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. 2024 Feb 12;19(1):88.
doi: 10.1186/s13019-024-02507-2.

Regulation of overexpression lncRNA ATP2B1-AS1 on lung adenocarcinoma progression

Affiliations

Regulation of overexpression lncRNA ATP2B1-AS1 on lung adenocarcinoma progression

Shiyi Chen et al. J Cardiothorac Surg. .

Abstract

Background: LncRNA ATP2B1-AS1 (ATP2B1-AS1) is involved in the occurrence and development of various diseases, while the relationship between lung adenocarcinoma (LUAD) and ATP2B1-AS1 is unclear. This study was to investigate the expression of ATP2B1-AS1 in LUAD and its influence on survival and prognosis of patients.

Methods: LUAD tissue samples from patients participating in this study were collected, and the expression levels of ATP2B1-AS1 and miR-141-3p in LUAD sampleswere detected by real-time quantitative polymerase chain reaction (RT-qPCR). The effect of ATP2B1-AS1 on the growth of A549 cells was investigated through cell counting kit-8 (CCK-8) and transwell experiments. Besides, the prognostic value of ATP2B1-AS1 in LUAD was assessed via Kaplan-Meier curve and multivariate Cox regression.

Results: ATP2B1-AS1 was downregulated in LUAD tissues and cells, whereas miR-141-3p was upregulated. After pcDNA3.1-ATP2B1-AS1 was transfected into A549 cells, the proliferation ability of A549 cells was decreased, and the migration level and invasion of A549 cells were also inhibited. High expression of ATP2B1-AS1 sponge miR-141-3p exerted prognostic value.

Conclusions: ATP2B1-AS1 sponge miR-141-3p alleviated the progression of LUAD, and ATP2B1-AS1 may be deemed as a prognostic marker for LUAD.

Keywords: Lung adenocarcinoma; Prognosis; Progression; lncRNA ATP2B1-AS1; miR-141-3p.

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Conflict of interest statement

The authors declare no competing interests.

Figures

Fig. 1
Fig. 1
LncRNA ATP2B1-AS1 was down-regulated in LUAD. (A) Compared with normal tissues, ATP2B1-AS1 was decreased in LUAD tissues. (B) Low expression of ATP2B1-AS1 in A549, H1792, NCI-H650 and NCI-H23 cells. ***P < 0.001
Fig. 2
Fig. 2
LncRNA ATP2B1-AS1 delayed the malignant progression of LUAD. (A) The level of ATP2B1-AS1 in A549 cells increased after transfection. (B) The CCK8 results of transfected A549 cells. (C) and (D) pcDNA3.1-ATP2B1 -AS1 attenuated the migratory and invasive abilities of A549 cells. ***P < 0.001
Fig. 3
Fig. 3
The mechanism of ATP2B1-AS1 sponged miR-141-3p. (A) ATP2B1-AS1 may interact with miR-141-3p. (B) Detection of luciferase activity in A549 cells. (C) and (D) The expression of miR-141-3p was increased in LUAD tissues and A549 cells. (E) ATP2B1-AS1 was negatively correlated with downstream miR-141-3p (r = -0.5562, P < 0.0001). ***P < 0.001
Fig. 4
Fig. 4
The expression of ATP2B1-AS1 predicted poor prognosis in LUAD patients. The Kaplan-Meier method suggested that the high expression of ATP2B1-AS1 was more conducive to the survival of patients (Log-Rank P = 0.024)

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