RETRACTED: Potential of β-elemene induced ferroptosis through Pole2-mediated p53 and PI3K/AKT signaling in lung cancer cells

Gong, Zheng; Liu, Ze-Gang; Du, Kun-Yu; Wu, Jiang-hai; Yang, Na; Shu, Jing-Kui

doi:10.1016/j.cbi.2022.110088

Cited by 9 publications

(3 citation statements)

References 21 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, the molecular mechanisms of POLE2 on BLCA tumorigenesis are poorly understood, despite several studies that have recently shown different molecular regulation mechanisms of POLE2 in other cancers. POLE2 knockdown in lung cancer activates cellular iron-dependent ferroptosis by increasing the production of lipid ROS, MDA and iron content in cells through modulation of P53 expression or PI3K/AKT signaling [54]. In glioblastoma, POLE2 knockdown suppresses cell proliferation and metastasis by controlling AURKA (Aurora kinase A) to promote ubiquitination and reduce the stability of the tumor-promoting factor FOXM1 (forkhead transcription factor) [50].…”

Section: Discussionmentioning

confidence: 99%

Prognostic and chemotherapeutic response prediction by proliferation essential gene signature: Investigating POLE2 in bladder cancer progression and cisplatin resistance

Yu,

Lin,

et al. 2024

J. Cancer

View full text Add to dashboard Cite

Background: Bladder cancer (BLCA) is the most common genitourinary malignancy. Proliferation essential genes (PEGs) are crucial to the survival of cancer cells. This study aimed to build a PEG signature to predict BLCA prognosis and treatment efficacy. Methods: BLCA PEGs and differentially expressed PEGs were identified using DepMap and TCGA-BLCA datasets, respectively. Based on the prognostic analysis of the differentially expressed PEGs, a PEG model was constructed. Subsequently, we analyzed the relationship between the PEG signature and prognosis of BLCA patients as well as their response to chemotherapy. Finally, we performed random forest analysis to target and functional experiments to validate the most significant PEG which is associated with BLCA progression. CCK-8, invasion, migration, and chemosensitivity assays were performed to assess effects of gene knockdown on BLCA cell proliferation, invasion and migration abilities, and cisplatin chemosensitivity. Results: We screened 10 prognostic PEGs from 201 differentially expressed PEGs and used them to construct a PEG signature model. Patients with high PEG signature score (PEGs-high) exhibited worse OS and lower sensitivity to chemotherapy than those with PEGs-low. We also found significant correlations between the PEG score and previously defined BLCA molecular subtypes. This suggests that the PEG score may effectively predict the molecular subtypes which have distinct clinical outcomes. Random forest analysis revealed that POLE2 (DNA polymerase epsilon subunit 2) was the most significant PEG differentiating BLCA tissue and normal tissue. Bioinformatic analysis and an immunohistochemistry staining assay confirmed that POLE2 was significantly up-regulated in tumor tissues and was associated with poor survival in BLCA patients. Moreover, POLE2 knockdown inhibited the ability of cell clone formation, proliferation, invasion, immigration and IC50 of cisplatin. Conclusion:The PEG signature acts as a potential predictor for prognosis and chemotherapy response in BLCA patients. POLE2 is a key PEG and plays a remarkable role in promoting the malignant progression and cisplatin resistance of BLCA.

show abstract

Section: Discussionmentioning

confidence: 99%

Prognostic and chemotherapeutic response prediction by proliferation essential gene signature: Investigating POLE2 in bladder cancer progression and cisplatin resistance

Yu,

Lin,

et al. 2024

J. Cancer

View full text Add to dashboard Cite

show abstract

“…p53 inhibits tumor formation and protects DNA from damage by inducing cell cycle arrest, DNA repair or apoptosis. Inhibition of P53 has been shown to be associated with drug resistance and poor prognosis in lung cancer patients, and increased P53 expression improves the sensitivity of lung cancer cells to cisplatin treatment [ 52 ]. As a result, P53 is a key molecule in the regulation of chemoresistance in lung cancer cells.…”

Section: Discussionmentioning

confidence: 99%

Predictive Value of Gene Databases in Discovering New Biomarkers and New Therapeutic Targets in Lung Cancer

