Obtained from p53 wild-type (p53 +/+), p53 knockdown In the present study, the characteristics of mBM-MSCs The differential characteristics of mouse (m)BM-MSCsĮxhibiting distinct p53 statuses has not been thoroughly The transformation of MSCs, which promotes mesodermal tumor ForĮxample, the absence of p53 can increase the osteogenicĪnd the inactivation of p53 skews MSCs towards an osteogenic fateĪnd impairs hematopoiesis-supporting activity ( 24). The cell cycle, and the aberrant transformation of MSCs. Loss of p53 expression occurs in ~50% of human cancers ( 19, 20),Īnd p53 mutations can lead to genome instability, functionalĪlterations in cell proliferation, migration, differentiation and Processes, such as cell cycle control and growth, differentiationĪnd DNA repair therefore, p53 is often referred to as the guardian Suppressor gene that regulates the homeostasis of cells ( 17), as well as several cellular P53 is a prominent transcription factor and tumor Represent promising potential for their use in cancer therapy withĭemonstrating that MSCs have potential beneficial effects forīreast cancer therapy through the targeting of fibronectin 1, CD44 Metastasis and angiogenesis of colon cancer by secreting galectin-3 Growth and metastasis of breast cancer ( 8). MSCs also reportedly induce theĮxpression of discoidin domain-containing receptor 2 to mediate the Inhibition of microRNA (miR)-155-5p promoted the transition ofīM-MSCs into gastric cancer-MSCs through the activation of the MSCs can promote the growth, metastasis and invasion of cancers Other tissues, to sites of inflammation, such as areas of injuryĪnd tumors ( 5– 8), respond to the local microenvironment,Īnd exert immunosuppressive and anti-inflammatory activities Hematopoiesis-supportive stroma ( 4) they can be mobilized from BM, and Including osteoblasts, adipocytes, chondrocytes and That enable them to develop into several different cell types, Marrow (BM), adipose tissue, umbilical cord, skeletal muscle, liverĪnd tumoral tissues ( 1– 3). The results of the present study indicated that p53 may serve an important role in the biology of mBM‑MSCs, and may provide novel insights into the role of cells with different p53 statuses in cancer progression.įibroblast-like, multipotent cells that can be isolated from bone Ubiquitin protein ligase E3 component n‑recognin 2, RING‑finger protein 31 and matrix metalloproteinase 19 were highly expressed in p53+/‑ and p53‑/‑ mBM‑MSCs. The expression levels of tumor necrosis factor‑α and interferon‑γ‑inducible protein‑10 were significantly upregulated in the supernatant of p53+/‑ and p53‑/‑ mBM‑MSCs. The expression levels of microRNA (miR)‑3152 and miR‑337 were significantly increased in p53+/‑ and p53‑/‑ mBM‑MSCs, whereas the expression levels of miR‑221, miR‑155, miR‑1288 and miR‑4669 were significantly decreased. The colony formation and migratory abilities of p53+/‑ and p53‑/‑ mBM‑MSCs were markedly enhanced, and the expression levels of stem cell‑associated proteins were significantly increased compared with p53+/+. The adipogenic and osteogenic differentiation of mBM‑MSCs was increased in the absence of p53. mBM‑MSCs from all three groups, representing distinct p53 statuses, were unable to form tumors over a 3‑month period in vivo. The p53+/‑ and p53‑/‑ mBM‑MSCs demonstrated an increased proliferation rate compared with mBM‑MSCs derived from p53+/+ mice. In the present study, p53 wild‑type (p53+/+), knockdown (p53+/‑) and knockout (p53‑/‑) mouse BM‑MSCs (mBM‑MSCs) were observed to be similar in appearance and in the expression of cell surface biomarkers, but expressed differential p53 protein levels. The present study aimed to investigate the role of p53 in the biology of BM‑MSCs. The tumor suppressor gene, p53, is functionally involved in cell cycle control, apoptosis and genomic stability, and is mutated and inactivated in most human cancers. Bone marrow MSCs (BM‑MSCs) are fibroblast‑like cells with multipotent differentiation ability, that localize to areas of tissue damage, including wounds and solid tumors. Mesenchymal stem cells (MSCs) affect diverse aspects of tumor progression, such as angiogenesis, tumor growth and metastasis.
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