PAQR3 Inhibits Non-small Cell Lung Cancer Growth by Regulating the NF-κB/p53/Bax Axis

Guo, Qiang; Ke, Xixian; Fang, Shixu; Gao, Wen; Song, Yimin; Chen, Cheng; Lu, Haojie; Xu, Gang

doi:10.3389/fcell.2020.581919

Cited by 18 publications

(22 citation statements)

References 35 publications

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“…With receiving more and more attention, an increasing number of key proteins have been identified in ALL 8–11 . PAQR3 has been uncovered to be a critical regulator into various cancers 15–18 . In particular, researchers found PAQR3 affect leukemic cells proliferation and apoptosis, 19 nevertheless, its role and relevant regulatory mechanism in ALL keeps unknown.…”

Section: Discussionmentioning

confidence: 99%

“…PAQR3 is one member of the PAQR family, a newly discovered tumor suppressor, and takes part in a variety of biological processes 13,14 . For instance, PAQR3 modulates the NF‐κB/p53/Bax axis to suppress non‐small‐cell lung cancer progression 15 . Furthermore, PAQR3 suppresses glioma progression by inactivating PI3K/Akt pathway 16 .…”

Section: Introductionmentioning

confidence: 99%

“… 13 , 14 For instance, PAQR3 modulates the NF‐κB/p53/Bax axis to suppress non‐small‐cell lung cancer progression. 15 Furthermore, PAQR3 suppresses glioma progression by inactivating PI3K/Akt pathway. 16 MiR‐15b/PAQR3 axis contributes to breast cancer progression.…”

Section: Introductionmentioning

confidence: 99%

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PAQR3 inhibits proliferation and aggravates ferroptosis in acute lymphoblastic leukemia through modulation Nrf2 stability

Jin

Tong

2021

Immunity Inflam & Disease

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Introduction Acute lymphoblastic leukemia (ALL) is a usual hematological tumor, which was featured by malignant proliferation of lymphoid progenitor cells. Many important factors participate into the regulation of ALL, including proteins. PAQR3 (also named RKTG) has been proved to take part in many human cancers by acting as a tumor suppressor. PAQR3 has bee n shown to repress human leukemia cells proliferation and induce cell apoptosis, but its role and relevant regulatory mechanism on cell proliferation and ferroptosis in ALL needs more exploration. Methods The genes expression was detected through quantitative reverse transcription polymerase chain reaction (mRNA) or western blot (protein). The cell proliferation was assessed through Cell Counting Kit‐8 and 5‐ethynyl‐2‐deoxyuridine assays. The levels of MDA, DCF, and intracellular free Fe in ALL cells were tested through the commercial kits. The cell apoptosis was determined through flow cytometry analysis. The binding ability of PAQR3 and nuclear factor erythroid 2‐related factor 2 (Nrf2) was verified through pull down assay. Results PAQR3 expression was firstly assessed in ALL patients and cell lines, and discovered to be downregulated. It was verified that PAQR3 suppressed ALL cells proliferation. Further experiments proved that PAQR3 aggravates ferroptosis in ALL. In addition, AQR3 bound with Nrf2, and modulated its expression through ubiquitination in ALL. Finally, through rescue assays, it was demonstrated that Nrf2 overexpression reversed the effects of PAQR3 on cell proliferation and ferroptosis. Conclusion Findings from our work uncovered that PAQR3 inhibited proliferation and aggravated ferroptosis in ALL through modulation Nrf2 stability. This study suggested that PAQR3 may serve as an effective biological marker for ALL treatment.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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PAQR3 inhibits proliferation and aggravates ferroptosis in acute lymphoblastic leukemia through modulation Nrf2 stability

Jin

Tong

2021

Immunity Inflam & Disease

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“…Giemsa dye A was added in each well for 5 min and continued to be stained with dye B for 15 min. 19 The images were scanned with a microscope. The clone count was calculated.…”

Section: Methodsmentioning

confidence: 99%

Circular RNA CircCDYL Regulates Proliferation and Apoptosis in Non-Small Cell Lung Cancer Cells by Sponging miR-185-5p and Upregulating TNRC6A

