Differential expression of miR‐21, miR‐125b and miR‐191 in breast cancer tissue

Mar‐Aguilar, Fermín; Luna-Aguirre, Claudia Maribel; Moreno‐Rocha, J. Claudio; Araiza‐Chávez, Juan; Treviño, Víctor; Rodríguez‐Padilla, Cristina; Reséndez‐Pérez, Diana

doi:10.1111/j.1743-7563.2012.01548.x

Cited by 61 publications

(39 citation statements)

References 28 publications

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“…For instance, miR-125b was downregulated in breast tumors compared with normal samples [6]. Moreover, overexpression of miR-125b inhibited cell growth and reduced migration and invasion in breast cancer cells [7].…”

Section: Discussionmentioning

confidence: 98%

MiR-548-3p functions as an anti-oncogenic regulator in breast cancer

Shi¹,

Qiu²,

Wu³

et al. 2015

Biomedicine & Pharmacotherapy

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Section: Discussionmentioning

confidence: 98%

MiR-548-3p functions as an anti-oncogenic regulator in breast cancer

Shi¹,

Qiu²,

Wu³

et al. 2015

Biomedicine & Pharmacotherapy

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“…Abundant studies about the expression levels of various miRNAs and their functions in breast cancer have been reported Zhang et al, 2013). Mar-Aguilar et al (2013) demonstrated upregulation of miR-21 and miR-191 and downregulation of miR125b in breast cancer patients. Overexpression of serum miR-155 was found in breast cancer patients (Sun et al, 2012).…”

Section: Discussionmentioning

confidence: 98%

Expression Level of miR-93 in Formalin-Fixed Paraffin-Embedded Tissues of Breast Cancer Patients

Deng

Qian

Liu

et al. 2014

Genetic Testing and Molecular Biomarkers

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MiR-93 is thought to be an onco-miRNA for its capabilities of enhancing tumor growth. The objective of this study was to evaluate the potential predictive value of miR-93 expression in formalin-fixed paraffin-embedded (FFPE) tissues of breast cancer patients. The expression of miR-93 was examined in 101 breast cancer patients and 40 controls using real-time quantitative PCR. We found that miR-93 was markedly upregulated in breast cancer patients compared with controls (p<0.01). The expression level of miR-93 was significantly correlated with miR-24/378 in breast cancer patients. MiR-93 exhibited great capability of discriminating between cancer patients and cancer-free controls by receiver-operator characteristic (ROC) curve analysis. MiR-93 showed 0.866 AUC (the area under the ROC curve) values. The MiR-93 level was found significantly correlated with breast cancer by univariable logistic regression. These results suggest that overexpression of miR-93 in FFPE tissues may serve as an indispensable source for biomarker discovery and validation in breast cancer patients.

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“…The mechanisms by which miRNAs are regulated and expressed under normal or disease conditions are currently of great interest. Although miR-125b has been implicated in various cancers [12, 25-27], and might contribute to persistent inflammation [28, 29], this is the first indication about the role of miR-125b in chondrocytes inflammatory response.…”

Section: Discussionmentioning

confidence: 99%

MiR-125b Inhibits LPS-Induced Inflammatory Injury via Targeting MIP-1α in Chondrogenic Cell ATDC5

Jia

Wang

Zhang

et al. 2018

Cell Physiol Biochem

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Background/Aims: Chondrocyte apoptosis is largely responsible for cartilage degeneration in osteoarthritis (OA). MicroRNAs (miRNAs) play an important role in chondrogenesis and cartilage remodeling. This study explored the effect of miR-125b on inflammatory injury in chondrogenic cells. Methods: LPS was used to simulate inflammatory injury in murine chondrogenic ATDC5 cell lines. Targeting effect of miR-125b on MIP-1α 3’UTR was assessed by dual luciferase activity assay. Regulatory effect of miR-125b on MIP-1α expression and the potential regulatory mechanism on inflammatory injury were assessed by Western blot. Results: miR-125b expression was decreased in LPS-induced ATDC5 cells and overexpression of miR-125b inhibited LPS-induced cell viability decline, the rise of apoptosis and inflammatory factors’ productions. MIP-1α expression was negatively related to miR-125b, and miR-125b directly targeted with 3’UTR of MIP-1α. Knockdown of miR-125b promoted LPS-induced inflammatory response via upregulation of MIP-1α. miR-125b expression in LPS-induced ATDC5 cells was negatively related with activations of NF-κB and JNK signaling pathways. Overexpression of miR-125b inhibited LPS-induced inflammation injury via suppressing MIP-1α expression and inhibiting activations of NF-κB and JNK signaling pathways. Conclusion: miR-125b could play an important role in inflammatory injury of chondrogenic cells and miR-125b affected inflammatory injury of ATDC5 cells via regulating expression of MIP-1α and regulating NF-κB and JNK signaling pathways.

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Differential expression of miR‐21, miR‐125b and miR‐191 in breast cancer tissue

Cited by 61 publications

References 28 publications

MiR-548-3p functions as an anti-oncogenic regulator in breast cancer

MiR-548-3p functions as an anti-oncogenic regulator in breast cancer

Expression Level of miR-93 in Formalin-Fixed Paraffin-Embedded Tissues of Breast Cancer Patients

MiR-125b Inhibits LPS-Induced Inflammatory Injury via Targeting MIP-1α in Chondrogenic Cell ATDC5

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