MiR‐202 inhibits cell proliferation, invasion, and migration in breast cancer by targeting ROCK1 gene

2019 ◽  
Vol 120 (9) ◽  
pp. 16008-16018 ◽  
Author(s):  
Fangfang Xu ◽  
Hui Li ◽  
Chengjiu Hu
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Invasion And Migration ◽  
And Migration ◽  
Rock1 Gene

Knockdown of SF3B1 inhibits cell proliferation, invasion and migration triggering apoptosis in breast cancer via aberrant splicing

Breast Cancer ◽  
2020 ◽  
Vol 27 (3) ◽  
pp. 464-476 ◽  
Author(s):  
Ling Zhang ◽  
Xiaojuan Zhang ◽  
Haitao Zhang ◽  
Feng Liu ◽  
Yanghui Bi ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Aberrant Splicing ◽  
Invasion And Migration ◽  
And Migration

scholarly journals Silencing of Prrx2 Inhibits the Invasion and Metastasis of Breast Cancer both In Vitro and In Vivo by Reversing Epithelial-Mesenchymal Transition

2017 ◽  
Vol 42 (5) ◽  
pp. 1847-1856 ◽  
Author(s):  
Zhi-Dong Lv ◽  
Hai-Bo Wang ◽  
Xiang-Ping Liu ◽  
Li-Ying Jin ◽  
Ruo-Wu Shen ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Epithelial Mesenchymal Transition ◽  
Association Studies ◽  
Mesenchymal Transition ◽  
Invasion And Migration ◽  
Node Metastasis ◽  
And Migration

Background/Aims: Epithelial-mesenchymal transition (EMT) is recognized as a crucial mechanism in breast cancer progression and metastasis. Paired-related homeobox 2 (Prrx2) has been identified as a new EMT inducer in cancer, but the underlying mechanisms are still poorly understood. Methods: The expression of Prrx2 was assessed by immunohistochemistry in breast cancer tissues to evaluate the clinicopathological significance of Prrx2, as well as the correlation between Prrx2 and EMT. Short hairpin RNA knockdown of Prrx2 was used to examine cellular effects of Prrx2, detecte the expression of Wnt/β-catenin signaling and EMT-associated proteins, and observe cell proliferation, invasion and migration abilities in vitro and in vivo. Results: Clinical association studies showed that Prrx2 expression was related to tumor size, lymph node metastasis, tumor node metastasis stages, EMT and poor survival. Results also showed that knockdown of Prrx2 could alter cell morphology, suppressed the abilities of cell proliferation, invasion and migration in breast cancer. Moreover, silencing of Prrx2 induced the mesenchymal-epithelial transition and prevented nuclear translocation of β-catenin, inhibited wnt/β-catenin signaling pathway. Conclusion: Our study indicated that Prrx2 may be an important activator of EMT in human breast cancer and it can serve as a molecular target of therapeutic interventions for breast cancer.

scholarly journals FAM96A and FAM96B Suppress Breast Cancer Proliferation and Migration via the Wnt/β-Catenin Signaling Pathway

2021 ◽  
Author(s):  
Di-Di Zhang ◽  
Xiao-Lin Sun ◽  
Zhao-Yuan Liang ◽  
Li-Na Zhang
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Cancer Progression ◽  
Breast Cancer Cells ◽  
Cancer Cell Proliferation ◽  
Breast Cancer Cell Proliferation ◽  
Invasion And Migration ◽  
And Migration

