scholarly journals Molecular Modelling, Synthesis and Biological Evaluation of novel benzimidazole derivatives for the treatment of Breast Cancer

2020 ◽  
Vol 01 ◽  
Author(s):  
Ishan Panchal ◽  
Animesh G. Devgirkar ◽  
Ashish D Patel ◽  
Afzal Nagani ◽  
Chaitali Lad
Keyword(s):  
Breast Cancer ◽  
Lung Cancer ◽  
Cell Line ◽  
Antitumor Agents ◽  
Mcf7 Cell ◽  
Mtor Inhibitors ◽  
Biological Evaluation ◽  
Benzimidazole Derivatives ◽  
Anticancer Activities ◽  
Mcf7 Cell Line

Background: The treatment of cancer must be needed with the scientific advancement. ATP-competitive mTOR inhibitors have been studied as potential antitumor agents. Objective: A series of substituted benzimidazole compounds were designed, synthesized and characterized via introducing 2-chloroquinolin into 2nd position and most title compounds exhibited enhanced anticancer activities. Methods: To study the anticancer mechanism, VIa-VIh was successfully docked by iGEMDOCK 2.0 which gives good affinity towards m-TOR/PI3K dual inhibitors. The anti-proliferative activities of these compounds were evaluated by on MCF-7 and A549 cell line for Brest and lung cancer respectively. Results: 2-(2-chloroquinolin-3-yl)-1H-benzoimidazol-1-yl)(phenyl)methanone (VIa) exhibited significant anti-proliferative activity, especially against brest cancer (IC50 197 µM) for MCF7 cell line and (2-(2-chloroquinolin-3-yl)-1H-benzo[d]imidazol-1-yl)(4-nitrophenyl)methanone (VIc) was significantly active against lung cancer (IC50 89 µM) for A579 cell line. Conclusion: VIa gives more activity on breast cancer and it gives IC50 197 µM for MCF7 cell line and (2-(2-chloroquinolin-3-yl)-1H-benzo[d]imidazol-1-yl) (4-nitrophenyl) methanone (VIc) lung cancer IC50 89 µM for A579 cell line.

Synthesis of artemisinic acid derived glycoconjugates and their anticancer studies

2020 ◽  
Vol 18 (12) ◽  
pp. 2252-2263
Author(s):  
Tharun K. Kotammagari ◽  
Sayantan Paul ◽  
Ganesh K. Barik ◽  
Manas K. Santra ◽  
Asish K. Bhattacharya
Keyword(s):  
Cell Line ◽  
Mcf7 Cell ◽  
Click Reaction ◽  
Anticancer Activities ◽  
Artemisinic Acid ◽  
Mcf7 Cell Line ◽  
Line P

Twenty-four artemisinic acid glycoconjugate hybrids were synthesized using click reaction and evaluated for their anticancer activities against the MCF7 cell line.

scholarly journals MicroRNA-126-5p Inhibits the Migration of Breast Cancer Cells by Directly Targeting CNOT7

2020 ◽  
Vol 19 ◽  
pp. 153303382097754
Author(s):  
Yuying Miao ◽  
Jiang Lu ◽  
Baozhen Fan ◽  
Lecan Sun
Keyword(s):  
Breast Cancer ◽  
Cell Line ◽  
Mcf7 Cell ◽  
Bioinformatic Analysis ◽  
Negative Control ◽  
Differentially Expressed ◽  
Luciferase Reporter ◽  
Differentially Expressed Mirnas ◽  
Mcf7 Cell Line ◽  
Breast Cancer Mcf7 Cell

