Project description:MCF7 cells were infected with retrovirus to overexpress wild-type and mutant miR-222 Measure miRNA expression level in MCF7 cells after overexpressing wild-type and mutant miR-222
Project description:Full title: Expression data from antisense miRNA-221/222 (si221/222) and control inhibitor (GFP) treated fulvestrant-resistant breast cancer cells The expression of miR-221/222 were found to be upregulated in fulvestrant resistant breast cancer cells MCF7-FR compared to its drug-sensitive counterpart MCF7. To investigate the role of miR-221/222 in acquired resistance to fulvestrant, we lowered the level of miR-221/222 in MCF7-FR cells using miRNA inhibitors (antagomirs), and compared gene expression profiles before and after treatment.
Project description:Full title: Expression data from antisense miRNA-221/222 (si221/222) and control inhibitor (GFP) treated fulvestrant-resistant breast cancer cells The expression of miR-221/222 were found to be upregulated in fulvestrant resistant breast cancer cells MCF7-FR compared to its drug-sensitive counterpart MCF7. To investigate the role of miR-221/222 in acquired resistance to fulvestrant, we lowered the level of miR-221/222 in MCF7-FR cells using miRNA inhibitors (antagomirs), and compared gene expression profiles before and after treatment. Fulvestrant-resistant breast cancer cells MCF7-FR (originated from drug-sentitive breast cancer model cell line MCF7) were transient-transfected by antigomirs targeting miR221 or miR222 (i.e. si221, si222). All three cell lines, MCF7-FR, siR221, siRNA222 were subjected to gene expression profiling.
Project description:mRNA breast cancer cell lines were profiled to study the function of hsa-mir-221 and hsa-mir-222. MCF7 cell lines were profiled after treatment with mir-221/222 mimics, and compared to profiles with transfection controls. Similarly, MDA-MB-231 cell lines were profiled after treatment with mir-221/222 inhibitors, and compared to profiles with transfection controls. Since ESR1 is a predicted target of mir-221/222 we also profiled MCF7 cell lines after disrupting ESR1 with an siRNA. Other breast cancer cell lines are provided because all cell lines were normalized together. Keywords: breast cancer, cell line, hsa-mir-221, hsa-mir-222, ESR1
Project description:A long-prevailing model has held that the “seed” region (nucleotides 2-8) of a microRNA is typically sufficient to mediate target recognition and repression. However, numerous recent studies, both within the context of defining miRNA/target pairs by direct physical association and by directly assessing this model in vivo in C. elegans have brought this model into question. To test the importance of miRNA 3' pairing in vivo, in a mammalian system, we engineered a mutant murine mir-146a allele in which the 5' half of the mature microRNA retains the sequence of the wild-type mir-146a but the 3ʹ half has been altered to be anti-complementary to the wild-type miR-146a sequence. Mice homozygous or hemizygous for this mutant allele are phenotypically indistinguishable from wild-type controls and do not recapitulate any of the immunopathology previously described for mir-146a-null mice. Our results strongly support the conclusion that 3ʹ pairing is dispensable in the context of the function of a key mammalian microRNA.
Project description:To identify the microRNA-27b (miR-27b) target genes in luminal-type breast cancer cells, we performed the microarray analysis using miR-27b knockdown MCF7-luc cell line (MCF7-luc anti-miR-27b), miR-27b overexpressing MCF7-luc cell line (MCF7-luc miR-27b o.e.) and their contro cell line (MCF7-luc anti-NC).
Project description:mRNA breast cancer cell lines were profiled to study the function of hsa-mir-221 and hsa-mir-222. MCF7 cell lines were profiled after treatment with mir-221/222 mimics, and compared to profiles with transfection controls. Similarly, MDA-MB-231 cell lines were profiled after treatment with mir-221/222 inhibitors, and compared to profiles with transfection controls. Since ESR1 is a predicted target of mir-221/222 we also profiled MCF7 cell lines after disrupting ESR1 with an siRNA. Other breast cancer cell lines are provided because all cell lines were normalized together. Experiment Overall Design: mRNA breast cancer cell line profiles with some samples in duplicate or triplicate. See summary for more information.
Project description:MicroRNAs (miRNAs), small non-coding RNAs, are powerful and extremely versatile regulators of the gene expression in cells, playing an important role in every step of cancer progression. Here, we report a list of transcripts regulated by miR-662 and miR-24-2-5p transient overexpressions using miRNA MIMIC transfection (MIMIC-miR-662 and MIMIC-miR-24-2-5p, respectively) compared to control (MIMIC-negCTRL-FAM+) at 36 hours post-transfection in human MDA-MB-231-luc2-NW1 (NW1) (for miR-662 and miR-24-2-5p) and MCF7 (only for miR-24-2-5p) breast cancer cell lines. We found 38 transcripts significantly deregulated (17 downregulated, 21 upregulated) in miR-662-overexpressing NW1 cells compared to mock-transfected cells; 222 (187 downregulated, 35 upregulated) and 34 (32 downregulated, 2 upregulated) transcripts deregulated in miR-24-2-5p-overexpressing NW1 and MCF7 cells, respectively, compared to mock-transfected cells. Furthermore, a total of 30 transcripts (29 downregulated, 1 upregulated) were shared between miR-24-2-5p-overexpressing NW1 and MCF7 cells compared to mock-transfected cells. For miR-662, which we found to promote breast cancer metastasis by stimulating cancer cell stemness (Puppo et al., 2023), we observed the deregulation of Cell Migration Inducing Hyaluronidase 1 (CEMIP), Interleukin 6 receptor (IL6R), High Mobility Group AT-Hook 2 (HMGA2), Small Ubiquitin Like Modifier 3 (SUMO3), and Polymerase (DNA) Delta Interacting Protein 2 (POLDIP2), which reinforced the evidence of the involvement of miR-662 in the acquisition of a stem-like phenotype by human NW1 breast cancer cells and miR-662 contribution to breast cancer bone metastasis formation. For miR-24-2-5p, we found that the downregulation of two transcripts, WD Repeat and FYVE Domain Containing 1(WDFY1) and SH3 Domain Binding Glutamate Rich Protein Like 2 (SH3BGRL2), might explain a possible role of miR-24-2-5p as a tumour suppressor by reducing breast cancer cell invasive properties.
Project description:To identify the microRNA-27b (miR-27b) target genes in luminal-type breast cancer cells, we performed the microarray analysis using miR-27b knockdown MCF7-luc cell line (MCF7-luc anti-miR-27b), miR-27b overexpressing MCF7-luc cell line (MCF7-luc miR-27b o.e.) and their contro cell line (MCF7-luc anti-NC). After establishing MCF7-luc anti-miR-27b, MCF7-luc miR-27b o.e. and MCF7-luc anti-NC using lentivirus vector, we performed the microarray analysis.