ArticleTranslational cancer research2025
Mechanistic study of LINC01296 mediating TRIP13 regulation of neuroblastoma progression.
Article in Translational cancer research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Neuroblastoma (NB) is an embryonic cancer arising from neural crest cells. Long non-coding RNA (lncRNA) plays an important role in the development of tumors. Several studies have reported that LINC01296 and thyroid hormone receptor interacting protein 13 (TRIP13) acts as oncogenic regulators of cancer. However, their deep specific biological mechanisms in tumor metastasis are not known. Here, we aimed to elucidate whether LINC01296 or TRIP13 drives NB proliferation and progression, and to assess their potential as therapeutic targets. Methods: In this study, we utilized the NB cell line SK-N-SH to investigate the roles of LINC01296 and TRIP13 by bacterial transformation and polymerase chain reaction (PCR) verification. Cells were infected with lentivirus, and fluorescence expression was monitored. Total RNA was extracted for reverse transcription quantitative PCR (RT-qPCR). Cell proliferation was assessed by using Cell Counting Kit-8 (CCK-8) assay. Migration was evaluated using wound-healing assays, and invasion was tested via Transwell with Matrigel-coated chambers. Apoptosis was analyzed by flow cytometry. For Results: In this study, we found that compared with negative control (NC) group, overexpression of LINC01296 (OE-LINC01296) or TRIP13 (OE-TRIP13) both promoted the proliferation, migration and invasion of SK-N-SH cells, while inhibiting apoptosis; and vice versa. In addition, we further demonstrated that LINC01296 stabilised knockdown via short hairpin RNA (shRNA) (sh-LINC01296) + OE-TRIP13, and TRIP13 stabilised knockdown via shRNA (sh-TRIP13) + OE-LINC01296 decreased SK-N-SH cell proliferation, migration and invasion, while promoting apoptosis. We also established a subcutaneous transplantation tumor model in NB NOD/scid mice, and sh-LINC01296 or sh-TRIP13 inhibited tumor growth in mice, and the tumor growth in the sh-LINC01296 + OE-TRIP13 group and the sh-TRIP13 + OE-LINC01296 group was between the NC group and the sh-LINC01296 or sh-TRIP13 group. Conclusions: These results suggest that LINC01296 may play a role as an oncogene in the development of tumorigenesis in NB by mediating TRIP13, and provide a marker for the prognosis of NB.
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