Identification of potential biomarkers for lung adenocarcinoma

Sayeeram, Deepak; Katte, Teesta; Bhatia, Saloni; Kumar, Anushree; Kumar, Avinesh; Jayashree, G.; Rachana, D.S.; Reddy, Harsha Vardhan; Rasalkar, Avinash Arvind; Malempati, Rajya Lakshmi; S, Divijendra Natha Reddy

doi:10.1016/j.heliyon.2020.e05452

Cited by 10 publications

(6 citation statements)

References 38 publications

(35 reference statements)

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“…Lung adenocarcinoma is one of the most common pathologic types in NSCLC, accounting for about 40-50% of NSCLC cases (2). In recent years, there have been many studies on NSCLC that have developed many new markers with diagnostic value (3)(4)(5), as well as new therapies. Unfortunately, the overall 5-year survival rate of NSCLC is still as low as 16% (2).…”

Section: Introductionmentioning

confidence: 99%

Down-regulation of FBP1 in lung adenocarcinoma cells promotes proliferation and invasion through SLUG mediated epithelial mesenchymal transformation

Wang¹,

He²,

Lv³

et al. 2023

Transl Cancer Res

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Background: Metabolic reprogramming and epithelial-mesenchymal transformation (EMT) play an important role in lung cancer. In recent studies, metabolic enzymes such as Fructose-1,6-bisphosphatase 1 (FBP1) have shown potential functions beyond regulating metabolism.Methods: Western blot assay was performed to detect glycolysis-related and EMT-related protein expression levels. The glucose uptake kit and adenosine triphosphate (ATP) detection kit were used to detect glucose uptake rate and ATP content. Transwell assay was used to determine the invasiveness of lung adenocarcinoma cells. Wound healing assay was used to determine the metastatic ability of lung adenocarcinoma cells. Methyl thiazolyl tetrazolium (MTT) assay and EdU staining were performed to investigate the effect of FBP1 overexpression on lung adenocarcinoma proliferation.Results: Overexpression of FBP1 down-regulated glycolysis-related protein levels and inhibited glucose uptake and ATP production, while knockdown of FBP1 had the opposite effect. Overexpression of FBP1 reversed EMT and inhibited Slug expression. Meanwhile, overexpression of FBP1 impaired the invasion, metastasis and proliferation ability of lung adenocarcinoma cells. In contrast, FBP1 knockdown promoted the EMT process, up-regulated Slug expression and enhanced the invasion, metastasis and proliferation of lung adenocarcinoma cells.Conclusions: Therefore, FBP1 can be used as one of the potential clinical targets through inhibiting glycolysis, cell invasion and proliferation by inhibiting Slug mediated EMT processes.

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Section: Introductionmentioning

confidence: 99%

Down-regulation of FBP1 in lung adenocarcinoma cells promotes proliferation and invasion through SLUG mediated epithelial mesenchymal transformation

Wang¹,

He²,

Lv³

et al. 2023

Transl Cancer Res

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“… 7 , 8 , 9 , 10 A previous bioinformatic study revealed that ZNF687 may be highly expressed in LUAD. 11 We previously found that ZNF687 may act as a transcription factor of oncogene cyclin‐dependent kinase regulatory subunit 2 (CKS2) via informatic analysis and luciferase assay (Li MC, unpublished data). Nevertheless, ZNF687 function and mechanism in LUAD remain unclear.…”

Section: Introductionmentioning

confidence: 99%

“…Recent studies indicate that ZNF687, which is elevated and mutated in giant cell tumors, hepatocellular carcinoma (HCC), acute myeloid leukemia, and bone cancer, has an oncogenic function in cancer 7–10 . A previous bioinformatic study revealed that ZNF687 may be highly expressed in LUAD 11 . We previously found that ZNF687 may act as a transcription factor of oncogene cyclin‐dependent kinase regulatory subunit 2 (CKS2) via informatic analysis and luciferase assay (Li MC, unpublished data).…”

Section: Introductionmentioning

confidence: 99%

Oncogenic zinc finger protein ZNF687 accelerates lung adenocarcinoma cell proliferation and tumor progression by activating the PI3K/AKT signaling pathway

