Interestingly, c-Jun enhanced miR-5188 transcription to form a positive regulatory loop, and Timeless interacted with Sp1/c-Jun to induce miR-5188 expression by promoting c-Jun-mediated transcription, which further activated miR-5188-FOXO1/β-catenin-c-Jun loop and facilitated breast cancer progression.
We identified increased β-catenin and Atk expression was associated with drug resistance and poor prognosis in breast cancer patients using public databases.
In addition, the Wnt/β-Catenin pathway inhibitor was found to be able to reverse the impact of DCLK1 overexpression on BCa cell proliferative and metastatic capacity.
The results indicate that CUL1 knockdown prohibited the metastasis behaviors of breast cancer cells through downregulation (dephosphorylation) of the EMT signaling pathways of EGFR and Akt/GSK3β/β-catenin in breast cancer.
Meanwhile, decreased expression of β-catenin and cyclin Dl was detected in MCM10 short hairpin RNA cells, implying that MCM10 might induce breast cancer metastasis via the Wnt/β-catenin pathway.MCM10 can be defined as a potential diagnostic tool and a promising target for breast carcinoma.
In addition, the expression of β-catenin activated targets including c-Jun, c-Myc, Cyclin D1 and CD44 were also decreased by panobinostat treatment in breast cancer cells.
Hence, we hypothesized that HER2/β-catenin mediates paclitaxel resistance in breast cancer and suppression of HER2/β-catenin signaling could overcome paclitaxel resistance.
The expression of β‑catenin in the Wnt signaling pathway was lower in SK‑BR‑3 cells compared with in MDA‑MB‑231 cells, which may be used as a prognostic indicator for breast cancer.
Finally, miR-107 could further reduce the decreased expression of TPD52, Wnt1, β-catenin and cyclin D1 that was induced by PTX in both mRNA and protein levels, which were rescued by pcDNA3.1-TPD52 indicating that miR-107 regulated breast cancer cell sensitivity to PTX may be targeting TPD52 through Wnt/β-catenin signaling pathway.
The results of qPCR showed that baicalin increase the expression of E-cadherin mRNA, and decrease the expression of vimentin, β-catenin, c-Myc and MMP-7 mRNA in LPS-induced breast cancer MDA-MB-231 cells (P < 0.05).
The Wnt/β-catenin signaling pathway regulates various processes that are important for cancer progression, and emerging evidences have shown a close interaction between Wnt/β-catenin and ERα signaling. miR-190 is also involved in ER signaling and our previous study indicated that miR-190 suppresses breast cancer metastasis.
In conclusion, rAd.DCN inhibits tumor growth and lung metastasis of breast cancer via regulating wnt/β-catenin, vascular endothelial growth factor (VEGF), and Met pathways, and modulating the antitumor inflammatory and immune responses.Considering that i.v. delivery was much more effective in preventing lung metastasis, systemic delivery of rAd.DCN might be a promising strategy to treat breast cancer lung metastasis.
Electrophoretic mobility shift assay (EMSA), luciferase reporter assay, and RNA immunoprecipitation (RIP) were performed to study the regulation and underlying mechanisms of RPRD1A and miR-454-3p expression and their correlation with the Wnt/β-catenin pathway in breast cancer.
Our results reveal that HEIH may contribute to breast cancer development via modulation of microRNA-200b/axis and inducing the activation of Wnt/β-catenin pathway.