Increased S100A15 expression and decreased DNA methylation of its gene promoter are involved in high metastasis potential and poor outcome of lung adenocarcinoma

Chen, Yung‐Che; Hsiao, Chang‐Chun; Zheng, Yixin; Chen, Kuang‐Den; Sung, Ming-Tse; Chen, Chung‐Jen; Wang, Ting‐Ya; Lin, Yann-Sheng; Chang, Hsien‐Kun; Chang, Jen-Chieh

doi:10.18632/oncotarget.17391

Cited by 14 publications

(10 citation statements)

References 35 publications

(37 reference statements)

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“… 36 In contrast to hypermethylation, increased expression of S100A15 and reduced DNA methylation of its gene promoter have also been proved to be associated with high metastatic potential and poor prognosis of LUAD. 37 In this study, we demonstrated that the AGR2 promoter region was hypomethylated and AGR2 was highly expressed in LUAD cells through bioinformatics analysis and molecular experiments, which was consistent with studies of AGR2 promoter methylation in other cancers. Sung HY et al found that the promoter of AGR2 is hypomethylated and AGR2 is highly expressed in ovarian cancer cells.…”

Section: Discussionsupporting

confidence: 90%

Hypomethylation-Mediated AGR2 Overexpression Facilitates Cell Proliferation, Migration, and Invasion of Lung Adenocarcinoma

He¹,

Fu²,

Hu³

et al. 2021

CMAR

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Objective Studies have indicated that AGR2 is crucial in many cancers. However, its methylation level in lung adenocarcinoma (LUAD) is rarely known. Hence, the effect of AGR2 methylation on LUAD was explored in the study. Methods qRT-PCR was adopted to detect the expression of AGR2 in LUAD cells and normal lung cells. Methylation-specific PCR (MSP) was used to detect the methylation of AGR2 promoter region in different cell lines. MTT, Transwell and wound healing assays were used to verify the progression of cells in each transfection group. Results The expression of AGR2 was significantly up-regulated in LUAD cells relative to that in normal cells. Moreover, the expression of AGR2 was inversely modulated by DNA methylation, and the hypomethylation of CpG islands would lead to the increased expression of AGR2. Finally, overexpression and hypomethylation of AGR2 facilitated the proliferation, invasion and migration of LUAD cells. Conclusion These results demonstrated that hypomethylation of AGR2 promoter region promoted the expression of AGR2 in LUAD cells, thus promoting the progression of LUAD cells.

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Section: Discussionsupporting

confidence: 90%

Hypomethylation-Mediated AGR2 Overexpression Facilitates Cell Proliferation, Migration, and Invasion of Lung Adenocarcinoma

He¹,

Fu²,

Hu³

et al. 2021

CMAR

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“…PCNA is a key eukaryotic replication accessory factor that plays an important role in the cell cycle and apoptosis [63]. In addition, PCNA can promote LC progression [64]. CDK1 and CDK2 belong to the cyclin-dependent kinases (CDKs) family.…”

Section: Discussionmentioning

confidence: 99%

Mechanisms of Compound Kushen Injection for the Treatment of Lung Cancer Based on Network Pharmacology

Meng

Liu

et al. 2019

Evidence-Based Complementary and Alternative Medicine

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Background. Compound Kushen Injection (CKI) is a Chinese patent drug that shows good efficacy in treating lung cancer (LC). However, its underlying mechanisms need to be further clarified. Methods. In this study, we adopted a network pharmacology method to gather compounds, predict targets, construct networks, and analyze biological functions and pathways. Moreover, molecular docking simulation was employed to assess the binding potential of selected target-compound pairs. Results. Four networks were established, including the compound-putative target network, protein-protein interaction (PPI) network of LC targets, compound-LC target network, and herb-compound-target-pathway network. Network analysis showed that 8 targets (CHRNA3, DRD2, PRKCA, CDK1, CDK2, CHRNA5, MMP1, and MMP9) may be the therapeutic targets of CKI in LC. In addition, molecular docking simulation indicated that CHRNA3, DRD2, PRKCA, CDK1, CDK2, MMP1, and MMP9 had good binding activity with the corresponding compounds. Furthermore, enrichment analysis indicated that CKI might exert a therapeutic role in LC by regulating some important pathways, namely, pathways in cancer, proteoglycans in cancer, PI3K-Akt signaling pathway, non-small-cell lung cancer, and small cell lung cancer. Conclusions. This study validated and predicted the mechanism of CKI in treating LC. Additionally, this study provides a good foundation for further experimental studies and promotes the reasonable application of CKI in the clinical treatment of LC.

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“…In LUAD, many studies reported that gene DNA methylation was associated with cancer growth. For example, Chen et al (2017) found that decreased DNA methylation of S100A15 was involved in high metastasis of LUAD. Wang, Lu, Shen, Wu, and Zhao (2014) reported that the SAMHD1 promoter, highly methylated in LUAD, impeded SAMHD1 expression.…”

Section: Discussionmentioning

confidence: 99%

Methylation of CLEC14A is associated with its expression and lung adenocarcinoma progression

Shi

Che

et al. 2018

Journal Cellular Physiology

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Our main objective is probing the effect of methylation of CLEC14A on its expression and lung adenocarcinoma (LUAD) progression. Microarray analysis was utilized to screen out differentially downregulated genes with hypermethylation in LUAD tissues. The CLEC14A expression level was measured by western blot analysis and qRT-PCR. Methylation-specific-PCR was performed to evaluate methylation status of CLEC14A. The 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromid (MTT) assay was used to check the relation between CLEC14A expression and cell proliferation. Cell cycle, cell apoptosis, migration, and invasion were respectively detected by the flow cytometry assay, wound healing assay, and transwell assay. Tumor xenograft models were established for investigating the effect of CLEC14A on tumor formation. CLEC14A expression in LUAD tissues was impaired compared with that in adjacent tissues, and CLEC14A promoter was highly methylated in LUAD. Overexpressing CLEC14A or inhibiting the methylation level of CLEC14A in A549 and LTEP-a-2 cells impeded the duplication of LUAD cells, promoted apoptosis, attenuated cell migration, and invasion ability, and arrested cell cycle at the G0/G1 phase. Overexpression of CLEC14A inhibited tumorigenesis of LUAD cells in nude mice. The promoter of CLEC14A is methylated in LUAD, leading to downregulation of CLEC14A in LUAD. CLEC14A acts as an antitumor role in LUAD by suppressing cell proliferation, migration, invasion, promoting cell apoptosis, and reducing tumorigenicity in nude mice. Thus, the inhibition of CLEC14A methylation is a novel strategy for the clinic treatment of LUAD.

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Increased S100A15 expression and decreased DNA methylation of its gene promoter are involved in high metastasis potential and poor outcome of lung adenocarcinoma

Cited by 14 publications

References 35 publications

Hypomethylation-Mediated AGR2 Overexpression Facilitates Cell Proliferation, Migration, and Invasion of Lung Adenocarcinoma

Hypomethylation-Mediated AGR2 Overexpression Facilitates Cell Proliferation, Migration, and Invasion of Lung Adenocarcinoma

Mechanisms of Compound Kushen Injection for the Treatment of Lung Cancer Based on Network Pharmacology

Methylation of CLEC14A is associated with its expression and lung adenocarcinoma progression

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