Liu

Hou

et al. 2023

Thoracic Cancer

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Background Zinc finger protein 687 (ZNF687) has previously been discovered as a potential oncogene in individuals with giant cell tumors of the bone, acute myeloid leukemia, and hepatocellular carcinoma. However, its role and mechanism in lung adenocarcinoma (LUAD) remain unclear. Methods In LUAD cells, tumor, and matched adjacent tissue specimens, quantitative real‐time RT‐ polymerase chain reaction (qRT‐PCR), western blotting analyses, and immunohistochemistry staining (IHC) were conducted. Cell counting kit‐8 (CCK8) assay, clonogenicity analysis, flow cytometry, and transwell assays were utilized to detect ZNF687 overexpression and knockdown impacts on cell growth, colony formation, cell cycle, migration, and invasion. Bioinformatic studies, qRT‐PCR and western blotting studies were employed to validate the underlying mechanisms and signaling pathways implicated in the oncogenic effect of ZNF687. Results This study demonstrated that ZNF687 expression was elevated in LUAD cells and tissues. Individuals with upregulated ZNF687 had a poorer prognosis than those with downregulatedZNF687 ( p < 0.001). ZNF687 overexpression enhanced LUAD growth, migration, invasion and colony formation, and the cell cycle G1‐S transition; additionally, it promoted the epithelial‐mesenchymal transition (EMT). In contrast, knocking down ZNF687 showed to have the opposite impact. Moreover, these effects were associated with the activity of the phosphatidylinositol 3‐kinase (PI3K)/protein kinase B (AKT) signaling mechanism. Conclusion ZNF687 was upregulated in LUAD, and high ZNF687 expression levels are associated with poor prognoses. The activation of the PI3K/AKT signaling pathway by upregulated ZNF687 increased the proliferation of LUAD cells and tumor progression. ZNF687 may be a beneficial predictive marker and a therapeutic target in LUAD.

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“…Since genetic alterations may precede obvious histopathological alterations in cancer detection, the construction of a novel biomarker which can stratify patients with LUAD at an early stage, and direct treatment for LUAD is urgently needed. In recent years, for LUAD and non-small cell lung cancer, constructing new tumor biomarkers is a trend and has achieved significant results (20)(21)(22)(23).…”

Section: Introductionmentioning

confidence: 99%

A cuproptosis-related lncRNAs risk model to predict prognosis and guide immunotherapy for lung adenocarcinoma

Li¹,

Wang²,

Zhu³

et al. 2023

Ann Transl Med

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Background Cuproptosis, one of the newest forms of cell death induction, is attracting mounting attention. However, the role of cuproptosis in lung cancer is currently unclear. In this study, we constructed a prognostic signature utilizing cuproptosis-related long noncoding RNAs (CRL) in lung adenocarcinoma (LUAD) and researched its clinical and molecular function. Methods RNA-related and clinical data were downloaded from The Cancer Genome Atlas (TCGA) database. Differentially expressed CRLs were screened using the ‘limma’ package of R software. We used coexpression analysis and univariate Cox analysis to further identify prognostic CRLs. Applying least absolute shrinkage and selection operator (LASSO) regression and Cox regression models, a prognostic risk model based on 16 prognostic CRLs was constructed. To validate prognostic CRL function in LUAD, vitro experiments were conducted to explore the expression of GLIS2-AS1, LINC01230, and LINC00592 in LUAD. Subsequently, according to a formula, patients in the training, test, and overall groups were split into high- and low-risk groups. Kaplan-Meier and receiver operating characteristic (ROC) analyses were applied to assess the predictability of the risk model. Finally, the associations between risk signature and immunity-related analysis, somatic mutation, principal component analysis (PCA), enriched molecular pathways, and drug sensitivity was investigated. Results A cuproptosis-related long noncoding RNAs (lncRNAs) signature was constructed. Using quantitative polymerase chain reaction (qPCR) trial, we verified that the expressions of GLIS2-AS1, LINC01230, and LINC00592 in LUAD cell lines and tissues were consistent with the above screening results. Based on this signature, a total of 471 LUAD samples from TCGA data set were split into two risk groups based on the computed risk score. The risk model showed a better capacity in predicting prognosis than traditional clinicopathological features. Moreover, significant differences were found in immune cell infiltration, drug sensitivity, and immune checkpoint expression between the two risk groups. Conclusions The CRLs signature was shown to be a prospective biomarker to forecast prognosis in patients with LUAD and presents new insights for personalized treatment of LUAD.

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Identification of potential biomarkers for lung adenocarcinoma

Cited by 10 publications

References 38 publications

Down-regulation of FBP1 in lung adenocarcinoma cells promotes proliferation and invasion through SLUG mediated epithelial mesenchymal transformation

Down-regulation of FBP1 in lung adenocarcinoma cells promotes proliferation and invasion through SLUG mediated epithelial mesenchymal transformation

Oncogenic zinc finger protein ZNF687 accelerates lung adenocarcinoma cell proliferation and tumor progression by activating the PI3K/AKT signaling pathway

A cuproptosis-related lncRNAs risk model to predict prognosis and guide immunotherapy for lung adenocarcinoma

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