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Anticancer Effects of Resveratrol-Loaded Solid Lipid Nanoparticles on Human Breast Cancer Cells
Results indicate that the resveratrol-loaded solid lipid nanoparticles (Res-SLN) may have great potential for breast cancer treatment.
Involvement of miR-451 in resistance to paclitaxel by regulating YWHAZ in breast cancer
It is shown that miR-451 is decreased in human breast cancer specimens and in paclitaxel-resistant (PR) cells, and the results of xenograft model in vivo showed that intratumor injection of miR -451 agomir induced a tumor-suppressive effect in SKBR3/PR drug-resistant xenografted model.
MiR-155-3p acts as a tumor suppressor and reverses paclitaxel resistance via negative regulation of MYD88 in human breast cancer.
[Effects of lncRNA RP11-770J1.3 and TMEM25 expression on paclitaxel resistance in human breast cancer cells].
- Y. Li, Yueyue Wang, Chang-jie Chen
- BiologyZhejiang da xue xue bao. Yi xue ban = Journal of…
- 25 July 2017
Down-regulation of lncRNA RP11-770J1.3 and TMEM25 enhanced the sensitivity of MCF-7/PR cells to paclitaxel, and inhibited the expression of MRP, BCRP and MDR1/P-gp (all P<0.05).
The N-terminal polypeptide derived from vMIP-II exerts its anti-tumor activity in human breast cancer by regulating lncRNA SPRY4-IT1
It is suggested that lncRNA SPRY4-IT1 could serve as a novel biomarker by NT21MP for breast cancer.
SGK1 in Human Cancer: Emerging Roles and Mechanisms
Evidence highlights the crucial role of SGK1 in tumorigenesis and cancer progression, revealing why it has emerged as a potential target for cancer therapy and summarizes the current understanding of the regulatory mechanisms ofSGK1 at the molecular level.
NT21MP negatively regulates paclitaxel-resistant cells by targeting miR-155-3p and miR-155-5p via the CXCR4 pathway in breast cancer
Findings suggested that miR-155-3p/5p and their target genes MYD88 and TP53INP1 may serve as novel biomarkers for NT21MP therapy through the CXCR4 pathway for improving sensitivity to paclitaxel in breast cancer.
N-peptide of vMIP-Ⅱ reverses paclitaxel-resistance by regulating miRNA-335 in breast cancer.
- Yangyang Wang, Haifeng Wang, Qing-ling Yang
- Biology, ChemistryInternational journal of oncology
- 1 September 2017
It is elucidated that NT21MP and miR‑335 mediated PR of breast cancer cells partly through regulation of Wnt/β‑catenin signaling pathway.
The N-terminal polypeptide derived from viral macrophage inflammatory protein II reverses breast cancer epithelial-to-mesenchymal transition via a PDGFRα-dependent mechanism
The results illustrated that NT21MP could reverse the phenotype of EMT in paclitaxel-resistant cells and indicated that CXCR4 overexpression drives acquired pac litaxel resistance, partly by activating the PDGFA and PDGFB/PDGFRα autocrine signaling loops that activate AKT and ERK1/2.
N-terminal polypeptide derived from vMIP-II exerts its antitumor activity by inhibiting the CXCR4 pathway in human glioma
The present study indicates that NT21MP plays a regulatory role in the SDF-1α/CXCR4 axis and further manages the invasion, migration, apoptosis and cell cycle of glioma cells.