String Analysis to identify the Activity of Gyrinops versteegii derived Lauric Acid against Breast Cancer

2021 ◽  
Vol 16 (7) ◽  
pp. 136-140
Author(s):  
Lisna Hidayati ◽  
Nur Fathurahman Ridwan ◽  
Nova Eka Margiyanti ◽  
Anggia Noor Ramadhani ◽  
Taufik Adhi Prasetya Wardana ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Androgen Receptor ◽  
Cancer Cell ◽  
Lauric Acid ◽  
Cellular Proliferation ◽  
B Cell Lymphoma ◽  
Mitogen Activated Protein Kinase ◽  
Cancer Cell Proliferation ◽  
String Analysis

Understanding the interactions between cellular proteins and compounds from agarwood (Gyrinops versteegii) could lead to effective approaches for the diagnosis and treatment of breast cancer. In this study, we aimed to identify the interaction between lauric acid, a compound derived from agarwood (G. versteegii) and its target proteins using String database analysis. String analysis showed that lauric acid affects cellular proliferation through interactions with the Androgen Receptor (AR) and binds to Aldo-Keto Reductase (AKR1C3). Lauric acid also interacted with mitogen-activated protein kinase 1 (MAPK1) and other proteins such as matrix metalloprotein (MMP2), chemokine (CXCL8), B-cell lymphoma protein (BCL2). Retinoid Acid Receptor (RARG) and Androgen Receptor (AR) sub network are bridging system of regulation in breast cancer molecular process. These results show that lauric acid may interact with many proteins by AR sub network to increase apoptosis and reduce cancer cell proliferation. These results show that lauric acid may interact with many proteins to increase apoptosis and reduce cancer cell proliferation.

Madhuca indica Inhibits Breast Cancer Cell Proliferation by Modulating COX-2 Expression

2019 ◽  
Vol 18 (7) ◽  
pp. 459-474 ◽  
Author(s):  
Paramita Ghosh ◽  
Debarpan Mitra ◽  
Sreyashi Mitra ◽  
Sudipta Ray ◽  
Samir Banerjee ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Cancer Cell Proliferation ◽  
Breast Cancer Cell Proliferation ◽  
Cox 2

Characterization of YY1 OPB Peptide for its Anticancer Activity

2019 ◽  
Vol 19 (6) ◽  
pp. 504-511 ◽  
Author(s):  
Yige Qi ◽  
Ting Yan ◽  
Lu Chen ◽  
Qiang Zhang ◽  
Weishu Wang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Amino Acids ◽  
Cell Proliferation ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Expression Vectors ◽  
Cancer Cell Proliferation ◽  
Breast Cancer Cell Proliferation ◽  
Oncogene Products ◽  
And Migration

Background:The oncoprotein binding (OPB) domain of Yin Yang 1 (YY1) consists of 26 amino acids between G201 and S226, and is involved in YY1 interaction with multiple oncogene products, including MDM2, AKT, EZH2 and E1A. Through the OPB domain, YY1 promotes the oncogenic or proliferative regulation of these oncoproteins in cancer cells. We previously demonstrated that a peptide with the OPB sequence blocked YY1-AKT interaction and inhibited breast cancer cell proliferation.Objective:In the current study, we characterized the OPB domain and determined a minimal region for peptide design to suppress cancer cellMethods:Using alanine-scan method, we identified that the amino acids at OPB C-terminal are essential to YY1 binding to AKT. Further studies suggested that serine and threonine residues, but not lysines, in OPB play a key role in YY1-AKT interaction. We generated GFP fusion expression vectors to express OPB peptides with serially deleted N-terminal and found that OPB1 (i.e. G201-S226) is cytoplasmic, but OPB2 (i.e. E206-S226), OPB3 (i.e. E206-S226) and control peptide were both nuclear and cytoplasmic.Results:Both OPB1 and 2 inhibited breast cancer cell proliferation and migration, but OPB3 exhibited similar effects to control. OPB1 and 2 caused cell cycle arrest at G1 phase, increased p53 and p21 expression, and reduced AKT(S473) phosphorylation in MCF-7 cells, but not in MDA-MB-231 cells.Conclusion:: Overall, the serines and threonines of OPB are essential to YY1 binding to oncoproteins, and OPB peptide can be minimized to E206-S226 that maintain inhibitory activity to YY1- promoted cell proliferation.

The epithelial sodium channel has a role in breast cancer cell proliferation

2021 ◽  
Vol 187 (1) ◽  
pp. 31-43
Author(s):  
Adam W. Ware ◽  
Joshua J. Harris ◽  
Tania L. Slatter ◽  
Heather E. Cunliffe ◽  
Fiona J. McDonald
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Sodium Channel ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Epithelial Sodium Channel ◽  
Cancer Cell Proliferation ◽  
Breast Cancer Cell Proliferation

scholarly journals MiR-205 Dysregulations in Breast Cancer: The Complexity and Opportunities

2019 ◽  
Vol 5 (4) ◽  
pp. 53 ◽  
Author(s):  
Xiao ◽  
Humphries ◽  
Yang ◽  
Wang
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Cancer Cell ◽  
Target Gene ◽  
Cancer Metastasis ◽  
Epithelial Mesenchymal Transition ◽  
Metastatic Breast ◽  
Therapy Resistance ◽  
Cancer Cell Proliferation ◽  
Mesenchymal Transition

MicroRNAs (miRNAs) are endogenous non-coding small RNAs that downregulate target gene expression by imperfect base-pairing with the 3′ untranslated regions (3′UTRs) of target gene mRNAs. MiRNAs play important roles in regulating cancer cell proliferation, stemness maintenance, tumorigenesis, cancer metastasis, and cancer therapeutic resistance. While studies have shown that dysregulation of miRNA-205-5p (miR-205) expression is controversial in different types of human cancers, it is generally observed that miR-205-5p expression level is downregulated in breast cancer and that miR-205-5p exhibits a tumor suppressive function in breast cancer. This review focuses on the role of miR-205-5p dysregulation in different subtypes of breast cancer, with discussions on the effects of miR-205-5p on breast cancer cell proliferation, epithelial–mesenchymal transition (EMT), metastasis, stemness and therapy-resistance, as well as genetic and epigenetic mechanisms that regulate miR-205-5p expression in breast cancer. In addition, the potential diagnostic and therapeutic value of miR-205-5p in breast cancer is also discussed. A comprehensive list of validated miR-205-5p direct targets is presented. It is concluded that miR-205-5p is an important tumor suppressive miRNA capable of inhibiting the growth and metastasis of human breast cancer, especially triple negative breast cancer. MiR-205-5p might be both a potential diagnostic biomarker and a therapeutic target for metastatic breast cancer.

scholarly journals MiR-138-5p targeting LIMK1 suppresses breast cancer cell proliferation and motility

RSC Advances ◽  
2017 ◽  
Vol 7 (82) ◽  
pp. 52030-52038 ◽  
Author(s):  
Dengfeng Li ◽  
Hongming Song ◽  
Tianqi Wu ◽  
Dan Xie ◽  
Jiashu Hu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Cancer Cell Proliferation ◽  
Breast Cancer Cell Proliferation

Breast cancer is the most frequently diagnosed female cancer.

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