breast cancer
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2022 ◽  
Vol 271 ◽  
pp. 117-124
Author(s):  
Chad Markey ◽  
Julie E. Weiss ◽  
Andrew P. Loehrer

2022 ◽  
Vol 146 ◽  
pp. 528-537
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GeorginaVenecia Bello-Martínez ◽  
Génesis García-Ramírez ◽  
Monserrat Olea-Flores ◽  
Napoleón Navarro-Tito ◽  
Alberto Hernández-Moreno ◽  
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2022 ◽  
Vol 271 ◽  
pp. 154-162
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Adeseye Adekeye ◽  
Divyansh Agarwal ◽  
Anupma Nayak ◽  
Julia Tchou

2022 ◽  
Vol 18 (1) ◽  
pp. 91-93
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Florence Vibert ◽  
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Raluca Andreea Ionescu ◽  
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Shanti Ame

2022 ◽  
Vol 18 (1) ◽  
pp. 79-84
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Xiaoyan Deng ◽  
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Kandace P. McGuire
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2022 ◽  
Vol 12 (4) ◽  
pp. 717-723
Author(s):  
Bing Pan ◽  
Binghui Liu ◽  
Juhua Pan ◽  
Jian Xin ◽  
Chenglin Fu

Introduction: Breast cancer (BC) developed in the glandular epithelial tissue of breast. microRNA (miR)-367 is an important player in cancer progression, but has never been studied in BC. This experiment tries to probe the mechanism of miR-367 in BC treatment with downstream target gene. Materials and Methods: Human BC cell lines and healthy breast epithelium cells were applied in this study. After the transfection of miR-367 inhibitor or mimic into BC cells, functional assays were conducted to measure cell growth. Afterwards, flow cytometry was employed in apoptosis verification. Then, target relation between miR-367 and ARID1B was certified. Furthermore, ARID1B level was also measured. Results: miR-367 was underexpressed in human BC cells (p < 0.05). Besides, overexpressed miR-367 inhibited BC cell proliferation and encouraged apoptosis, while underexpressed miR-367 led to an opposite outcome (p < 0.05). This experiment then implied that miR-367 dramatically suppressed the activity of cell transfected with ARID1B-wild type. miR-367 overexpression quenched ARID1B level in BC cells; while silencing miR-367 upregulated ARID1B expression (p < 0.05). Conclusion: Our experiment discovered that miR-367 quenched BC cell growth and promoted apoptosis by targeting ARID1B. This investigation may provide novel insights in BC treatment.


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