Breast cancer

Pearce, Lynne

doi:10.7748/ns.30.51.15.s16

Cited by 17 publications

(14 citation statements)

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“…The morbidity of BC has been rising, over 2 million females were diagnosed with BC according to the statistic [ 2 ]. Although improved prognosis of patients with BC had achieved, BC remains leading reason of cancer mortality among females [ 3 ]. Therefore, it is meaningful to look into pathogenesis and find diagnosis biomarkers of BC.…”

Section: Introductionmentioning

confidence: 99%

CircMMP11 regulates proliferation, migration, invasion, and apoptosis of breast cancer cells through miR-625-5p/ZEB2 axis

Sun

Yang

et al. 2021

Cancer Cell Int

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Background Circular RNAs (circRNAs) have been demonstrated to play significant roles in regulating gene expression in tumorigenesis, including breast cancer (BC). This study was designed to explore the role and underlying molecular mechanisms of circMMP11 in BC. Methods The real-time quantitative polymerase chain reaction (RT-qPCR) assay was used for examining expression of circMMP11, microRNA-625-5p (miR-625-5p), and Zinc finger E-box binding homeobox-2 (ZEB2). The protein expression of ZEB2, Vimentin, and E-cadherin was assessed by western blot assay. The proliferation ability of BC cells was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazol-3-ium bromide (MTT) and colony-forming assays. The transwell assay was used to measure migration and invasion of BC cells. The apoptotic cells were examined by flow cytometry assay. The interaction association among circMMP11, miR-625-5p, and ZEB2 was confirmed by RNA pull-down and dual-luciferase report assays. A xenograft experiment was established to clarify the role of circMMP11 silencing in vivo. Results We found that circMMP11 and ZEB2 were overexpressed in BC tissues and cells compared with controls. The suppression of circMMP11 or ZEB2 repressed proliferation, migration, and invasion while induced apoptosis of BC cells. Additionally, miR-625-5p, interacted with ZEB2, was a target of circMMP11 in BC cells. CircMMP11 regulated the expression of ZEB2 by targeting miR-625-5p. Knockdown of circMMP11-mediated effects on BC cells could be abolished by overexpression of ZEB2. Consistently, silencing of circMMP11 impeded the tumor growth in vivo. Conclusions CircMMP11/miR-625-5p/ZEB2 axis affected proliferation, migration, invasion, and apoptosis of BC cells through the mechanism of competing endogenous RNAs (ceRNA), indicating that circMMP11 was an oncogenic circRNA in BC.

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Section: Introductionmentioning

confidence: 99%

CircMMP11 regulates proliferation, migration, invasion, and apoptosis of breast cancer cells through miR-625-5p/ZEB2 axis

Sun

Yang

et al. 2021

Cancer Cell Int

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“…According to data provided by the charity Breast Cancer Care, approximately 60,000 people are diagnosed with breast cancer each year, and the risk of developing the disease in a person’s lifetime is 1 in 8 [ 44 ]. With the continuous progress of surgical techniques, there is an increasing number of treatment options for breast cancer patients [ 45 ].…”

Section: Pharmacological Activities Of Protopinementioning

confidence: 99%

Identification and Quantification, Metabolism and Pharmacokinetics, Pharmacological Activities, and Botanical Preparations of Protopine: A Review

