scholarly journals LINC00665 promotes breast cancer progression through regulation of the miR-379-5p/LIN28B axis

2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Wei Ji ◽  
Yu-Ling Diao ◽  
Yi-Ran Qiu ◽  
Jie Ge ◽  
Xu-Chen Cao ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Progression ◽  
Epithelial Mesenchymal Transition ◽  
Normal Breast ◽  
Breast Cancer Progression ◽  
Migration And Invasion ◽  
Breast Tumorigenesis ◽  
Mesenchymal Transition ◽  
Tumorigenesis And Progression ◽  
Mirna Sponges

AbstractBreast cancer is the most common malignant tumor among women worldwide. Although increasing evidence indicates that long noncoding RNAs (lncRNAs) play critical roles during breast tumorigenesis and progression, the involvement of most lncRNAs in breast cancer remains largely unknown. In the current study, we demonstrated that LINC00665 promotes breast cancer cell proliferation, migration, and invasion. Accumulating evidence indicates that many lncRNAs can function as endogenous miRNA sponges by competitively binding common miRNAs. In this study, we demonstrated that LINC00665 functions as a sponge for miR-379-5p, reducing the ability of miR-379-5p to repress LIN28B. LINC00665 promoted breast cancer progression and induced an epithelial–mesenchymal transition-like phenotype via the upregulation of LIN28B expression. Clinically, LINC00665 expression was increased but miR-379-5p expression was decreased in breast cancer tissues compared with that in normal breast tissues in the TCGA database. Furthermore, the expression of LINC00665 was negatively related with miR-379-5p expression. Collectively, our results reveal the LINC00665–miR-379-5p–LIN28B axis and shed light on breast cancer therapy.

scholarly journals Expression of epithelial-mesenchymal transition-related markers and phenotypes during breast cancer progression

2020 ◽  
Vol 181 (2) ◽  
pp. 369-381 ◽  
Author(s):  
Charlotte Levin Tykjær Jørgensen ◽  
Carina Forsare ◽  
Pär-Ola Bendahl ◽  
Anna-Karin Falck ◽  
Mårten Fernö ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Progression ◽  
Epithelial Mesenchymal Transition ◽  
Breast Cancer Progression ◽  
Mesenchymal Transition

scholarly journals SOX4 Induces Epithelial–Mesenchymal Transition and Contributes to Breast Cancer Progression

2012 ◽  
Vol 72 (17) ◽  
pp. 4597-4608 ◽  
Author(s):  
Jianchao Zhang ◽  
Qian Liang ◽  
Yang Lei ◽  
Min Yao ◽  
Lili Li ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Progression ◽  
Epithelial Mesenchymal Transition ◽  
Breast Cancer Progression ◽  
Mesenchymal Transition

scholarly journals Cancer-associated fibroblast-derived exosomal miR-18b promotes breast cancer invasion and metastasis by regulating TCEAL7

2021 ◽  
Vol 12 (12) ◽  
Author(s):  
Ziqian Yan ◽  
Zhimei Sheng ◽  
Yuanhang Zheng ◽  
Ruijun Feng ◽  
Qinpei Xiao ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Cancer Progression ◽  
Breast Cancer Cells ◽  
Epithelial Mesenchymal Transition ◽  
Xenograft Model ◽  
Migration And Invasion ◽  
Invasion And Metastasis ◽  
Mesenchymal Transition ◽  
Mouse Xenograft Model

AbstractStudies 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. In this study, we compared the effects of CAFs-derived exosomes and normal fibroblasts (NFs)-derived exosomes on breast cancer cells migration and invasion. 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 cells migration and invasion than NFs-derived exosomes. Furthermore, microRNA (miR)-18b was upregulated in CAFs-derived exosomes, and CAFs-derived exosomes miR-18b can promote breast cancer cell migration and metastasis by specifically binding to the 3′UTR of Transcription Elongation Factor A Like 7 (TCEAL7). The miR-18b-TCEAL7 pathway promotes nuclear Snail ectopic activation by activating nuclear factor-kappa B (NF-κB), thereby inducing epithelial-mesenchymal transition (EMT) and promoting cell invasion and metastasis. Moreover, CAFs-derived exosomes miR-18b could promote mouse xenograft model tumor metastasis. Overall, our findings suggest that CAFs-derived exosomes miR-18b promote nuclear Snail ectopic by targeting TCEAL7 to activate the NF-κB pathway, thereby inducing EMT, invasion, and metastasis of breast cancer. Targeting CAFs-derived exosome miR-18b may be a potential treatment option to overcome breast cancer progression.

scholarly journals CDKL2 promotes epithelial-mesenchymal transition and breast cancer progression

Oncotarget ◽  
2014 ◽  
Vol 5 (21) ◽  
pp. 10840-10853 ◽  
Author(s):  
Linna Li ◽  
Chunping Liu ◽  
Robert J. Amato ◽  
Jeffrey T. Chang ◽  
Guangwei Du ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Progression ◽  
Epithelial Mesenchymal Transition ◽  
Breast Cancer Progression ◽  
Mesenchymal Transition

Development of improved SRC-3 inhibitors as breast cancer therapeutic agents

2021 ◽  
Author(s):  
Li Qin ◽  
Jianwei Chen ◽  
Dong Lu ◽  
Prashi Jain ◽  
Yang Yu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Progression ◽  
High Throughput Screening ◽  
Epithelial Mesenchymal Transition ◽  
Therapeutic Agents ◽  
Migration And Invasion ◽  
Mesenchymal Transition ◽  
Steroid Receptor Coactivators ◽  
Plasma Half Life

Steroid receptor coactivators (SRCs) possess specific and distinct oncogenic roles in the initiation of cancer and in cancer progression to a more aggressive disease. These coactivators interact with nuclear receptors and other transcription factors to boost transcription of multiple genes which potentiate cancer cell proliferation, migration, invasion, tumor angiogenesis and epithelial mesenchymal transition (EMT). Targeting SRCs using small molecule inhibitors (SMIs) is a promising approach to control cancer progression and metastasis. By high throughput screening analysis, we recently identified SI-2 as a potent SRC SMI. To develop therapeutic agents, SI-10 and SI-12, the SI-2 analogs, are synthesized that incorporate the addition of fluorine atoms to the SI-2 chemical structure. As a result, these analogs exhibit a significantly prolonged plasma half-life, minimal toxicity and improved hERG activity. Biological functional analysis showed that SI-10 and SI-12 treatment (5-50 nM) can significantly inhibit viability, migration and invasion of breast cancer cells in vitro and repress the growth of breast cancer PDX organoids. Treatment of mice with 10 mg/kg/day of either SI-10 or SI-12 was sufficient to repress growth of xenograft tumors derived from MDA-MB-231 and LM2 cells. Furthermore, in spontaneous and experimental metastasis mouse models developed from MDA-MB-231 and LM2 cells respectively, SI-10 and SI-12 effectively inhibited progression of breast cancer lung metastasis. These results demonstrate that SI-10/SI-12 are promising therapeutic agents and are specifically effective in blocking tumor metastasis, a key point in tumor progression to a more lethal state that results in patient mortality in the majority of cases.

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