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Although transfection with synthetic anti-miR-494 inhibitors failed to block drug-induced apoptosis or miR-494 upregulation, it induced the transcriptional repression of the PVRIG gene. Surprisingly, miR-494 inhibition in conjunction with low doses of Trichostatin A enhanced the weak T cell receptor-mediated apoptosis, indicating a subtle pro-survival role of miR-494. Interestingly, this pro-survival effect was overwhelmed by mitogen-mediated T cell activation and higher drug doses, which mediated caspase-dependent apoptosis.
Our results unravel a pro-survival function of miR-494 and its putative interaction with the PVRIG gene and the apoptotic machinery in Jurkat cells.
Our results unravel a pro-survival function of miR-494 and its putative interaction with the PVRIG gene and the apoptotic machinery in Jurkat cells.
Triple-negative breast cancer (TNBC) accounts for 15% of all breast cancer (BC) cases and is a severe type of BC. Since medicinal herbs containing biocompatible substances that are accepted by patient more than chemical therapeutics, they can be considered a safe option for treating BC.
This study evaluated the effect of Sambucus Ebulus (S. ebulus) extract on a model of TNBC.
S. ebulus extract was prepared using petroleum ether, ethyl acetate, and methanol. https://www.selleckchem.com/products/BafilomycinA1.html The petroleum ether extract was fractionated and analyzed using vacuum liquid chromatography and GC-MS, respectively. MDA-MB-231 and MCF-10A were used as TNBC and normal breast cells, respectively. Flowcytometry and MTT assays were performed to evaluate cell cycle, apoptosis, and viability of the cells. Gene expression analysis was performed using RT-qPCR. Nude mouse allograft tumor models were used, and pathological sections were evaluated.
The findings indicated that S. ebulus extract remarkably decreased cell proliferation and viability. The extract had no toxicity to the normal breast cells but efficiently killed the cancer cells. Cell cycle- and apoptosis-related gene expression showed that fraction 4 of S. ebulus extract significantly increased the expression of Bax, Bak, P53, and c-MYC.
This study showed satisfactory results of the effect of S. ebulus extract on clearing BC cells both in vitro and in vivo. Thus, S. ebulus extract may be a safe herbal compound for eliminating BC cells without toxicity to host cells.
This study showed satisfactory results of the effect of S. ebulus extract on clearing BC cells both in vitro and in vivo. Thus, S. ebulus extract may be a safe herbal compound for eliminating BC cells without toxicity to host cells.
In the current era, development of molecular techniques involves nanotechniques and the synthesis of nanoparticles is considered as the preferred field in nanotechnology.
The aim of the present work is to analyze the anticancer activity of the thymoquinone conjugated ZnO nanoparticles and to understand its mechanism of action in triple negative breast cancer cell line MDA-MB-231.
Zinc Oxide (ZnO) nanoparticles have extensive applications and it was synthesized using a chemical precipitation method. Thymoquinone (TQ) is the major bioactive component of the seeds of Nigella sativa. Synthesized nanoparticles were characterized using various spectroscopic techniques. Thymoquinone coated nanoparticles were checked for its efficiency. The cytotoxicity of ZnO, TQ and TQ conjugated ZnO nanoparticles against MDA-MB-231. Colony forming and cell migration assay were performed to measure the proliferative competence of the breast cancer cells on exposure to nanoparticles. The mechanism of apoptosis was probed by assessing MMP, interplay between ER stress and ROS.
The results of the characterization techniques confirmed the particles synthesized were ZnO and TQ-ZnO nanoparticles. pH dependent release of the compound was observed. Anti-proliferative effect that impairs the formation of colony was found to be enhanced in cells exposed to combined treatment with the nanoconjugate.
Hence, the TQ conjugated ZnO nanoparticles can act as an efficient carrier for drug delivery at the target site in TNBC cells.
Hence, the TQ conjugated ZnO nanoparticles can act as an efficient carrier for drug delivery at the target site in TNBC cells.
Cancer stem cells could influence tumor recurrence and metastasis.
To develop a new effective treatment modality targeting breast cancer stem cells (BCSCs), and to explore the role of Apatinib in BCSCs.
BCSCs were isolated from MDA-MB-231 cells by immune magnetic beads method. BCSCs were treated with Apatinib, lentiviral plasmids (lncRNA ROR) and iCRT-3 (Wnt pathway inhibitors). Viability, colony numbers, sphere numbers, apoptosis, migration, invasion of BCSCs were detected by MTT, colony formation, tumor sphere, flow cytometry, wound-healing, transwell assays, respectively. The expressions of markers (ABCG2, CD44, CD90, and CD24), epithelial-mesenchymal transition (EMT)-related molecules (E-cadherin, N-cadherin, Vimentin, MMP-2, MMP-9), and Wnt/β-catenin pathway-related proteins (Wnt3a, Wnt5a, β-catenin) in breast cancer stem cells were determined by performing Western blot and qRT-PCR analysis.
Apatinib decreased the viability and colony numbers of BCSCs in a concentration-dependent manner, and it also reduced sphere numbers, suppressed migration, invasion and lncRNA ROR expression, and induced apoptosis of BCSCs. However, these results were partially reversed by lncRNA ROR overexpression. Apatinib suppressed stem property, EMT process and Wnt/β-catenin pathway in BCSCs, which was partially reversed by lncRNA ROR overexpression. Moreover, lncRNA ROR overexpression increased the colony and sphere numbers, and promoted the cell viability, apoptosis inhibition, migration and invasion of BCSCs, but these effects were partially reversed by iCRT-3. LncRNA ROR overexpression increased the stem property, EMT process and Wnt/β-catenin pathway, which were partially counteracted by iCRT-3.
Apatinib inhibited stem property and malignant biological behaviors of BCSCs by blocking Wnt/β-catenin signal pathway through down-regulating lncRNA ROR.
Apatinib inhibited stem property and malignant biological behaviors of BCSCs by blocking Wnt/β-catenin signal pathway through down-regulating lncRNA ROR.