Background: To assess the effect of microRNA-126-5p (miR-126-5p) on the migration of the breast cancer MCF7 cell line. Methods: GSE143564 was downloaded from the Gene Expression Omnibus (GEO; http://www.ncbi.nlm.nih.gov/geo ) to identify the differentially expressed miRNAs between breast cancer and adjacent tissues. Quantitative reverse transcription PCR (RT-qPCR) was used to assess miR-126-5p levels in the normal 184A1 breast cell line and the breast cancer MCF7 cell line. The MCF7 cell line was then transfected with miR-126-5p mimics or corresponding negative control (NC-mimic). The proliferation and migration abilities of the MCF7 cell line were measured by methyl thiazolyl tetrazolium (MTT), Transwell and scratch healing assays. CCR4-NOT transcription complex and subunit 7 (CNOT7) expression levels in the NC-mimic and miR-126-5p mimic groups were measured by Western blot analysis. Bioinformatic analysis and a dual-luciferase reporter assay were performed to identify the miR-126-5p target gene. Results: One hundred forty-eight differentially expressed miRNAs (downregulated = 55, upregulated = 93) were identified. MiR-126-5p expression in the MCF7 cell line was significantly downregulated relative to that of 184A1 cell line (P < 0.05). Compared with that observed in the control and NC-mimic groups, cell proliferation in the miR-126-5p mimic group was significantly decreased at 48 and 72 h posttransfection (P < 0.05). In addition, the scratch healing rate and number of membrane-piercing cells in the miR-126-5p overexpression group were lower than those detected in the control and NC groups (P < 0.05). Furthermore, miR-126-5p could reduce the luciferase activity for the wild-type CNOT7 gene 3’-untranslated region (UTR) reporter (P < 0.05) but had no effect on the mutant 3’UTR reporter (P > 0.05). Compared with that observed in the NC and control groups, the levels of CNOT7 in the miR-126-5p overexpression group decreased (P < 0.05). Conclusion: Upregulation of miR-126-5p can inhibit the migration of the breast cancer MCF7 cell line, which may involve its direct targeting of the 3’UTR of CNOT7.

Induction of breast cancer progression and metastasis by HOXB9 gene’s activation by sequence specific binding factors.

2013 ◽  
Vol 31 (26_suppl) ◽  
pp. 26-26
Author(s):  
Aisulu Zhussupova ◽  
Tetsu Hayashida ◽  
Maiko Takahashi ◽  
Hiromitsu Jinno ◽  
Yuko Kitagawa
Keyword(s):  
Breast Cancer ◽  
Cell Line ◽  
Cell Lines ◽  
Cancer Progression ◽  
Promoter Region ◽  
Mcf7 Cell ◽  
Luciferase Activity ◽  
Luciferase Assay ◽  
Chip Assay ◽  
Mcf7 Cell Line

26 Background: HOXB9 is a member of class I HOX genes and is known to be overexpressed in human breast cancer and related to EMT, tumor angiogenesis, and radio-resistance (PNAS 2010), being significant prognostic factor in breast cancer patients. (Ann Surg Oncol 2012). Methods: We analyzed the upstream promoter region to determine the critical sequence for HOXB9 transcription. The multiple lengths of HOXB9 promoter region were cloned into pGL3 luciferase vector and each of them were checked by luciferase assay. Then made E2F1 overexpressed cell-lines: MCF7, MCF10A and MDA-MB231 to check HOXB9 gene expression. ChIP assay performed using E2F1 induced MCF7 cell-line model and EMSA made with T47D cells and E2F1 antibody. Results: We demonstrated luciferase activity of MDA-MB231 cells and overexpressed HOXB9 was determined at the region from -404 to -392 bps, showing that the mentioned region plays the critical role for the transcription of HOXB9. Computer prediction system for the binding ability to critical sequence raised several candidate: E2F1, PAX-5, P53, ETS-1, NFY-A, Sp-1, which are known to be related with cancer progression and we confirmed these genes could induce HOXB9. E2F1 overexpressed breast cancer cell-lines indicate high expression of HOXB9 show the correlation between E2F1 and HOXB9 expression. Luciferase assay method done by constructing pGL3 with HOXB9 critical sequence and analyzed using wild-type MCF7 and E2F1 induced MCF7 cells showed high luciferase activity of HOXB9 critical sequence plasmid in E2F1 induced MCF7 cell-line by compare to WT. ChIP assay and EMSA assay methods performed using E2F1 overexpressed MCF7 and T47D cell-lines model revealed high precipitation rate with E2F1 antibody and HOXB9 expression than negative control. Conclusions: HOXB9 is plays the role as the accelerator of breast cancer progression and discovering the properties of the gene and related factors will help to understand new signaling pathways of breast cancer development. E2F1 is a strong candidate direct binds to HOXB9 critical sequence and correlates with HOXB9 expression. Manipulating of E2F1 expression may regulate HOXB9 and reduce cancer progression and metastasis.