Abstract Background: Family with sequence similarity 96 member A and B (FAM96A and FAM96B) are two highly conserved homologous proteins belonging to MIP18 family. Many studies have shown that FAM96A and FAM96B play many different functions mainly through interacting with other different proteins. Recently, several studies show that FAM96A and FAM96B are significantly down-regulated compared in human gastrointestinal stromal tumors, colon cancer, liver cancer and gastric cancer with corresponding normal tissues. However, the molecular regulatory mechanisms of FAM96A and FAM96B in breast cancer development and metastasis are still unclear. In this work, we aimed to explore the molecular mechanisms of FAM96A and FAM96B in breast cancer progression.Methods: We used specific siRNAs to down-regulate FAM96A and FAM96B expression, and used recombinant plasmids to up-regulate FAM96A and FAM96B expression in breast cancer cells. Cell proliferation was measured using MTT and colony formation assays. Cell cycle and apoptosis were detected by flow cytometry analysis. Wound healing and transwell assays were used to examine cell migration and invasion abilities. The relationships among FAM96A/B, EMT and Wnt/β-catenin signaling pathway were determined by analyzing the expression changes of classical markers and biological functional changes after XAV-939 inhibitor treatment. Results: We found that FAM96A and FAM96B expression in breast cancer was down-regulated. FAM96A/B overexpression suppressed breast cancer cell proliferation, invasion and migration, induced cell apoptosis and led to cell cycle arrested in G0/G1 phase. Conversely, FAM96A/B knockdown exhibited the opposite effects on breast cancer cells. Moreover, our data demonstrated that FAM96A/B overexpression suppressed EMT and Wnt/β-catenin signaling pathway, while FAM96A/B knockdown showed the promoting effects on EMT and Wnt/β-catenin signaling pathway in breast cancer cells. Furthermore, a Wnt pathway inhibitor, XAV-939 treatment reversed the promoting effects of FAM96A and FAM96B knockdown on breast cancer cell proliferation, invasion and migration.Conclusions: Our findings revealed that FAM96A and FAM96B may act as tumor suppressor genes and inhibit breast cancer progression via modulating the Wnt/β-catenin pathway, which can provide the potential markers for the diagnosis and treatment of breast cancer.

Silencing of miR-200a-3p Inhibits Proliferation, Invasion and Migration of Breast Cancer Cells by Targeting Ephrin-A5

2021 ◽  
Vol 11 (7) ◽  
pp. 1227-1235
Author(s):  
Yongmei Zhang ◽  
Huayi Zhang ◽  
Gang Guo
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Cell Lines ◽  
The Cancer Genome Atlas ◽  
Luciferase Reporter Assay ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Reporter Assay ◽  
Invasion And Migration ◽  
And Migration

Increasing evidence suggests microRNAs (miRs/miRNAs) exert considerable functions in the pathogenesis of malignancies, including breast cancer (BC). The miR-200a-3p has previously been reported to promote tumorigenesis in different types of cancers. The present study aimed to investigate the potential role of and possible mechanisms of miR-200a-3p in BC. In this study miR-200a-3p and ephrin-A5 (EFNA5) expression in tissues of patients with BC was analyzed using The Cancer Genome Atlas (TCGA) database. And several BC cell lines were employed to determine the expression levels of miR-200a-3p and EFNA5. Then, miR-200a-3p expression was silenced by transfection with miR-200a-3p inhibitor. Cell proliferation was evaluated using a cell counting kit-8 kit and colony formation assay, whilst cell invasion and migration were detected using Transwell and wound healing assays, respectively. Then, the potential interaction between miR-200a-3p and EFNA5 was verified using luciferase reporter assay. Subsequently, rescue assays were conducted by co-transfection with miR-200a-3p inhibitor and short hairpin RNA (shRNA) targeted against EFNA5 (shRNA-EFNA5) to study the effects of TTN-AS1 and miR-211-5p on BC development. Results indicated that miR-200a-3p expression was significantly upregulated while EFNA5 was notably downregulated in BC tissues and cell lines. Cells transfected with miR-200a-3p inhibitor presented lower abilities of cell proliferation, invasion and migration. Moreover, the luciferase reporter assay confirmed that EFNA5 was a direct target of miR-200a-3p. And EFNA5 silencing reversed the inhibitory effects of miR-200a-3p inhibitor on proliferation, invasion and migration of BC cells. Taken together, these findings revealed that miR-200a-3p silencing inhibits proliferation, invasion and migration of BC cells by targeting EFNA5, which provides insights into the regulatory mechanism of BC and new strategies for developing therapeutic interventions for this disease.

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