Kmt2c restricts G-CSF-driven HSC mobilization and granulocyte production in a methyltransferase-independent manner.

Granulocyte colony-stimulating factor (G-CSF) is widely used to enhance myeloid recovery after chemotherapy and to mobilize hematopoietic stem cells (HSCs) for transplantation. Unfortunately, through the course of chemotherapy, cancer patients can acquire leukemogenic mutations that cause therapy-related myelodysplastic syndrome (MDS) or acute myeloid leukemia (AML). This raises the question of whether therapeutic G-CSF might potentiate therapy-related MDS/AML by disproportionately stimulating mutant HSCs and other myeloid progenitors.

Identification and characterization of TGF-β1-responsive Runx2 acetylation sites for matrix Metalloproteinase-13 expression in osteoblastic cells.

In skeletal tissues, transforming growth factor-beta 1 (TGF-β1) serves a number of activities. For example, in osteoblastic cells, TGF-β1 stimulates the expression of matrix metalloproteinase-13 (MMP-13, a bone remodeling gene), which requires the bone transcription factor Runx2. Although TGF-β1 is known to stimulate Runx2 acetylation, the sites involved in MMP-13 gene activation remain unknown.

Regulation of transforming growth factor-β1-stimulation of Runx2 acetylation for matrix metalloproteinase 13 expression in osteoblastic cells.

Transforming growth factor beta 1 (TGF-β1) functions as a coupling factor between bone development and resorption. Matrix metalloproteinase 13 (MMP13) is important in bone remodeling, and skeletal dysplasia is caused by a deficiency in MMP13 expre-ssion. Runx2, a transcription factor is essential for bone development, and MMP13 is one of its target genes.

Regulation of Runx2 and Its Signaling Pathways by MicroRNAs in Breast Cancer Metastasis.

As a major threat among women globally, breast cancer (BC) emerges as a primary research focus for several researchers. Although various therapeutic regimens are available, there is an increased chance of metastasis of BC cells, which raises the severity of this malignancy. Of multiple preferred secondary targets, metastasis to bone is extensively studied.

Regulation of Breast Cancer Progression by Noncoding RNAs.

Background: Breast cancer (BC) is the cardinal cause of cancer-related deaths among women across the globe. Our understanding of the molecular mechanisms underlying BC invasion and metastasis remains insufficient. Recent studies provide compelling evidence on the prospective contribution of noncoding RNAs (ncRNAs) and the association of different interactive mechanisms between these ncRNAs with breast carcinogenesis.

miR-873-3p targets HDAC4 to stimulate matrix metalloproteinase-13 expression upon parathyroid hormone exposure in rat osteoblasts.

Matrix metalloproteinase-13 (MMP-13) plays a predominant role in endochondral bone formation and bone remodeling. Parathyroid hormone (PTH) stimulates the expression of MMP-13 via Runx2, a bone transcription factor in rat osteoblastic cells (UMR106-01), and histone deacetylase 4 (HDAC4) acts as a corepressor of Runx2. Moreover, microRNAs (miRNAs) play an important role in regulating genes posttranscriptionally.