LncRNA SAMD12-AS1 down-regulates P53 to promote malignant progression of glioma.

OBJECTIVE

To study the expression level of long non-coding RNA (LncRNA) SAMD12-AS1 in glioma and its influence on the invasive ability of glioma cells; meanwhile, the regulation mechanism of LncRNA SAMD12-AS1 promoting the development of glioma was further explored.

PATIENTS AND METHODS

The expression level of SAMD12-AS1 in 40 pairs of tumor tissue specimens and paracancerous ones collected from glioma patients were examined through Real Time quantitative-Polymerase Chain Reaction (qRT-PCR) method, and the interplay between SAMD12-AS1 expression and clinical indicators of glioma patients was also analyzed. Meanwhile, the expression of SAMD12-AS1 in glioma cell lines was further verified by qRT-PCR. In addition, SAMD12-AS1 knockdown model was constructed using glioma cell lines (T98-G and U87). Cell Counting Kit-8 (CCK-8), cell wound healing test, and transwell assays were conducted to examine the impact of SAMD12-AS on glioma cell functions. Additionally, whether it exerted its biological characteristics through P53 was finally explored.

RESULTS

qPCR results in the study revealed that SAMD12-AS1 expression in tumor tissue specimens of glioma patients was remarkably higher than that in the adjacent ones, and the difference was statistically significant. Compared with patients with low expression of SAMD12-AS1, patients with high expression of SAMD1-AS1 had a higher incidence of lymph node or distant metastasis. In addition, compared to the NC group, knocking down SAMD12-AS1 markedly attenuated the proliferation rate, as well as the invasiveness and migration ability of glioma cells. Subsequently, in glioma tissues, it was verified that P53 expression was remarkably decreased and negatively correlated with SAMD12-AS1. Finally, cell recovery experiment also demonstrated that there may exist a mutual regulation between SAMD12-AS1 and P53, which then together affected the malignant progression of glioma.

CONCLUSIONS

LncRNA SAMD12-AS1 may accelerate the invasion and migratory capacities of glioma cells by modulating P53, and its expression was confirmed to be significantly relevant to the incidence of lymph node or distant metastasis.