MiR-6838-5p suppresses cell metastasis and the EMT process in triple-negative breast cancer by targeting WNT3A to inhibit the Wnt pathway.

Triple-negative breast cancer (TNBC) has become a common tumor that harms women's physical and mental health, as characterized by a relatively rapid recurrence and a high incidence of brain metastasis. Research increasingly suggests that microRNAs play key roles in the progress of TNBC. However, the function of miR-6838-5p in TNBC has not yet been reported, and requires additional exploration. In the present study, we uncovered miR-6838-5p expression in TNBC cells via a quantitative reverse transcriptase-polymerase chain reaction. Functionally, the impacts of up-regulated or down-regulated miR-6838-5p on TNBC invasiveness, Wnt pathway activation and epithelial-mesenchymal transition (EMT) were investigated via transwell and western blot assays. Mechanical analyses were utilized to unmask the miR-6838-5p mechanism in TNBC, including luciferase reporter, western blot and RIP assays. Rescue assays manifested the miR-6838-5p/WNT3A network in TNBC invasiveness through the Wnt pathway. Under-expressed miR-6838-5p was found in TNBC cells. Up-regulation of miR-6838-5p suppressed TNBC cell invasion, migration and blockade of the Wnt pathway. However, down-regulation of miR-6838-5p led to opposite results. Furthermore, we found, via luciferase reporter, western blot and RIP assays, that miR-6838-5p could bind with WNT3A and negatively regulate WNT3A expression. Through rescue experiments, we demonstrated that the overexpression of WNT3A partially rescued the miR-6838-5p overexpression-mediated inhibitory effect, and knockdown of WNT3A partially rescued the miR-6838-5p suppression-mediated promotive effect on the progression of TNBC. In summary, the results of the present study indicate that miR-6838-5p suppresses cell proliferation, metastasis and the EMT process in TNBC by targeting WNT3A to inhibit the Wnt pathway, which may provide a new insight into the therapeutic strategies of TNBC.

Liu G ，Wang P ，Zhang H 《-》

MiR-212-5p Suppresses the Epithelial-Mesenchymal Transition in Triple-Negative Breast Cancer by Targeting Prrx2.

Triple-negative breast cancer (TNBC) is the most aggressive breast cancer subtype. Our study investigated the functional role of miR-212-5p in TNBC. Realtime PCR was used to quantify miR-212-5p expression levels in 30 paired TNBC samples and adjacent normal tissues. Wound healing and Transwell assays were used to evaluate the effects of miR-212-5p expression on the invasiveness of TNBC cells. Luciferase reporter and Western blot assays were used to verify whether the mRNA encoding Prrx2 is a major target of miR-212-5p. MiR-212-5p was downregulated in TNBC, and its expression levels were related to tumor size, lymph node status and vascular invasion in breast cancer. We also observed that the miR-212-5p expression level was significantly correlated with a better prognosis in TNBC. Ectopic expression of miR-212-5p induced upregulation of E-cadherin expression and downregulation of vimentin expression. The expression of miR212-5p also suppressed the migration and invasion capacity of mesenchymal-like cancer cells accompanied by a morphological shift towards the epithelial phenotype. Moreover, our study observed that miR-212-5p overexpression significantly suppressed Prrx2 by targeting its 3'-untranslated region (3'-UTR) region, and Prrx2 overexpression partially abrogated miR-212-5p-mediated suppression. Our study demonstrated that miR-212-5p inhibits TNBC from acquiring the EMT phenotype by downregulating Prrx2, thereby inhibiting cell migration and invasion during cancer progression.

Lv ZD ，Yang DX ，Liu XP ，Jin LY ，Wang XG ，Yang ZC ，Liu D ，Zhao JJ ，Kong B ，Li FN ，Wang HB ... -  《-》

miR-124 regulates EMT based on ZEB2 target to inhibit invasion and metastasis in triple-negative breast cancer.

Triple-negative breast cancer (TNBC) is highly invasive and aggressive and lacks specific molecular targets to improve the prognosis. MicroRNAs (miRNAs) serve a role in promoting and suppressing tumors in various types of malignant cancer, including TNBC. However, the regulatory mechanism of miR-124 in TNBC has still remains unclear. Reverse transcription quantitative polymerase chain reaction (RT-qPCR) was used to detect the expression of miR-124. Cell viability was analyzed with CCK-8 assay. Cell colony formation ability was detected with colony formation assay. Cell invasion was measured with transwell assay. Dual luciferase reporter assay was conducted to verify whether ZEB2 is a target gene of miR-124. The mRNA and protein expression levels of ZEB2 and EMT markers were detected by quantitative real time PCR and western blot, respectively. Our results showed that miR-124 was down-regulated in TNBC tissues and cells. Overexpression of miR-124 inhibited the proliferation, metastasis and epithelial-mesenchymal transition (EMT) of TNBC cells. Furthermore, ZEB2 3'UTR was considered to be a direct target of miR-124 with luciferase reporter assay. Rescue experiments confirmed that EMT was regulated by miR-124 via suppression of ZEB2. miR-124 suppresses EMT and metastasis via ZEB2. Therefore, miR-124 may represent a potential therapeutic target for TNBC.

Ji H ，Sang M ，Liu F ，Ai N ，Geng C ... -  《-》

The Antimicrobial Peptide Merecidin Inhibit the Metastasis of Triple-Negative Breast Cancer by Obstructing EMT via miR-30d-5p/Vimentin.

Ma F ，Song J ，He M ，Wang X ... -  《-》

MicroRNA-211-5p suppresses tumour cell proliferation, invasion, migration and metastasis in triple-negative breast cancer by directly targeting SETBP1.

Chen LL ，Zhang ZJ ，Yi ZB ，Li JJ ... -  《-》