Genes & genomics · 2026
c-Myc regulated long noncoding RNA TRD-AS1 to affect the progression of oral squamous cell carcinoma.
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Feng Ziyue, Han Yuxuan, Qin Xiaofeng, Fu Miaoting, Li Xiangyang, Zhu Youming
Аннотация
BACKGROUND: Oral squamous cell carcinoma (OSCC) progression is closely associated with dysregulated oncogenic transcription programs and noncoding RNA networks. c-Myc is a key transcription factor in tumor biology, but the role of c-Myc-regulated long noncoding RNAs such as TRD-AS1 (LNC TRD-AS1) in OSCC progression remains to be clarified.
OBJECTIVE: To investigate the effect of c-Myc-regulated LNC TRD-AS1 on the progression of OSCC.
METHODS: The effects of c-Myc on LNC TRD-AS1 were detected. Expression of c-Myc and LNC TRD-AS1 in OSCC and paracancerous tissues. Dual luciferase reporter assay verified the binding of c-Myc to the promoter region of LNC TRD-AS1. The localization of LNC TRD-AS1 in OSCC was determined by nucleocytoplasmic isolation assay and RNA FISH experiments. The effects of overexpression, knockdown of LNC TRD-AS1 and rescue experiments on migration, metabolism, and proliferation of OSCC cells were observed by quantitative real-time polymerase chain reaction (qRT-PCR), western blots, scratch tests, Transwell assays, medium color and pH changes, ATP measurement, CCK-8 assays, and colony formation assays.
RESULTS: It was found that c-Myc positively regulated the expression of LNC TRD-AS1 in OSCC cell lines and tissues. The binding of c-Myc to the LNC TRD-AS1 promoter region was verified by dual-luciferase reporter assays. Both nucleoplasmic separation assays and RNA FISH showed that LNC TRD-AS1 was localized to the nuclei in OSCC cells. Overexpression of LNC TRD-AS1 promoted migration, metabolism and proliferation in OSCC cell lines, while knockdown had the opposite effect.
CONCLUSION: c-Myc positively regulated LNC TRD-AS1 in OSCC. LNC TRD-AS1 affected the migration, proliferation and metabolism of OSCC by affecting the tumor acid metabolism.
OBJECTIVE: To investigate the effect of c-Myc-regulated LNC TRD-AS1 on the progression of OSCC.
METHODS: The effects of c-Myc on LNC TRD-AS1 were detected. Expression of c-Myc and LNC TRD-AS1 in OSCC and paracancerous tissues. Dual luciferase reporter assay verified the binding of c-Myc to the promoter region of LNC TRD-AS1. The localization of LNC TRD-AS1 in OSCC was determined by nucleocytoplasmic isolation assay and RNA FISH experiments. The effects of overexpression, knockdown of LNC TRD-AS1 and rescue experiments on migration, metabolism, and proliferation of OSCC cells were observed by quantitative real-time polymerase chain reaction (qRT-PCR), western blots, scratch tests, Transwell assays, medium color and pH changes, ATP measurement, CCK-8 assays, and colony formation assays.
RESULTS: It was found that c-Myc positively regulated the expression of LNC TRD-AS1 in OSCC cell lines and tissues. The binding of c-Myc to the LNC TRD-AS1 promoter region was verified by dual-luciferase reporter assays. Both nucleoplasmic separation assays and RNA FISH showed that LNC TRD-AS1 was localized to the nuclei in OSCC cells. Overexpression of LNC TRD-AS1 promoted migration, metabolism and proliferation in OSCC cell lines, while knockdown had the opposite effect.
CONCLUSION: c-Myc positively regulated LNC TRD-AS1 in OSCC. LNC TRD-AS1 affected the migration, proliferation and metabolism of OSCC by affecting the tumor acid metabolism.