive metastasis and invasion capability. However, little is known on the molecular process by which this disease develops and progresses. Objective: In this study, we explored the effects of sex-determining region Y-box 4 (SOX4) protein on proliferation, migration, apoptosis and tumourigenesis of breast adenocarcinoma and its possible mechanisms. Methods: The SOX4 overexpression or knockdown Michigan Cancer Foundation-7 (MCF-7) cell lines were established. Among the SOX4 overexpression or MCF-7 knockdown cell lines, proliferation, migration ability and apoptosis rate were detected. The expression levels of apoptosis-related proteins (Bax and Cleaved caspase-3) were analysed using Western blot. The effect of SOX4 on tumourigenesis was analysed using the clone formation assay in vitro and tumour xenograft experiment in nude mice. Results: Compared with the overexpression of control cells, proliferation and migration ability of SOX4 overexpression cells significantly increased, the apoptosis rate significantly decreased in addition to the expression levels of Bax and Cleaved caspase-3 (P < 0.05). Compared with the knockdown of control cells, proliferation and migration ability of SOX4 knockdown cells significantly decreased, and the apoptosis rate and expression levels of Bax and Cleaved caspase-3 significantly increased (P < 0.05). Clone formation and tumour growth abilities of SOX4 overexpression cells were significantly higher than those of the control cells (P < 0.05), whereas SOX4 knockdown cells had the opposite effect. Conclusion: SOX4 plays an oncogenic role in breast adenocarcinoma tumourigenesis by promoting cell proliferation, migration and inhibiting apoptosis. It can be used as a potential molecular target for breast cancer gene therapy.

scholarly journals Metformin suppresses the proliferation and invasion through NF-kB and MMPs in MCF-7 cell line

2019 ◽  
Vol 45 (3) ◽  
pp. 295-304
Author(s):  
Nail Besli ◽  
Guven Yenmis ◽  
Matem Tunçdemir ◽  
Elif Yaprak Sarac ◽  
Sibel Doğan ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Cell Line ◽  
Cancer Cell Line ◽  
Immunocytochemical Staining ◽  
Breast Adenocarcinoma ◽  
Control Group ◽  
Expression Levels ◽  
Er Positive ◽  
Mcf 7

AbstractObjectiveMCF-7 cells, a breast cancer cell line, are used for experiments of estrogen receptor (ER)-positive breast cancer and many sub-clones representing different classes of ER-positive tumors. We aimed to determine the efficacy of metformin, a potential anti-cancer agent, on the cell proliferation, and the expressions of NF-kB (p65), MMP-2 and MMP-9 in MCF-7 cell line.Materials and methodsMCF-7 cells (human breast adenocarcinoma) were treated with elevating doses of metformin (0–50 mM) for 24 h. The anti-proliferative effect of metformin was studied by BrdU proliferation assay, and the expression levels of NF-kB (p65), MMP-2 and MMP-9 were analyzed by immunocytochemical staining.ResultsThe percentage of cell proliferation was reduced significantly by 10 and 50 mM doses of metformin (p < 0.001). The expression levels of nuclear NF-kB (p65), MMP-9 and MMP-2 were considerably reduced in 50 mM metformin treated cells while the expression of cytoplasmic NF-kB (p65) elevated compared to control group (p < 0.05). Ten millimolar metformin also reduced expression of MMP-9 significantly (p < 0.05).ConclusionMetformin may act on the proliferation, and the processes of invasion and metastasis of MCF-7 cells through blocking NF-kB, which is intensely expressed in breast cancer cells, and through diminishing the expression of MMP-2 and MMP-9 significantly.

scholarly journals The Inhibitory Effect of Hsa-miR-330 Replacement on the Proliferation and Migration of Breast Cancer MCF-7 Cells

2018 ◽  
Vol 7 (3) ◽  
pp. 360-365
Author(s):  
Elham Hosseinzadeh ◽  
Behzad Mansoori ◽  
Ali Mohammadi ◽  
Vahid Khaze ◽  
Maryam Rezazadeh ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Wound Healing ◽  
Imaging System ◽  
Target Therapy ◽  
Cellular Migration ◽  
Inhibitory Role ◽  
And Migration ◽  
Mcf 7 ◽  
Proliferation And Migration

