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RNA-seq analysis JARID2 knockdown effect on MDA-MB-231 cells

ABSTRACT: The JmjC domain-containing protein JARID2 is an important regulator of gene expression in embryonic stem cells. However, what role JARID2 play in tumorigenesis is poorly understood. Here, we reported that JARID2 was highly expressed in multiple types of cancer, including breast cancer. And JARID2 promoted the glycolysis, lipid metabolism, stemness, proliferation, and invasion of breast cancer cells. Furthermore, we found that JARID2 was physically interacted with the nucleosome remodeling and deacetylase (NuRD) complex transcriptionally repressing a series of tumor suppressor genes. Overall, our data propose that JARID2 promotes tumorigenesis and development, endorsing the proposal of JARID2 as a target for cancer therapy.

ORGANISM(S): Homo sapiens

PROVIDER: GSE202868 | GEO | 2025/05/11

REPOSITORIES: GEO

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Project description:JARID2 is a chromatin remodeler, member of the Jumonji family of transcription factor genes that belongs to the polycomb repressive complex 2 (PRC2) (Peng JC et al. Cell 2009) and is frequently deleted in leukemic transformation of chronic myeloid malignancies (Puda A et al. Am J Hematol. 2012). In this work, we compared gene expression profile (GEP) of CD34+ cells from Primary Myelofibrosis (PMF) patients with healthy donors and we found JARID2 among downregulated genes. In addition, integrative analysis of gene and miRNA profiles highlighted JARID2 as a shared target of several miRNAs aberrantly expressed in PMF CD34+ cells. Since the role of JARID2 in normal and malignant hematopoiesis has never been investigated, we performed JARID2 silencing experiments on normal Cord Blood (CB) CD34+ cells to evaluate its involvement in proliferation and commitment. Therefore, CD34+ cells were transfected with a mixture of 3 Silencer Select siRNAs targeting JARID2 mRNA and with a non-targeting siRNA as control (NegCTR). The expression level of JARID2 in control samples and JARID2-siRNA cells was assessed by QRT-PCR at 24h (RQ 0,2 ± SEM 0,036, p <.001) and 48h (RQ 0,32 ± SEM 0,026, p<.001) after the last nucleofection. Flow cytometric analysis of CD41 Megakaryocyte (MK) lineage differentiation marker performed on serum-free multilineage culture at day 8, 10 and 12 pointed out that JARID2 inhibition induces a significant increase in the MK fraction compared to NegCTR sample. In addition, we demonstrated that JARID2 silencing induces a remarkable increase in percentage of CFU-megakaryocyte (CFU-MK) colonies and a strong decrease of non-megakaryocyte colonies (CFU non-MK) in collagen-based clonogenic assay. Moreover, morphological evaluation of May-Grunwald-Giemsa (MGG)–stained cytospins of TPO treated cells at day 8, 10 and 12 after the last nucleofection clearly displayed a considerable enrichment in MK precursors at different stages of maturation in JARID2-siRNA sample compared to NegCTR. Finally, to better characterize changes in gene expression induced by JARID2 gene silencing, we performed mRNA expression profile microarray analysis in NegCTR and JARID2-siRNA CD34+ cells.

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RNA-seq analysis JARID2 knockdown effect on MDA-MB-231 cells

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