MicroRNA-132 suppresses cell proliferation in human breast cancer by directly targeting FOXA1

Wang, Dan; Ren, Jin; Ren, Hui; Fu, Jing; Yu, Dan

doi:10.1038/aps.2017.89

Cited by 35 publications

(17 citation statements)

References 45 publications

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“…In the present study, prediction software analysis showed that multiple miRNAs may regulate LAPTM4B, and common predictive results were evident in at least three databases for hsa-miR-132-3p, hsa-miR-139-5p, hsa-miR-582-5p and hsa-miR-625-5p. [27][28][29][30][31] Moreover, luciferase Multiple studies have proven that differentially expressed miRNAs could widely modulate the proliferation, invasion and metastasis of breast cancer. miR-99a inhibited the activation process of the phosphorylation of mTOR and its downstream molecules 4E-BP1 and S6K1, eventually suppressing the proliferation of MCF-7 and MDA-MB-231.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‐132‐3p inhibits tumor malignant progression by regulating lysosomal‐associated protein transmembrane 4 beta in breast cancer

Zhang

2019

Cancer Science

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Lysosomal‐associated protein transmembrane 4 beta (LAPTM4B), a proto‐oncogene, has been shown to be a positive modulator in cancer progression. However, the mechanism of LAPTM4B regulation is not fully elucidated. Aberrant microRNAs (miRNAs) can regulate gene expression by interfering with target transcripts and/or translation to exert tumor‐suppressive or oncogenic effects in breast cancer. In the present study, miR‐132‐3p, which was predicted by relevant software, was confirmed to directly bind to the 3′ untranslated region (3′UTR) of LAPTM4B and negatively regulate its expression in luciferase reporter and western blot assays. Subsequently, we validated that miR‐132‐3p was downregulated in breast cancer tissues. Receiver‐operating characteristic curve analysis indicated that miR‐132‐3p had accurate diagnostic value, and a Kaplan‐Meier and Cox regression model showed that miR‐132‐3p was a potential prognostic marker for recurrence, showing low levels in breast cancer patients. In addition, we showed that miR‐132‐3p was inversely correlated with LAPTM4B expression in the above samples. Functionally, miR‐132‐3p suppressed the migration and invasion of breast carcinoma cells through LAPTM4B by mediating epithelial‐mesenchymal transition signals, and partially reversed the carcinogenic effects of LAPTM4B by inhibiting the PI3K‐AKT‐mTOR signaling pathway. Taken together, these findings provide the first comprehensive analysis of miR‐132‐3p as a direct LAPTM4B‐targeted miRNA, and shed light on miR‐132‐3p/LAPTM4B as a significant functional axis involved in the oncogenesis and metastasis of breast cancer.

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Section: Discussionmentioning

confidence: 99%

MicroRNA‐132‐3p inhibits tumor malignant progression by regulating lysosomal‐associated protein transmembrane 4 beta in breast cancer

Zhang

2019

Cancer Science

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“…The expression of miR-132, which was shown to target FOXA1, was reduced in peripheral blood of both HF patients and HF-induced rats. In vitro studies demonstrated that miR-132 overexpression in cells treated with H 2 O 2 reduced apoptosis and oxidative stress through increasing SOD levels and reducing MDA levels [58]. In addition, miR-132 overexpression reduced Transforming growth factor-β1 (TGF-β1) and Smad3, two important pro-fibrotic factors, suggesting an overall cardioprotective role for miR-132, which was abolished by its downregulation in HF [59].…”