Objectives: miRNAs comprise a group of master gene expression regulators, exerting their effects after transcription through targeting specific mRNAs, hence, influencing cellular processes. A considerable number of miRNAs are known to affect cell proliferation and migration in breast cancer, one of which is hsa-miR-330, a key player in various types of cancers. The purpose of this study was to evaluate the anti-proliferative and anti-migrative effects of hsa-miR-330 on MCF-7 cell line. Materials and Methods: MCF-7 cells were transfected with pCMV-miR-330 vector and cell selection was performed in media containing Geneticin (G418). Subsequently, MTT assay was performed to evaluate the effect of hsa-miR-330 on proliferation and scratch wound healing assay was employed to evaluate cellular migration. Finally, using real-time PCR, the expression of hsamiR-330 as well as the repressive impact on the expression of E2F was investigated. Results: Upon confirmation of hsa-miR-330 induction in MCF-7 cells via GFP channel imaging system, miR-330 expression was demonstrated to be increased 10 folds in stable cells. The results of MTT and wound-healing assays demonstrated an inhibitory role for hsa-miR-330 in proliferation and migration of stable hsa-miR-330-transfected MCF-7 cancer cells compared to controls. In addition, after transfecting cells with hsa-miR-330, E2F1 was down-regulated in comparison with controls. Conclusions: Based on the results of the current study, we suggest a potential inhibitory role for hsa-miRNA-330 in cell proliferation as well as cell migration in breast cancer by targeting E2F1 mRNA. Additionally, a therapeutic role can be suggested for hsa-miR-330 in terms of target therapy for breast cancer.

scholarly journals USP13 Regulates the Breast Tumor Proliferation and Migration through the Stabilization of PDCD4 Protein

2021 ◽  
Author(s):  
Jun Tian ◽  
Bei Li ◽  
Jing Qiao ◽  
Xinfeng Pang ◽  
Xiaojing Yue
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Cell Lines ◽  
Breast Tumor ◽  
Soft Agar ◽  
Tumor Proliferation ◽  
Soft Agar Assay ◽  
And Migration ◽  
Cancer Tissues ◽  
Proliferation And Migration

Abstract Background: Programmed cell death protein 4 (PDCD4), which serves as a tumor suppressor protein, plays a important role in cell proliferation,apoptosis, cell migration and DNA-damage response.However, the exact mechanism for the deubiquitination of PDCD4 remain unclear.Methods: Western blotting was used to detect the expression of PDCD4 in the breast cancer tissues and BC cell lines. We identified the potential PDCD4 associated deubiquitinase by RNAi screening. GST-Pull down and domain-mapping analysis were used to reveal that USP13 and PDCD4 directly interact with each other.Flow cytometry was used to detect the changes of G1 to S phase. Soft agar assay was used to measure the changes of the cell proliferation efficiency.Results: The expression of PDCD4 was decreased in the breast cancer tissues and BC cell lines. USP13 as a potential PDCD4 associated deubiquitinase. USP13 physically interacted with PDCD4 and greatly increased the steady state of PDCD4 through the ubiquitin-proteasome pathway.Importantly, silencing of the USP13 facilitated cell cycle from G1 to Sphase, promoted breast tumor cells proliferation and migration through downregulation of PDCD4. Conclusions: Together, these results suggest that USP13 plays an important role in the breast tumor proliferation and migration through modulating PDCD4 stability.

scholarly journals Identification of CTRP1 as a Prognostic Biomarker and Oncogene in Human Glioblastoma

2019 ◽  
Vol 2019 ◽  
pp. 1-11
Author(s):  
Liyan Chen ◽  
Gang Su
Keyword(s):  
Cell Proliferation ◽  
Mrna Expression ◽  
Genetic Alterations ◽  
Expression Levels ◽  
Cell Proliferation And Migration ◽  
Ccl2 Expression ◽  
Human Gbm ◽  
And Migration ◽  
Mrna Expression Levels ◽  
Proliferation And Migration

