miR‑125a is upregulated in cancer stem‑like cells derived from TW01 and is responsible for maintaining stemness by inhibiting p53

microRNA (miR)‑125a and miR‑125b were demonstrated to translationally and transcriptionally inhibit the mRNA level of p53 following the induction of chemo‑reagents in our previous report. As a small subpopulation of nasopharyngeal carcinoma (NPC), cancer stem‑like cells (CSCs) function critically in multi‑malignant behaviors, including tumorigenesis and metastasis; however, the expression pattern and regulatory role of miR‑125a, miR‑125b and p53 in CSCs derived from NPC remain unclear. In order to investigate the potential regulatory role of miR‑125 on p53, firstly CSCs was isolated from TW01 by culturing in serum‑free medium. The stemness of isolated CSCs was examined via self‑renewal capacity and side population assays. Following this, the miR‑125a, miR‑125b and p53 mRNA levels were evaluated via reverse‑transcription quantitative polymerase chain reaction. Following the transfections of wild‑type p53 or p53 without DNA binding activity (p53‑mutR248Q) into TW01 or CSCs, Chromatin Immunoprecipitation (ChIP), and cell cycle analyses using flow cytometry or Cell Counting Kit‑8 assays were performed. Notably, it was determined that miR‑125a was significantly upregulated in CSCs derived from TW01, but not miR‑125b, and the mRNA and protein levels of p53 were downregulated. The transfection of p53 significantly decreased the cell viability and stopped cell cycle at the G0/G1 phases in TW01 and CSCs. The ChIP assay confirmed that the ectopic expression of wild‑type p53 transcriptionally regulates its downstream gene, p21, but not B‑cell lymphoma 2 nor Sco2. Taken together, the results of the present study indicated that p53 regulates CSCs via its DNA binding activity and potentially, in CSCs, miR‑125a regulates the expression of p53, maintaining stemness.