Posted: Monday, January 23, 2023
According to Xu et al, of the First Affiliated Hospital, Hengyang Medical School, University of South China, and colleagues, the role of long noncoding RNA nuclear-enriched abundant transcript 1 (NEAT1) in tumorigenesis of bladder cancer is poorly understood. To further elucidate the mechanism of NEAT1, the investigators modulated the microRNA (miR)-101/VEGF-C pathway to provide insight into the potential therapeutic applications of these RNAs in bladder cancer. This study was published in BMC Urology.
“Comparison with the normal tissues indicated that NEAT1 was upregulated in bladder cancer and was associated with an unfavorable prognosis,” mentioned the study authors. “In addition, we demonstrated that NEAT1 promoted the malignant development of bladder cancer cells.”
The investigators retrospectively reviewed the records of 60 patients diagnosed with bladder cancer undergoing surgical resection. Tumor samples and adjacent healthy tissue were collected for use in the experimental and control groups, respectively, and evaluated for NEAT1, miR-101, and VEGF-C using quantitative real time-polymerase chain reaction. In vitro experiments to determine the impact of NEAT1 on bladder cancer cell behavior were carried out with human bladder cancer cell lines T24 and 5637.
NEAT1 and VEGF-C were expressed at high levels compared with respective levels in normal tissues, whereas miR-101 was significantly downregulated. Consequently, the upregulation of NEAT1 was associated with poorer recurrence-free survival, and the downregulation of miR-101 suggested it was a target of NEAT1. Heightened expression of NEAT1 was also observed to promote the migration, proliferation, and invasion of bladder cancer cells.
Furthermore, miR-101 overexpression in T24 and 5637 cells appeared to downregulate VEGF-C levels, and miR-101 deletion facilitated VEGF-C expression. As such, miR-101 repressed the protein and messenger RNA levels of VEGF-C in bladder cancer cells. Of note, miR-101 upregulation seemed to reverse the promoting effects of NEAT1, and miR-101 inhibition heightened the effects of NEAT1.
Disclosure: The study authors reported no conflicts of interest.