scholarly journals Recent Advancements in the Development of Anti-Breast Cancer Synthetic Small Molecules

Molecules ◽  
2021 ◽  
Vol 26 (24) ◽  
pp. 7611
Author(s):  
Eslam B. Elkaeed ◽  
Hayam A. Abd El Salam ◽  
Ahmed Sabt ◽  
Ghada H. Al-Ansary ◽  
Wagdy M. Eldehna
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Multidrug Resistance ◽  
Small Molecules ◽  
Breast Cancer Treatment ◽  
Cancer Cell Proliferation ◽  
Invasion And Metastasis ◽  
Chemical Structures ◽  
Long Time ◽  
Cancer Types

Among all cancer types, breast cancer (BC) still stands as one of the most serious diseases responsible for a large number of cancer-associated deaths among women worldwide, and diagnosed cases are increasing year by year worldwide. For a very long time, hormonal therapy, surgery, chemotherapy, and radiotherapy were used for breast cancer treatment. However, these treatment approaches are becoming progressively futile because of multidrug resistance and serious side effects. Consequently, there is a pressing demand to develop more efficient and safer agents that can fight breast cancer belligerence and inhibit cancer cell proliferation, invasion and metastasis. Currently, there is an avalanche of newly designed and synthesized molecular entities targeting multiple types of breast cancer. This review highlights several important synthesized compounds with promising anti-BC activity that are categorized according to their chemical structures.

Raddeanoside R13 inhibits breast cancer cell proliferation, invasion, and metastasis

Tumor Biology ◽  
2016 ◽  
Vol 37 (7) ◽  
pp. 9837-9847 ◽  
Author(s):  
Yingchun Liang ◽  
Xiaojie Xu ◽  
Haiming Yu ◽  
Ling Li ◽  
Tian Hong ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Cancer Cell Proliferation ◽  
Invasion And Metastasis ◽  
Breast Cancer Cell Proliferation

scholarly journals Cancer-Associated Fibroblasts Exosomal miR-106a Promotes Breast Cancer Invasion and Metastasis by Down -regulation of TCEAL7

2021 ◽  
Author(s):  
Ziqian Yan ◽  
Zhimei Sheng ◽  
Yuanhang Zheng ◽  
Ruijun Feng ◽  
Lihong Shi ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Cancer Associated Fibroblasts ◽  
Cancer Cell Proliferation ◽  
Invasion And Metastasis ◽  
Breast Cancer Cell Proliferation ◽  
Mesenchymal Transition ◽  
Mouse Xenograft Model

Abstract Studies have shown that cancer-associated fibroblasts (CAFs) play an irreplaceable role in the occurrence and development of tumors. Therefore, exploring the action and mechanism of CAFs on tumor cells is particularly important for designing new and effective treatments and improving prognosis of tumors. For exosomes have been shown to play vital roles in intercellular communication, in this study, we compared the effects of CAFs-derived exosomes and NFs-derived exosomes on breast cancer cell proliferation, migration, and metastasis. The results showed that exosomes from both CAFs and NFs could enter into breast cancer cells and CAFs-derived exosomes had a more enhancing effect on breast cancer cell proliferation and invasion than NFs-derived exosomes. Furthermore, it was found that the expression levels of miR-106a in exosomes derived from CAFs were significantly up-regulated than that of NFs-derived exosomes and what’s more, in vitro and in vivo studies have shown that miR-106a can promote breast cancer cell proliferation, migration and metastasis by specifically binding to the 3'UTR of TCEAL7. It is inspiring to find that the miR-106a-TCEAL7 pathway promotes Snail nuclear ectopic activation by activating NF-κB, thereby inducing epithelial-mesenchymal transition and promoting cell proliferation and metastasis. Moreover, a mouse xenograft model confirmed that CAFs-derived exosomes miR-106a could promote tumor metastasis. The above data shows that CAFs-derived exosomes miR-106a promote Snail nuclear ectopic by targeting TCEAL7 to activate the NF-κB pathway, thereby inducing EMT, invasion and metastasis of breast cancer. Targeting CAFs-derived exosome miR-106a may be a potential treatment option to overcome breast cancer progression.

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
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