Recent research suggests curcumin extracted from the turmeric plant may inhibit the proliferation of cancer cells by controlling the expression of microRNAs (miRNAs). The effect of phenolic curcumin on miR-638-5p and potential target gene expressions in the triple negative breast cancer (TNBC) cell line MDA-MB-231 was investigated in this study. GSE154255 and GSE40525 datasets were downloaded and analyzed using GEO2R to identify dysregulated miRNAs in TNBC. To find differently expressed genes in breast cancer (BRCA), The Cancer Genome Atlas Program data was examined. Utilizing in silico tools, KEGG, GO, and other enrichment analyses were performed. The databases miRNet, miRTarBase v8.0, and TarBase v.8 were used for miRNA and mRNA matching. Real-time quantitative reverse transcription polymerase chain reaction was used to examine the levels of miRNA and its targets in miRNA mimic transfected/curcumin-treated MDA-MB-231 cultures and controls. The cell viability detection kit-8 method was used to assess cell viability, and the scratch assay was used to conduct migration assessment. Bioinformatics analysis showed that miR-638-5p was significantly reduced in TNBC patients. Experimental results showed that miR-638-5p was upregulated in MDA-MB-231 treated with curcumin, while the potential target genes of miR-638-5p, CFL1, SIX4, MAZ, and CDH1 were downregulated. Mimic miR-638-5p transfection inhibited MDA-MB-231 cell proliferation and reduced migration and expression of CFL1, SIX4, and MAZ genes was decreased in mimic miR-638-5p transfected cells. These findings suggest that curcumin exerts its anticancer effects on MDA-MB-231 cells by modulating the expression of miR-638-5p and its possible target genes.
Background: Multiple Myeloma (MM) is plasma cell dyscrasia characterized by transformation of B cells into malignant cells. Although there are data regarding molecular pathology of multiple myeloma, molecularmechanisms of the disease has not been fully explained. Aims: To investigate gene expression profiles in bone marrow myeloma cells via RNA sequencing technology. Study Design: Cell study. Methods: Four untreated MM patients myeloma cells and 4 healthy donors B cells from bone marrow were sorted using FACSAria II. It was occurred two groups as patient pool from myeloma cells and the control pool from B cells. Transcriptome analysis was performed and results were analyzed using bioinformatic tools. Results: Total result of transcriptome data 18.806 transcripts (94.4%) were in pooled MM patients. 992 regions were detected as new exon candidates or altenative splicing regions. In addition, 490 mutations (deletion or insertion) and 1397 SNV were, 415 fusion transcripts, 132 frameshift mutations and 983 fusions which were reported before in NCBI were detected with unknown function were identified in patients. 35.268 transcripts were obtained (71%) (25.355 transcripts were defined previously) in the control pool. This preliminary study, the first 50 genes analyzed with a gene set enchriment analysis program by MSigDB, Enrichr and Panther.Molecular functions, cellular component, pathway and biological process of the genes obtained statistical values by means of bioinformatics tools were presented as supplemental file. Conclusion: EEF1G, ITM2C, FTL, CLPTM1L, and CYBA possible candidate genes were identified in this study which may be associated with myelomagenesis.
Objectives: Multiple myeloma (MM) is a common hematological cancer. Hence, it is important to conduct further studies investigating the molecular mechanisms in detail that contributes to myeloma genesis. In addition to genetic changes, epigenetic factors such as miRNAs may influence the expression of myeloma-related genes. Methods: Our study aimed to detect genes closely related to MM and miRNAs involved in the cancer process by changing the expression of these genes with bioinformatics tools and in vitro methods. Bioinformatics approaches identified hub miRNAs in our study that may have a role in the expression change of genes connected to myeloma. The functional impacts of the chosen miRNA on RPMI8226 and U266 cell lines and the effect of this miRNA on the expression changes of putative target genes were investigated. Results: The viability of miR-145-5p transfected cells was found to decrease compared to control cells and the expression of IGF1R and NRAS genes were found to be significantly suppressed in both cell lines at mRNA level. Decreased levels of the IGF1R and NRAS genes were confirmed in miR-145-5p transfected cells at the protein level as well as compared to control cells. In addition, IGF1R /miR-145-5p interaction was demonstrated via luciferase reporter assay. However, expression levels of EGFR , KLF4 , IRS1 , CDK4 and CDK6 candidate genes had no statistically significant difference in miR-145-5p transfected cells compared to control cells. Conclusions: Mir-145-5p was demonstrated to act as a tumor suppressor miRNA and inhibit the proliferation in MM cell lines via targeting IGF1R and NRAS .
26 September 2024 in European Journal of Breast Health
Fifty‐six adult patients with newly diagnosed acquired severe aplastic anemia (SAA) received horse antilymphocyte globulin (ALG), cyclosporin A (CyA), methylprednisolone (Mpred), granulocyte colony‐stimulating factor (G‐CSF) as first‐line therapy. The median age was 34 (range, 17–72) and median neutrophil count 0.280 × 109/L. Trilineage hematologic recovery (at a median interval of 105 days from treatment) was seen in 46 patients (37 complete, 9 partial) after one (n = 38) or two (n = 8) courses of ALG. Cytogenetic abnormalities were observed in three unresponders, clonal hematologic disease in three complete responders, and relapse of marrow aplasia in four complete responders. Median follow up for surviving patients was 1,668 days (range, 237–4,012). The actuarial survival at 5 years was 82%, falling to 77.1% at 7 years and was stationary at 7 and 8 years. Survival was not influenced by the neutrophil count (72% vs. 87%, for neutrophils less than vs. greater than 0.2 × 109/L; P = 0.54). Immunosuppressive treatment of SAA with the 4‐drug combination appears to be effective. The significant prognostic effect of an enduring increase of the white blood cell (WBC) count during G‐CSF treatment may suggest complete and partial response to therapy. In nonresponders, the WBC count either did not change or elevated values gradually returned to nearly their initial levels while the patients were still under G‐CSF treatment. In patients not responsive to treatment but living under CyA and G‐CSF, the possibility of developing cytogenetic abnormalities does not seem to be low, despite the absence of findings attributable to manifest myelodysplastic syndrome. Am. J. Hematol., 2007.