Section: Mirna Induction Of Oxidative Stress In Hfmentioning

confidence: 99%

MicroRNA and ROS Crosstalk in Cardiac and Pulmonary Diseases

Climent

Viggiani

Lin

et al. 2020

IJMS

101

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Reactive oxygen species (ROS) affect many cellular functions and the proper redox balance between ROS and antioxidants contributes substantially to the physiological welfare of the cell. During pathological conditions, an altered redox equilibrium leads to increased production of ROS that in turn may cause oxidative damage. MicroRNAs (miRNAs) regulate gene expression at the post-transcriptional level contributing to all major cellular processes, including oxidative stress and cell death. Several miRNAs are expressed in response to ROS to mediate oxidative stress. Conversely, oxidative stress may lead to the upregulation of miRNAs that control mechanisms to buffer the damage induced by ROS. This review focuses on the complex crosstalk between miRNAs and ROS in diseases of the cardiac (i.e., cardiac hypertrophy, heart failure, myocardial infarction, ischemia/reperfusion injury, diabetic cardiomyopathy) and pulmonary (i.e., idiopathic pulmonary fibrosis, acute lung injury/acute respiratory distress syndrome, asthma, chronic obstructive pulmonary disease, lung cancer) compartments. Of note, miR-34a, miR-144, miR-421, miR-129, miR-181c, miR-16, miR-31, miR-155, miR-21, and miR-1/206 were found to play a role during oxidative stress in both heart and lung pathologies. This review comprehensively summarizes current knowledge in the field.

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“…FOXA1 is expressed in various organs, including breast, liver, pancreas, and prostate, and can influence the expression of a large number of genes associated with metabolic processes, regulation of signaling, and the cell cycle [29,30]. It has been reported that Foxa1 was a direct target of miR-132 in breast cancer, thyroid cancer, and nasopharyngeal carcinoma [31][32][33]. In consistent with the above results, our research further proved that FOXA1 was a direct target of miR-132 in KGN cells proliferation.…”

Section: Discussionmentioning

confidence: 99%

miR-132 is up-regulated in polycystic ovarian syndrome and inhibits granulosa cells proliferation via targeting Foxa1

Cui

Xuan

Liu

et al. 2020

Preprint

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Background: Polycystic ovary syndrome (PCOS) is one of the most common endocrine metabolic disorders characterized by hyperandrogenism, polycystic ovaries and ovulatory dysfunction. Several studies have suggested that the aberrant expression of miRNAs serves an important role in the pathogenesis of PCOS, though the role and underling mechanism of microRNA-132 (miR-132) in the development of PCOS remain unclear. Methods: The expression of miR-132 in granulosa cells (GCs) derived from 26 PCOS patients and 30 healthy controls was detected through RT-qPCR. And the apoptosis levels of granulosa cells were measured by TUNEL.Granulosa-like tumor cell line (KGN) was cultured for cell counting kit-8 (CCK-8) was assays after over-expression of miR-132 or knockdown TargetScan was applied to analysis the potential targets of miR-132, which was further verified by luciferase assay, RT-qPCR and western blot. Results: The expression of miR-132 was declined in granulosa cells of PCOS patients. Meanwhile, the significantly increased apoptotic nuclei were present GCs of PCOS patients. Furthermore, over-expressed of miR-132 inhibited the proliferation of KCN cells. In addition, our results verified that miR-132 directly targeted Foxa1, knockdown of which suppressed KGN cells proliferation. Conclusion: Our results revealed that miR-132 inhibits the cell viability and induces apoptosis by directly interacting with Foxa1, indicating a role of miR-132 to be a potential target in the PCOS patients.

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MicroRNA-132 suppresses cell proliferation in human breast cancer by directly targeting FOXA1

Cited by 35 publications

References 45 publications

MicroRNA‐132‐3p inhibits tumor malignant progression by regulating lysosomal‐associated protein transmembrane 4 beta in breast cancer

MicroRNA‐132‐3p inhibits tumor malignant progression by regulating lysosomal‐associated protein transmembrane 4 beta in breast cancer

MicroRNA and ROS Crosstalk in Cardiac and Pulmonary Diseases

miR-132 is up-regulated in polycystic ovarian syndrome and inhibits granulosa cells proliferation via targeting Foxa1

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