Erratum: Ovarian cancer proliferation and apoptosis are regulated by human transfer RNA methyltransferase 9-like via LIN9.

[This corrects the article DOI: 10.3892/ol.2017.6750.].

Ovarian cancer proliferation and apoptosis are regulated by human transfer RNA methyltransferase 9-likevia LIN9.

Current traditional treatment options have little impact on the long-term survival of patients with ovarian cancer due to a lack of understanding of the molecular transformations that occur in ovarian carcinoma. Transfer RNAs (tRNAs) perform a key role in protein translational fidelity. Enzymes involved in tRNA modification may function as regulators of cancer progression. Human tRNA methyltransferase 9-like (hTRM9L) catalyzes tRNA wobble base modifications, which regulate ovarian cancer growth and apoptosis via the retinoblastoma protein (pRB) and p53 signaling pathways. The aim of the present study was to confirm the role of hTRM9L in the proliferation and apoptosis of ovarian cancer. Immunohistochemistry was performed to investigate the expression of hTRM9L and LIN9 in 70 ovarian tissues. hTRM9L was amplified by polymerase chain reaction (PCR) and inserted into the Ubi-multiple cloning site-enhanced green fluorescent protein (EGFP)-internal ribosome entry site-puromycin lentiviral expression vector to create the Ubi-KIAA1456-EGFP-puromycin (LV-KIAA1456) vector. The lentiviruses were subsequently compounded and transduced into HO8910PM cells. hTRM9L, LIN9 and B-cell lymphoma 2 (Bcl-2)/Bcl-2 associated X protein (Bax) expression levels were examined by PCR and western blot analysis. Apoptosis was verified by flow cytometry, and cell proliferation was evaluated using Cell Counting Kit-8. hTRM9L and LIN9 expression were reduced in the ovarian cancer group, and there was a positive correlation between hTRM9L and LIN9 expression according to Pearson's correlation coefficient (r=0.406; P<0.05). hTRM9L was increased by 2-3-foldin HO8910PM cells following LV-hTRM9L transduction. The expression of hTRM9L at the mRNA and protein levels in HO8910PM cells that were transfected with LV-hTRM9L was significantly increased compared with the negative control, as confirmed by reverse transcription-quantitative PCR and western blot analysis, respectively (P<0.05). The same was observed for LIN9 and Bax (P<0.05). By contrast, Bcl-2 was downregulated in LV-hTRM9L (P<0.05). Furthermore, cell growth was inhibited (P<0.05) and apoptosis increased (P<0.05). In the present study, hTRM9L was shown to prevent tumor growth and promote apoptosis by regulating LIN9, which is associated with the pRB and p53 signaling pathways. This maybe a novel breakthrough in the treatment of ovarian cancer.