Abstract
Background ANLN and miR-30a-5p may be involved in the progression of lung adenocarcinoma (LUAD). However, their underlying mechanism in LUAD has not been completely comprehended. Methods Differential expression analysis, binding site prediction, and survival analysis were conducted by bioinformatics approaches. ANLN mRNA and miR-30a-5p expression were detected by qRT-PCR. ANLN protein expression was detected by western blot. Cell behaviors in LUAD were examined by functional experiments. Results ANLN was activated in LUAD cells in terms of mRNA and protein. High ANLN level was positively correlated with poor prognosis. Enforced ANLN stimulated protumorigenesis LUAD cell behaviors. miR-30a-5p could target ANLN mRNA, as revealed and verified through assays. Remarkably low miR-30a-5p expression was observed in LUAD cells, and it could repress ANLN expression. The accelerated cell behaviors by overexpression of ANLN were counteracted by upregulating miR-30a-5p. Conclusion Overall, miR-30a-5p remarkably restrained the malignant progression of LUAD cells by constraining ANLN expression. Thus, ANLN and miR-30a-5p could be novel therapeutic targets of LUAD.
Highlights
Lung cancer is an unbearably painful illness as well as a fetal tumor [1]
ANLN is aberrantly expressed in many cancers like cervical cancer [6], breast cancer [7], pancreatic cancer [8], prostatic cancer [9], and anaplastic thyroid carcinoma [10]
Expression data of mRNAs downloaded from the TCGA-lung adenocarcinoma (LUAD) dataset indicated that the ANLN level in normal tissues was remarkably lower than that in LUAD tissues (Figure 1(b))
Summary
Lung cancer is an unbearably painful illness as well as a fetal tumor [1]. Missed diagnosis in its early-stage triggers poor prognosis of patients [2]. Activation of ANLN hastens epithelial-mesenchymal transition (EMT) of tumor cells [13]. ANLN and miR-30a-5p may be involved in the progression of lung adenocarcinoma (LUAD). Their underlying mechanism in LUAD has not been completely comprehended. ANLN mRNA and miR-30a-5p expression were detected by qRT-PCR. ANLN was activated in LUAD cells in terms of mRNA and protein. Enforced ANLN stimulated protumorigenesis LUAD cell behaviors. Low miR-30a-5p expression was observed in LUAD cells, and it could repress ANLN expression. The accelerated cell behaviors by overexpression of ANLN were counteracted by upregulating miR-30a-5p. MiR-30a-5p remarkably restrained the malignant progression of LUAD cells by constraining ANLN expression. ANLN and miR-30a-5p could be novel therapeutic targets of LUAD
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