Liu

et al. 2023

Medicina

View full text Add to dashboard Cite

Background and Objectives: The molecular mechanisms of lung cancer are still unclear. Investigation of immune cell infiltration (ICI) and the hub gene will facilitate the identification of specific biomarkers. Materials and Methods: Key modules of ICI and immune cell-associated differential genes, as well as ICI profiles, were identified using lung cancer microarray data from the single sample gene set enrichment analysis (ssGSEA) and weighted gene co-expression network analysis (WGCNA) in the gene expression omnibus (GEO) database. Protein–protein interaction networks were used to identify hub genes. The receiver operating characteristic (ROC) curve was used to assess the diagnostic significance of the hub genes, and survival analysis was performed using gene expression profiling interactive analysis (GEPIA). Results: Significant changes in ICI were found in lung cancer tissues versus adjacent normal tissues. WGCNA results showed the highest correlation of yellow and blue modules with ICI. Protein–protein interaction networks identified four hub genes, namely CENPF, AURKA, PBK, and CCNB1. The lung adenocarcinoma patients in the low hub gene expression group showed higher overall survival and longer median survival than the high expression group. They were associated with a decreased risk of lung cancer in patients, indicating their potential role as cancer suppressor genes and potential targets for future therapeutic development. Conclusions: CENPF, AURKA, PBK, and CCNB1 show great potential as biomarkers and immunotherapeutic targets specific to lung cancer. Lung cancer patients’ prognoses are often foreseen using matched prognostic models, and genes CENPF, AURKA, PBK, and CCNB1 in lung cancer may serve as therapeutic targets, which require further investigations.

show abstract

“…The occurrence of this disease is closely associated with the mutation of the P53 oncogene which, under normal conditions, would induce cancer cells to produce ferroptosis, ie, mutated P53 can inhibit ferroptosis in lung carcinogenesis so that cancer cells avoid cell death. 112 In the process of lung cancer development, it has been found that lung cancer tissues highly express ferritin, but it remains to be established whether this represents the underlying mechanism through which lung cancer cells avoid ferroptosis. In terms of classification, lung cancer is typically divided into two types, namely small cell lung cancer and non-small cell lung cancer, with both representing 15% and 85% of total cases, respectively.…”

Section: Ferroptosis In Respiratory Diseasesmentioning

confidence: 99%

Unraveling the Molecular Regulation of Ferroptosis in Respiratory Diseases

Zhu,

Zhou,

et al. 2024

JIR

View full text Add to dashboard Cite

Ferroptosis, a type of programmed cell death that relies on iron, is distinct in terms of its morphological, biochemical and genetic features. Unlike other forms of cell death, such as autophagy, apoptosis, necrosis, and pyroptosis, ferroptosis is primarily caused by lipid peroxidation. Cells that die due to iron can potentially trigger an immune response which intensifies inflammation and causes severe inflammatory reactions that eventually lead to multiple organ failure. In recent years, ferroptosis has been identified in an increasing number of medical fields, including neurological pathologies, chronic liver diseases and sepsis. Ferroptosis has the potential to cause an inflammatory tempest, with many of the catalysts and pathological indications of respiratory ailments being linked to inflammatory reactions. The growing investigation into ferroptosis in respiratory disorders has also garnered significant interest to better understand the mechanism of ferroptosis in these diseases. In this review, the recent progress in understanding the molecular control of ferroptosis and its mechanism in different respiratory disorders is examined. In addition, this review discusses current challenges and prospects for understanding the link between respiratory diseases and ferroptosis.

show abstract

RETRACTED: Potential of β-elemene induced ferroptosis through Pole2-mediated p53 and PI3K/AKT signaling in lung cancer cells

Cited by 9 publications

References 21 publications

Prognostic and chemotherapeutic response prediction by proliferation essential gene signature: Investigating POLE2 in bladder cancer progression and cisplatin resistance

Prognostic and chemotherapeutic response prediction by proliferation essential gene signature: Investigating POLE2 in bladder cancer progression and cisplatin resistance

Predictive Value of Gene Databases in Discovering New Biomarkers and New Therapeutic Targets in Lung Cancer

Unraveling the Molecular Regulation of Ferroptosis in Respiratory Diseases

Contact Info

Product

Resources

About