Bian¹,

Xue²,

Wang³

et al. 2021

CMAR

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A series of research reveal that circular RNA (circRNA) plays a vital role in regulating the development of tumor cells. In this research, we would explore the role and mechanism of circCDYL in non-small cell lung cancer (NSCLC). Methods: RT-PCR was performed to detect the expression of circCDYL in NSCLC tissues, plasma, and cell lines. The tumor cell proliferation ability was evaluated by clone formation assay, and cell cycle determination. Flow cytometry was used to detect apoptosis in NSCLC cell lines. Western blot and RT-PCR were used to assess the expression of proteins and genes. Luciferase assay was performed to confirm the relationship of circRNA-miRNA-mRNA.Results: The decreased level of circCDYL was observed in NSCLC patients' tissues and plasma, which was also downregulated in NSCLC cell lines. Forced expression of circCDYL inhibited cell viability, proliferation and induced apoptosis in A549 cells. Luciferase assay verified that circCDYL could bind with miR-185-5p and confirmed that TNRC6A was a downstream target of miR-185-5p. Overexpression of miR-185-5p or silencing of TNRC6A could inhibit the anti-tumor effect of circCDYL in A549 cells via regulating the ERK1/2 signal. Conclusion: Here, we revealed that circCDYL inhibited proliferation and induced apoptosis in NSCLC cell lines via regulating ERK1/2 signal, and the mechanism of this progression may target miR-185-5p/TNRC6A, which provided a theoretical basis for clinical therapy.

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“…Gene Set Enrichment Analysis (GSEA) was commonly used to evaluate the signaling mechanisms involved in influencing factors. In this study, we divided the TCGA NSCLC gene expression data into high-and low-risk groups based on the median value of risk scores, and the signaling mechanisms involved in the high-and low-risk groups were explored via the GSEA (13). The program was run for 1,000 cycles, and nominal P value (NOM P) <0.05 was used as the screening criterion.…”

Section: The Signaling Mechanisms Of the Risk Modelmentioning

confidence: 99%

Evaluation of the roles and regulatory mechanisms of PD-1 target molecules in NSCLC progression

Zhang¹,

Yao

Zhang

et al. 2021

Ann Transl Med

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Background: Targeted programmed cell death protein 1 (PD-1) therapy could effectively improve the long-term prognosis of patients with non-small cell lung cancer (NSCLC). The role of PD-1 targets in the progression of NSCLC has not been fully revealed. Methods:The differentially expressed genes (DEGs) in patients' blood after NSCLC treatment with PD-1 blocker nivolumab in the GSE141479 dataset were analyzed by GEO2R and identified in the TCGA database. The mechanism of action involved in the PD-1 target molecules via the Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG). The protein-protein interaction (PPI) network shows the relationship between PD-1 target molecules. The factors affecting the prognosis of NSCLC patients were identified via the COX regression analysis and survival analysis to build the risk model and nomogram. Results: There were 64 DEGs in patients' blood after nivolumab treatment and 48 DEGs in NSCLC tissues. The PD-1 target molecules involved cell proliferation, DNA replication, cell cycle, lung cancer, and other cellular processes. The prognostic factors CCNA2, CHEK1, DLGAP5, E2F8, FOXM1, HIST1H2BH, HJURP, MKI67, PLK1, TPX2, and TYMS, and the independent factors HIST1H2BH and PLK1, influenced the prognosis of NSCLC patients. HIST1H2BH and PLK1 were overexpressed in LUAD and LUSC tissues. The elevated expression levels of HIST1H2BH and PLK1 were related to the overall survival (OS) and the progression-free survival of NSCLC patients. High-risk NSCLC patients had a poor prognosis and were an independent factor influencing the poor prognosis of NSCLC patients. The high-risk model group was enriched with signaling mechanisms such as cell cycle, DNA replication, and homologous recombination.Conclusions: The risk model based on PD-1 target molecules was helpful to assess the prognosis of NSCLC patients. HIST1H2BH and PLK1 might become prognostic biomarkers of NSCLC patients.

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PAQR3 Inhibits Non-small Cell Lung Cancer Growth by Regulating the NF-κB/p53/Bax Axis

Cited by 18 publications

References 35 publications

PAQR3 inhibits proliferation and aggravates ferroptosis in acute lymphoblastic leukemia through modulation Nrf2 stability

PAQR3 inhibits proliferation and aggravates ferroptosis in acute lymphoblastic leukemia through modulation Nrf2 stability

Circular RNA CircCDYL Regulates Proliferation and Apoptosis in Non-Small Cell Lung Cancer Cells by Sponging miR-185-5p and Upregulating TNRC6A

Evaluation of the roles and regulatory mechanisms of PD-1 target molecules in NSCLC progression

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