Abstract
This paper aims to explore the lncRNA PROX1-AS1 effect on proliferation, migration, invasion, and apoptosis of lung cancer cells together with its targeted regulation on miR-1305. To adopt qRT-PCR to test PROX1-AS1 and miR-1305 expression levels in lung cancer tissues and adjacent tissues. Lung cancer cells A549 were cultured in vitro and randomly divided into several groups, which are si-NC, si-PROX1-AS1, miR-NC, miR-1305, si-PROX1-AS1 plus anti-miR-NC, and si-PROX1-AS1 plus anti-miR-1305. To adopt the CCK-8 method to test cell proliferation and to adopt the Transwell chamber experiment to test cell migration and invasion. To adopt the flow cytometry method to test the apoptosis rate. Through a dual luciferase experiment, we decided to find out the targeting relationship between PROX1-AS1 and miR-1305. Then we adopted the western blot method to test CyclinD1, MMP-2, MMP-9, Bcl-2, p21, and Bax expression levels. Compared with adjacent tissues (P < 0.05), the expression of PROX1-AS1 in lung cancer tissue was remarkably higher, while the expression of miR-1305 was remarkably lower (P < 0.05). After PROX1-AS1 knockdown expression or miR-1305 overexpression, cell activity, migration, and invasion ability were outstandingly lowered (P < 0.05), but the apoptosis rate was obviously raised (P < 0.05), CyclinD1, MMP-2, Bcl-2, and MMP-9 protein data were remarkably reduced (P < 0.05), but p21 and Bax protein conditions were outstandingly enhanced (P < 0.05). The dual luciferase experiment confirmed that PROX1-AS1 had a targeting relationship with miR-1305. After cotransfection with si-PROX1-AS1 and anti-miR-1305, the cell viability, migration and invasion ability were remarkably enhanced (P < 0.05), the apoptosis rate was remarkably reduced (P < 0.05), CyclinD1, MMP-2, Bcl-2, and MMP-9 protein were increased remarkably (P < 0.05), and p21 or Bax protein was lowered remarkably (P < 0.05). On the one hand, PROX1-AS1 can promote lung cancer proliferation, migration, and invasion. On the other hand, it may restrain apoptosis, possibly through inhibiting miR-1305 expression.
Highlights
Tumor cell metastasis and invasion lead to a decrease in the treatment effect and affect the prognosis of patients. erefore, related research about lung cancer occurrence and metastasis molecular mechanism is helpful to improve lung cancer diagnosis and treatment and improve the patient’s prognosis [1, 2]
As mentioned in the above paper, these results show that PROX1-AS1 expression levels in lung cancer tissues are elevated, suggesting that PROX1-AS1 may play an oncogene part in the development of lung cancer. is paper showed that the cell proliferation ability was significantly reduced by knocking down PROX1-AS1 expression in lung cancer cells
Studies have reported that CyclinD1 can positively regulate the generation cycle and improve cell-cell multiplication, while P21 does the opposite [14]. It suggests that PROX1AS1 knockdown expression may inhibit lung cancer proliferation through inducing cell cycle arrest. e results of this paper indicated that lung cancer cell migration and invasion ability were remarkably reduced after knocking miR-NC
Summary
Lung cancer is known as a common malignant tumor, and nonsmall cell lung cancer seems to be the main pathological type. Tumor cell metastasis and invasion lead to a decrease in the treatment effect and affect the prognosis of patients. Long noncoding RNA (lncRNA) is an endogenous noncoding RNA, which is not expressed normally in lung cancer cells and could regulate downstream microRNA (miRNA) to affect cell biological behavior [3–5]. Long noncoding RNA PROX1-AS1 (lncRNA PROX1-AS1) is upregulated in prostate cancer cells and can promote proliferation, migration, and invasion of prostate cancer cells [6]. MiR1305 expression decreased in cervical cancer cells, under the condition expression raising could restrain its proliferation, Journal of Healthcare Engineering migration, and invasion [7]. Whether PROX1-AS1 has an effect on lung cancer cell’s biological behavior through regulating miR-1305 expression is not yet known. Erefore, this paper mainly explores the influence of PROX1-AS1 on lung cancer migration, proliferation, invasion, apoptosis, and miR-1305 regulation, providing potential targets for lung cancer targeted therapy
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