Emerging ways to treat breast cancer: will promises be met?

Samadi, Pouria; Saki, Sahar; Dermani, Fatemeh Karimi; Pourjafar, Mona; Saidijam, Massoud

doi:10.1007/s13402-018-0409-1

Cited by 46 publications

(23 citation statements)

References 207 publications

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“…Breast cancer is the most common cancer among women and is responsible for more than 40 000 deaths in the United States and more than 500 000 deaths worldwide each year. 24 Although the breast cancer mortality rates have decreased over the past decades, these rates are anticipated to decrease further with a better understanding of risk factors, prevention strategies and effective therapies. In this article, we investigated the effect of a miR-199a-5p mimic-based approach and its molecular signaling pathway; additionally, the role of combined treatment with a miR-199a-5p mimic and Gemcitabine was unraveled, for the rst time, in breast cancer cells.…”

Section: Discussionmentioning

confidence: 99%

Retracted Article: Gemcitabine aggravates miR-199a-5p-mediated breast cancer cell apoptosis by promoting VEGFA downregulation via inactivating the AKT signaling pathway

et al. 2019

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Section: Discussionmentioning

confidence: 99%

Retracted Article: Gemcitabine aggravates miR-199a-5p-mediated breast cancer cell apoptosis by promoting VEGFA downregulation via inactivating the AKT signaling pathway

et al. 2019

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“…1,2 However, most patients obtain only modest survival benefits and die from tumor recurrence and distant metastasis. [3][4][5] Therefore, understanding the mechanisms of the growth and metastasis of BC cells and identifying more efficacious therapeutic targets is extremely important.…”

Section: Introductionmentioning

confidence: 99%

<p>Long Non-Coding RNA NEAT1 Promotes the Proliferation, Migration, and Metastasis of Human Breast-Cancer Cells by Inhibiting miR-146b-5p Expression</p>

Hao

Yun

et al. 2020

CMAR

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Background: Breast cancer (BC) is the most commonly diagnosed cancer in women. Tumor recurrence and metastasis are the key causes of death in BC patients. Long noncoding RNA (lncRNA) is closely associated with BC progression. lncRNA nuclear-enriched abundant transcript (NEAT)1 has been reported to regulate the proliferation and mobility of several types of cancer cells. However, how lncRNA NEAT1 affects the proliferation and invasion of BC cells is not known. Methods: Quantitative real time-polymerase chain reaction (qRT-PCR) was used to measure expression of lncRNA NEAT1 and microRNA (miR)-146b-5p in BC tissues and cell lines. Cell Counting Kit (CCK)-8, cell colony-formation, wound-healing, and Transwell™ assays were undertaken to determine the effects of lncRNA NEAT1 and miR-146b-5p on progression of BC cells. The interaction between lncRNA NEAT1 and miR-146b-5p was examined by luciferase reporter, RNA-binding protein immunoprecipitation (RIP), and RNA-pulldown assays. Results: Expression of lncRNA NEAT1 was upregulated in BC tissues and cell lines. High expression of lncRNA NEAT1 predicted poor overall survival in BC patients. Silencing of expression of lncRNA NEAT1 inhibited epithelial-mesenchymal transition (EMT) and suppressed the proliferation, migration and invasion of BC cells. Ectopic expression of lncRNA NEAT1 induced EMT and promoted BC progression. Mechanistic investigations revealed that miR-146b-5p was a direct target of lncRNA NEAT1, and its expression was correlated negatively with expression of lncRNA NEAT1 in BC tissues. Conclusion: lncRNA NEAT1 could (i) serve as a novel prognostic marker for BC and (ii) be a potential therapeutic target for BC.

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“…The breast tumors lacking these three proteins are referred to as triple negative breast cancer (TNBC), which generally affects young women . In terms of strategies towards breast cancer treatment, therapies including chemotherapy, radiotherapy, surgical mastectomy, hormone based therapies and antiangiogenic therapies are well‐recognized approaches; nevertheless, undesired effects such as acquired resistance, metastasis and recurrence always accompany these antitumor strategies. Moreover, lack of early diagnosis methods and biomarkers are also attributed to the high mortality of patients with breast cancer.…”

Section: Introductionmentioning

confidence: 99%

Knockdown of long noncoding RNA TP73‐AS1 suppresses the malignant progression of breast cancer cells in vitro through targeting miRNA‐125a‐3p/metadherin axis

Liu¹,

Wei

Ma³

et al. 2020

Thoracic Cancer

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Background: TP73 antisense RNA 1 (TP73-AS1) is a long noncoding RNA which has been shown to be involved in the progression of multiple malignant tumors. Previous studies have demonstrated the oncogenic role of TP73-AS1 in breast cancer. However, its molecular mechanism remains largely unknown in breast tumorigenesis. Methods: Expression of TP63-AS1, miRNA-125a-3p (miR-125a) and metadherin (MTDH) was detected by real-time quantitative PCR and western blotting. The malignancy was evaluated by cell counting kit 8 (CCK-8), transwell assays, flow cytometry and western blotting. The target binding was confirmed by dual luciferase reporter assay. Xenograft tumor model was performed to detect tumor growth in vivo. Results: Expression of TP73-AS1 was higher in breast cancer tissues and cell lines. Biologically, its knockdown could promote cell apoptosis rate, and inhibit proliferative capacity, migration and invasion ability in HCC-70 and MB231 cells, accompanied with higher cleaved caspase 3 level and lower Ki67, Ncadherin and Vimentin level. Moreover, TP73-AS1 downregulation restrained the tumor growth of HCC-70 cells in vivo. Mechanically, TP73-AS1 functioned as a molecular "sponge" for miR-125a to modulate MTDH, a downstream target of miR-125a. Intriguingly, both miR-125a overexpression and MTDH silencing exerted a tumor-suppressive effect in the malignant progression of HCC-70 and MB231 cells, which was counteracted by TP73-AS1 upregulation and miR-125a downregulation, respectively. Conclusion: Knockdown of TP73-AS1 inhibited cell proliferation, migration and invasion, but facilitated apoptosis in breast cancer cells in vitro through targeting miR-125a and upregulating MTDH, suggesting a novel TP73-AS1/miR-125a/MTDH pathway in the malignant progression of breast cancer.

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Emerging ways to treat breast cancer: will promises be met?

Cited by 46 publications

References 207 publications

Retracted Article: Gemcitabine aggravates miR-199a-5p-mediated breast cancer cell apoptosis by promoting VEGFA downregulation via inactivating the AKT signaling pathway

Retracted Article: Gemcitabine aggravates miR-199a-5p-mediated breast cancer cell apoptosis by promoting VEGFA downregulation via inactivating the AKT signaling pathway

<p>Long Non-Coding RNA NEAT1 Promotes the Proliferation, Migration, and Metastasis of Human Breast-Cancer Cells by Inhibiting miR-146b-5p Expression</p>

Knockdown of long noncoding RNA TP73‐AS1 suppresses the malignant progression of breast cancer cells in vitro through targeting miRNA‐125a‐3p/metadherin axis

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