Background: A hormonal role in the development of non-small cell lung cancer (NSCLC) has been well documented, and the classic estrogen receptors (ERs)-ERα and ERβ have been extensively investigated over the past decade. The expression of ERβ was found to be high and display biological activity in NSCLC, but anti-estrogen therapy targeting this receptor has shown limited efficacy for the disease. The third estrogen receptor, G protein-coupled estrogen receptor 1 (GPER1/GPR30), was recently found to be highly expressed in NSCLC. Herein, we aimed to investigate the expression profile of GPER1 and correlate it with clinicopathological factors as well as postoperative prognosis in NSCLC. Methods:We examined GPER1 and ERβ expression using immunohistochemistry among 183 NSCLC cases, including 132 lung adenocarcinoma (LUAD) with identified epidermal growth factor receptor (EGFR) mutation status and 51 squamous cell carcinoma (SCC) patients. We then conducted correlation analysis between the expression of GPER1 and clinicopathological factors and patients' postoperative prognosis.Results: Positive expression of GPER1 was categorized into 2 main classes: nuclei-GPER1 (nGPER1) and concurrent nuclei-and cytoplasm-GPER1 (n/cGPER1), according to its subcellular localization. The LUAD with wild-type EGFR (wt-EGFR) had a higher frequency of n/cGPER1 (50%) but a lower frequency of nGPER1 (31%) when compared with those with mutated EGFR (n/cGPER1: 31%, nGPER1: 41%, respectively). The expression of GPER1, regardless of subcellular localization, was positively correlated with tumor stage and lymph node metastasis. The median recurrence-free survival (mRFS) and overall survival (OS) were significantly worse in participants with n/cGPER1 expression than in those with nGPER1 or without GPER1 expression.Conclusions: This study revealed that GPER1 is aberrantly highly expressed and presents a unique GPER1 expression profile in NSCLC. The n/cGPER1 expression was significantly associated with EGFR mutation status, tumor stage, lymph node metastasis, and poor postoperative prognosis in NSCLC.
Long non coding RNA FOXP4‐AS1 exerted crucial functions in various human cancers, while its role in non‐small cell lung cancer (NSCLC) remains unclear. A total of 30 pairs of NSCLC tissues and matched adjacent normal tissues were used to evaluate the expression of FOXP4‐AS1 and miR‐3184‐5p. Cell proliferation was assessed by CCK‐8 assay and colony formation assay. Cell apoptosis was measured by flow cytometry. Bioinformatic analysis and luciferase reporter assay were performed to determine the regulatory relationship among FOXP4‐AS1, miR‐3184‐5p and EIF5A. The xenograft tumor model was constructed to confirm the function of FOXP4‐AS1 in NSCLC progression. The results showed that FOXP4‐AS1 was upregulated and miR‐3184‐5p was downregulated in NSCLC tissues and cell lines. Downregulation of FOXP4‐AS1 significantly reduced cell proliferation and induced apoptosis of NSCLC cells in vitro. FOXP4‐AS1 could regulated the expression of EIF5A by binding to miR‐3184‐5p. Rescue experiments showed that downregulation of miR‐3184‐5p or overexpression of EIF5A obviously attenuated the inhibitory effects of si‐FOXP4‐AS1 on cell proliferation, as well as the stimulating effects on cell apoptosis. Moreover, knockdown of FOXP4‐AS1 could efficiently inhibited tumor development of NSCLC in vivo. Downregulation of FOXP4‐AS1 attenuated the progression of NSCLC by regulating miR‐3184‐5p and EIF5A.
Lung adenocarcinoma (LUAD) is one of the major causes of cancer death in the world. Studies show that the effective anticancer component in blister beetles is cantharidin, which can improve chemotherapy efficacy, median survival, and prognosis of LUAD. However, the antitumor mechanism of blister beetles has not been fully clarified. This study aimed to identify the key targets of the treatment of LUAD by blister beetles based on the principle of network pharmacology. An integrated approach including network pharmacology and a molecular docking technique was conducted, which mainly comprises target prediction, weighted gene correlation network analysis (WGCNA) analysis, network construction, gene ontology, and pathway enrichment analysis. 35 key targets were obtained and significantly associated with response to external stimuli, collagen binding, cyclin binding, organic acid binding, pyruvate metabolism, glycolysis, and amino acid biosynthesis pathways. Both LASSO regression and the RF model had a high predictive ability, and 9 candidate genes were screened, among which BIRC5 and PLK1 were the key targets for the treatment of LUAD by using blister beetles and showed significant survival significance. Cantharidin exerts its antitumor effects through 8 targets in 32 pathways, while BIRC5 and PLK1 have obvious survival significance.
Objective: The aim of our study was to investigate the expression of Survivin in lung adenocarcinoma of Xuanwei and Kunming patients. Methods: Twenty-five specimens of Xuanwei patients and 28 specimens of Kunming patients were observed and analyzed. The Survivin expression was detected by immunohistochemistry. The results were quantitatively analyzed by image analysis system. Results: There were significant differences in Survivin expression (P < 0.01) between Xuanwei patients and Kunming patients. Conclusion: Survivin expression in lung adenocarcinoma of Xuanwei patients was significantly higher than that of Kunming patients. The pathogenesis of lung adenocarcinoma might be different between Xuanwei patients and Kunming patients. High Survivin expression might be one of the reasons to explain high incidence of lung cancer in Xuanwei.
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