MIAT lncRNA is overexpressed in breast cancer and its inhibition triggers senescence and G1 arrest in MCF7 cell line

2018 ◽  
Vol 119 (8) ◽  
pp. 6470-6481 ◽  
Author(s):  
Firooz J. Alipoor ◽  
Malek H. Asadi ◽  
Masoud Torkzadeh‐Mahani
Keyword(s):  
Breast Cancer ◽  
Cell Line ◽  
Mcf7 Cell ◽  
G1 Arrest ◽  
Mcf7 Cell Line

scholarly journals A New CDK2 Inhibitor with 3-Hydrazonoindolin-2-One Scaffold Endowed with Anti-Breast Cancer Activity: Design, Synthesis, Biological Evaluation, and In Silico Insights

Molecules ◽  
2021 ◽  
Vol 26 (2) ◽  
pp. 412
Author(s):  
Mohammad M. Al-Sanea ◽  
Ahmad J. Obaidullah ◽  
Mohamed E. Shaker ◽  
Garri Chilingaryan ◽  
Mohammed M. Alanazi ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Cell Line ◽  
Inhibitory Activity ◽  
Flow Cytometric Analysis ◽  
Docking Studies ◽  
Biological Evaluation ◽  
Intrinsic Activity ◽  
Binding Interaction ◽  
Mcf 7

Background: Cyclin-dependent kinases (CDKs) regulate mammalian cell cycle progression and RNA transcription. Based on the structural analysis of previously reported CDK2 inhibitors, a new compound with 3-hydrazonoindolin-2-one scaffold (HI 5) was well designed, synthesized, and biologically evaluated as a promising anti-breast cancer hit compound. Methods: The potential anti-cancerous effect of HI 5 was evaluated using cytotoxicity assay, flow cytometric analysis of apoptosis and cell cycle distribution, ELISA immunoassay, in vitro CDK2/cyclin A2 activity, and molecular operating environment (MOE) virtual docking studies. Results: The results revealed that HI 5 exhibits pronounced CDK2 inhibitory activity and cytotoxicity in human breast cancer MCF-7 cell line. The cytotoxicity of HI 5 was found to be intrinsically mediated apoptosis, which in turn, is associated with low Bcl-2 expression and high activation of caspase 3 and p53. Besides, HI 5 blocked the proliferation of the MCF-7 cell line and arrested the cell cycle at the G2/M phase. The docking studies did not confirm which one of geometric isomers (syn and anti) is responsible for binding affinity and intrinsic activity of HI 5. However, the molecular dynamic studies have confirmed that the syn-isomer has more favorable binding interaction and thus is responsible for CDK2 inhibitory activity. Discussion: These findings displayed a substantial basis of synthesizing further derivatives based on the 3-hydrazonoindolin-2-one scaffold for favorable targeting of breast cancer.

scholarly journals Methoxy and bromo scans on N-(5-methoxyphenyl) methoxybenzenesulphonamides reveal potent cytotoxic compounds, especially against the human breast adenocarcinoma MCF7 cell line

2021 ◽  
Vol 36 (1) ◽  
pp. 1029-1047
Author(s):  
Myriam González ◽  
María Ovejero-Sánchez ◽  
Alba Vicente-Blázquez ◽  
Manuel Medarde ◽  
Rogelio González-Sarmiento ◽  
...  
Keyword(s):  
Cell Line ◽  
Mcf7 Cell ◽  
Breast Adenocarcinoma ◽  
Human Breast ◽  
Human Breast Adenocarcinoma ◽  
Cytotoxic Compounds ◽  
Mcf7 Cell Line
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