et al. 2021

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Through pharmacological activity research, an increasing number of natural products and their derivatives are being recognized for their therapeutic value. In recent years, studies have been conducted on Corydalis yanhusuo W.T. Wang, a valuable medicinal herb listed in the Chinese Pharmacopoeia. Protopine, one of its components, has also become a research hotspot. To illustrate the identification, metabolism, and broad pharmacological activity of protopine and the botanical preparations containing it for further scientific studies and clinical applications, an in-depth and detailed review of protopine is required. We collected data on the identification and quantification, metabolism and pharmacokinetics, pharmacological activities, and botanical preparations of protopine from 1986 to 2021 from the PubMed database using “protopine” as a keyword. It has been shown that protopine as an active ingredient of many botanical preparations can be rapidly screened and quantified by a large number of methods (such as the LC-ESI-MS/MS and the TLC/GC-MS), and the possible metabolic pathways of protopine in vivo have been proposed. In addition, protopine possesses a wide range of pharmacological activities such as anti-inflammatory, anti-platelet aggregation, anti-cancer, analgesic, vasodilatory, anticholinesterase, anti-addictive, anticonvulsant, antipathogenic, antioxidant, hepatoprotective, neuroprotective, and cytotoxic and anti-proliferative activities. In this paper, the identification and quantification, metabolism and pharmacokinetics, pharmacological activities, and botanical preparations of protopine are reviewed in detail to lay a foundation for further scientific research and clinical applications of protopine.

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“…Breast cancer (BC) is a common malignant tumor, mainly deriving from breast epithelial tissues. 1,2 The occurrence and development of BC is a very complex pathological process. Family genetic history, unhealthy lifestyle, and excessive mental stress are several common factors for BC.…”

Section: Introductionmentioning

confidence: 99%

Exosome miR‐134‐5p restrains breast cancer progression via regulating PI3K/AKT pathway by targeting ARHGAP1

Yang

Zhang

et al. 2021

J of Obstet and Gynaecol

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Aim: Exosomes has been shown to be involved in the regulation of cancer progression. However, the role of exosome miR-134-5p in breast cancer (BC) progression is unclear. Methods: Exosomes were extracted from BC cells (MCF-7 and MDA-MB-231) using differential centrifugation and were observed by transmission electron microscope (TEM). The protein levels of exosome markers, apoptosis markers, Rho GTPase activating protein 1 (ARHGAP1, an important oncogene in BC) and phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) markers were detected by western blot (WB) assay. Quantitative real-time PCR was used to measure the expression levels of miR-134-5p and ARHGAP1. Cell cycle and apoptosis, colony number, viability, migration, and invasion were determined by flow cytometry, colony formation assay, MTT assay, and transwell assay, respectively. The interaction between miR-134-5p and ARHGAP1 was confirmed using a dual-luciferase reporter assay. Xenograft models were constructed to verify the role of exosome miR-134-5p in BC tumor growth in vivo. Results: MiR-134-5p was lowly expressed in BC cells and in the exosomes of BC cells. Overexpressed exosome miR-134-5p suppressed the proliferation, migration, invasion, and promoted the apoptosis of BC cells. ARHGAP1 was a target of miR-134-5p, and its silencing could inhibit BC progression. In addition, ARHGAP1 overexpression could reverse the negative regulation of miR-134-5p on BC progression. MiR-134-5p could target ARHGAP1 to inhibit the activity of PI3K/AKT pathway. Exosome miR-134-5p overexpression could suppress BC tumor growth via targeting ARHGAP1 in vivo. Conclusion: Exosome miR-134-5p restrained BC progression through regulating ARHGAP1/PI3K/AKT signaling pathway, suggesting that miR-134-5p might be a therapeutic target for BC.

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Breast cancer

Abstract: Essential facts Breast cancer is the most common cancer in the UK, with around 60,000 new cases diagnosed each year, according to the charity Breast Cancer Care. Over a lifetime, women have a one in eight risk of developing it.

Cited by 17 publications

References 0 publications

CircMMP11 regulates proliferation, migration, invasion, and apoptosis of breast cancer cells through miR-625-5p/ZEB2 axis

CircMMP11 regulates proliferation, migration, invasion, and apoptosis of breast cancer cells through miR-625-5p/ZEB2 axis

Identification and Quantification, Metabolism and Pharmacokinetics, Pharmacological Activities, and Botanical Preparations of Protopine: A Review

Exosome miR‐134‐5p restrains breast cancer progression via regulating PI3K/AKT pathway by targeting ARHGAP1

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