Objective: To investigate the expression characteristics of long noncoding ribonucleic acid (lncRNA) lnc01614 in gastric cancer, so as to further investigate its roles in the occurrence and development of gastric cancer and its potential regulatory mechanism.
Patients and methods: Quantitative Real-time polymerase chain reaction (qRT-PCR) was used to detect the expression levels of lnc01614 in 79 pairs of gastric cancer tissues and normal adjacent tissues. The correlations of lnc01614 expression with pathological parameters of gastric cancer and prognoses of patients were also analyzed. QRT-PCR was employed to further verify the expression of lnc01614 in gastric cancer cells. Lnc01614 knockdown expression models were established using small interfering RNA (siRNA) in gastric cancer cell strains (SGC-7901 and AGS). The effect of lnc01614 on the biological function of gastric cancer cells was analyzed by Cell Counting Kit-8 (CCK-8) and transwell invasion and migration assay. Lastly, Western blotting was performed to explore its potential mechanism.
Results: The results of qRT-PCR showed that the expression of lnc01614 in gastric cancer tissues was significantly higher than that in normal tissues. Compared with patients with low expression of lnc01614, patients with high expression of lnc01614 had higher tumor staging, greater lymph node metastasis and distant metastasis rates, and lower overall survival rate. In comparison with the negative control si-NC group, cell proliferation, invasion and migration abilities in lnc01614 knockdown expression group (si-lnc01614) were significantly decreased. Western blotting results indicated that si-lnc01614 group exhibited increased E-cadherin expression, and significantly reduced vimentin and snail expression.
Conclusions: Lnc01614 was upregulated in gastric cancer and significantly correlated with gastric cancer staging, lymph node metastasis, distant metastasis and poor prognosis. Lnc01614 may promote the proliferation, invasion and migration capabilities of gastric cancer through the regulation of epithelial-mesenchymal transition (EMT) pathway.