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Aberrant microRNA (miRNA) expression has been linked to cancer development. In this study, we aimed to investigate whether the anti‑cancer effect of miRNA‑299‑3p on laryngeal cancer Hep‑2 cells is mediated through targeting human telomerase reverse transcriptase (hTERT). The expression of miR‑299‑3p in laryngeal cancer Hep‑2 cells and human osteosarcoma U2OS cells was quantified by stem‑loop‑mediated reverse transcription quantitative polymerase chain reaction. miR‑299‑3p mimic was transfected into Hep‑2 cells to induce overexpression of miR‑299‑3p. A CCK‑8 assay was performed to identify the effects of miR‑299‑3p overexpression on the proliferation of Hep‑2 cells. Western blot analysis was carried out to determine the expression of hTERT protein. A significant decrease was noted in the expression of miR‑299‑3p in Hep‑2 cells compared with that of U2OS cells (P0.05). Overexpression of miR‑299‑3p resulted in a notable inhibition of cellular proliferation (P0.05), as well as downregulation of hTERT mRNA and protein in Hep‑2 cells (P0.05). The expression of miR‑299‑3p is downregulated in human laryngeal cancer Hep‑2 cells. Overexpression of miR‑299‑3p inhibits Hep‑2 cell growth by targeting the 3'‑untranslated region of hTERT mRNA.

Global DNA hypomethylation, in particular that of the gene promoter sequence in gene hypermethylation, is a well-known characteristic of human cancer. Subtelomeres are enriched CpG islands; methylation is believed to be a potential epigenetic regulator. However, regulation on the telomere length remains largely unknown. To demonstrate this correlation, four nasopharyngeal carcinoma cell lines (CNE, CNE1, CNE2, 5-8F) were treated for 72 hours with 0, 1, or 2.5 μM of the demethylating agent 5-aza-2'-deoxycytidine (5-aza-dC). Subtelomeric (D4Z4) level methylation was evaluated with a bisulfite assay, the human telomerase catalytic subunit (hTERT) expression was assayed by reverse transcription-polymerase chain reaction, the telomerase activity was detected using a telomeric repeat amplification protocol assay, and the telomere length was measured by Southern blot terminal restriction fragment analysis. There was significant demethylation following 5-aza-dC treatment, and a strongly repressed hTERT expression decreased the telomerase activity and remarkably shortened telomeres. Thus, partial subtelomeric methylation does not repress hTERT expression; conversely, demethylation may downregulate hTERT expression and shorten telomeres.