Introduction. Glioblastoma (GBM) is the most frequent and malignant type of primary brain tumors in adults. The valuable prognostic biomarkers and therapeutic targets for GBM remain to be elucidated. The association of adipokines with cancer has been well documented. The C1q/TNF-related protein 1 (CTRP1), a novel adipokine, belongs to the CTRP family.Methods. In the present study, the expression and potential roles of CTRP1 in GBM were explored based on in silico evaluation, including GEPIA, the Pathology Atlas of the Human Protein Atlas, cBioPortal, TIMER, and SurvExpress. The CCK8, transwell, and wound healing assays were used to detect cell proliferation and migration.Results. It was found that mRNA expression levels ofCTRP1were significantly upregulated in GBM tissues compared with those in nontumor tissues according to the analysis on public dataset and immunohistochemical results of GBM tissues (P<0.05). CTRP1 was mainly localized in the cytoplasm and cell membrane of GBM cells. The genetic alterations of CTRP1 occurred at a low rate in GBM (2 of 591 sequenced cases/patients, 0.33%). The mRNA expression levels ofCTRP1were positively associated with the tumor-infiltrating macrophages and CCL2 in GBM (P<0.05, respectively). The higher mRNA expression levels ofCTRP1were significantly correlated with higher risk and shorter overall survival time in GBM (P<0.05). CTRP1 knockdown significantly inhibited the proliferation and migration in human GBM cells, suggesting the inhibition of CTRP1 on human GMB progression. Moreover, CTRP1 knockdown inhibited CCL2 expression, and CCL2 overexpression reversed the inhibition of cell proliferation and migration induced by CTRP1 knockdown, suggesting that CTRP1 promoted tumor progression by regulating CCL2 expression.Conclusions. These findings suggest that CTRP1 potentially indicates poor prognosis in GBM and promotes the progression of human GBM.

Sprouty4 interferes with cell proliferation and migration of breast cancer-derived cell lines

Tumor Biology ◽  
2014 ◽  
Vol 35 (5) ◽  
pp. 4447-4456 ◽  
Author(s):  
Vanita Vanas ◽  
Elsa Mühlbacher ◽  
Rosana Kral ◽  
Hedwig Sutterlüty-Fall
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Cell Lines ◽  
Cell Proliferation And Migration ◽  
And Migration ◽  
Proliferation And Migration

scholarly journals miR-3188 Regulates Cell Proliferation, Apoptosis, and Migration in Breast Cancer by Targeting TUSC5 and Regulating the p38 MAPK Signaling Pathway

2018 ◽  
Vol 26 (3) ◽  
pp. 363-372 ◽  
Author(s):  
Xiaowen Chen ◽  
Jianli Chen
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Signaling Pathway ◽  
P38 Mapk ◽  
Molecular Mechanisms ◽  
Mapk Signaling ◽  
Mapk Signaling Pathway ◽  
Luciferase Reporter ◽  
And Migration ◽  
Mcf 7

This study intended to investigate the effects of miR-3188 on breast cancer and to reveal the possible molecular mechanisms. miR-3188 was upregulated and TUSC5 was downregulated in breast cancer tissues and MCF-7 cells compared to normal tissue and MCF-10 cells. After MCF-7 cells were transfected with miR-3188 inhibitor, cell proliferation and migration were inhibited, whereas apoptosis was promoted. Luciferase reporter assay suggested that TUSC5 was a target gene of miR-3188. In addition, miR-3188 overexpression increased the p-p38 expression, while miR-3188 suppression decreased the p-p38 expression significantly. miR-3188 regulated breast cancer progression via the p38 MAPK signaling pathway. In conclusion, miR-3188 affects breast cancer cell proliferation, apoptosis, and migration by targeting TUSC5 and activating the p38 MAPK signaling pathway. miR-3188 may serve as a potential therapeutic agent for the treatment of breast cancer.

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