PRDM14 mediates chemosensitivity and glycolysis in drug‑resistant A549/cisplatin cells and their progenitor A549 human lung adenocarcinoma cells

He, Saifei; Ma, Xiaokun; Zheng, Ni; Wang, Guoyu; Wang, Menghan; Xia, Weiya; Yu, Dunxi

doi:10.3892/mmr.2020.11788

Cited by 4 publications

(1 citation statement)

References 38 publications

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“…Recently, multiple studies have emphasized the importance of active glycolysis as a key promotor in tumorigenesis [27,28]. Importantly, the function of PRDM14 in promoting chemoresistance in A549/cisplatinresistant cells, including their progenitor A549 human lung adenocarcinoma cells, has been elucidated by He et al [29]. Furthermore, Li et al revealed that heightened expression of GLUT-4 not only enhances cell propagation but also drives glycolysis, with significant effects for NSCLC patients.…”

Section: Discussionmentioning

confidence: 99%

<i>STIL</i> enhances the development of lung adenocarcinoma by regulating the glycolysis pathway

WANG,

XIE

2025

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Background: To investigate STIL centriolar assembly protein (STIL)'s role and prognostic significance in lung adenocarcinoma (LUAD) progression, we examined STIL and E2 promoter binding factor 1 (E2F1) expressions and their impacts on LUAD prognosis using Gene Expression Profiling Interactive Analysis (GEPIA). Methods: Functional assays including CCK-8, wound-healing, 5-ethynyl-2-deoxyuridine (EdU), Transwell assays, and flow cytometry, elucidated STIL and E2F1's effects on cell viability, proliferation, apoptosis, and migration. GSEA identified potential pathways, while metabolic assays assessed glucose metabolism. Results: Our findings reveal that STIL and E2F1 are overexpressed in LUAD, correlating with adverse outcomes. It enhances cell proliferation, migration, and invasion, and suppresses apoptosis, activating downstream of E2F1. Silencing E2F1 reversed the promotion effect of the STIL overexpression on cell viability and invasiveness. Importantly, STIL modulates glycolysis, influencing glucose consumption, lactate production, and energy balance in LUAD cells. Conclusion: Our model, incorporating STIL, age, and disease stage, robustly predicts patient prognosis, underscoring STIL's pivotal role in LUAD pathogenesis through metabolic reprogramming. This comprehensive approach not only confirms STIL's prognostic value but also highlights its potential as a therapeutic target in LUAD.

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Section: Discussionmentioning

confidence: 99%

<i>STIL</i> enhances the development of lung adenocarcinoma by regulating the glycolysis pathway

WANG,

XIE

2025

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TRIM47 inhibits cisplatin chemosensitivity and endoplasmic reticulum stress-induced apoptosis of ovarian cancer cells

Zhao,

Zhang,

Tong

et al. 2024

Molecular and Cellular Probes

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PRDM1/BLIMP1 induces cancer immune evasion by modulating the USP22-SPI1-PD-L1 axis in hepatocellular carcinoma cells

Zhang

You

et al. 2022

Nat Commun

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Programmed death receptor-1 (PD-1) blockade have achieved some efficacy but only in a fraction of patients with hepatocellular carcinoma (HCC). Programmed cell death 1 ligand 1 (PD-L1) binds to its receptor PD1 on T cells to dampen antigen-tumor immune responses. However, the mechanisms underlying PD-L1 regulation are not fully elucidated. Herein, we identify that tumoral Prdm1 overexpression inhibits cell growth in immune-deficient mouse models. Further, tumoral Prdm1 overexpression upregulates PD-L1 levels, dampening anti-tumor immunity in vivo, and neutralizes the anti-tumor efficacy of Prdm1 overexpression in immune-competent mouse models. Mechanistically, PRDM1 enhances USP22 transcription, thus reducing SPI1 protein degradation through deubiquitination, which enhances PD-L1 transcription. Functionally, PD-1 mAb treatment reinforces the efficacy of Prdm1-overexpressing HCC immune-competent mouse models. Collectively, we demonstrate that the PRDM1-USP22-SPI1 axis regulates PD-L1 levels, resulting in infiltrated CD8+ T cell exhaustion. Furthermore, PRDM1 overexpression combined with PD-(L)1 mAb treatment provides a therapeutic strategy for HCC treatment.

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PRDM14 mediates chemosensitivity and glycolysis in drug‑resistant A549/cisplatin cells and their progenitor A549 human lung adenocarcinoma cells

Cited by 4 publications

References 38 publications

<i>STIL</i> enhances the development of lung adenocarcinoma by regulating the glycolysis pathway

<i>STIL</i> enhances the development of lung adenocarcinoma by regulating the glycolysis pathway

TRIM47 inhibits cisplatin chemosensitivity and endoplasmic reticulum stress-induced apoptosis of ovarian cancer cells

PRDM1/BLIMP1 induces cancer immune evasion by modulating the USP22-SPI1-PD-L1 axis in hepatocellular carcinoma cells

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