PRDX1 stimulates non-small-cell lung carcinoma to proliferate via the Wnt/β-Catenin signaling

Song, Changshan; Xiong, Gang; Yang, Shuai; Wei, Xiaopeng; Ye, Xiao-Wei; Huang, Wei; Zhang, Riwen

doi:10.23736/s0031-0808.20.03978-6

Cited by 13 publications

(12 citation statements)

References 24 publications

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“…The Wnt/β-catenin signal pathway played an important role in regulating the growth and metastasis of glioblastoma cells (34). Another study also confirmed that the Wnt/β-catenin signaling pathway could promote the growth and progression of numerous cancers, including NSCLC (35). The Wnt/β-catenin signaling pathway could be activated by frizzled and low-density lipoprotein receptor-related protein 5/6.…”

Section: Discussionmentioning

confidence: 76%

MicroRNA‑20a promotes non‑small cell lung cancer proliferation by upregulating PD‑L1 by targeting PTEN

et al. 2022

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Non-small cell lung cancer (NSCLC) remains one of the most common malignant tumors worldwide. The aim of the present study was to investigate the possibility of microRNA-20a (miR-20a) as a biomarker and therapeutic target for the diagnosis and treatment of NSCLC. Bioinformatics prediction, together with functional validation, confirmed miR-20a bound to programmed death ligand-1 (PD-L1) 3'-untranslated region to upregulate PD-L1 expression. Both miR-20a and PD-L1 could promote the proliferation of NSCLC cells. The expression level of PD-L1 was controlled by PTEN; however, further upstream regulation of PD-L1 expression was largely unknown. The present study showed that miR-20a could not restore the inhibition of PD-L1 expression levels by PTEN. Knockdown of PTEN expression upregulated the expression level of PD-L1 and promoted the proliferation of NSCLC cells. PTEN negatively regulated the Wnt/β-catenin signaling pathway by inhibiting β-catenin and Cyclin D1. Interestingly, PTEN could reverse miR-20a-mediated proliferation of NSCLC cells and the inhibitory effect was similar to that of XAV-939. miR-20a promotes the proliferation of NSCLC cells by inhibiting the expression level of PTEN and upregulating the expression level of PD-L1. It is suggested that miR-20a could be used as a biomarker and therapeutic target for the treatment of NSCLC.

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Section: Discussionmentioning

confidence: 76%

MicroRNA‑20a promotes non‑small cell lung cancer proliferation by upregulating PD‑L1 by targeting PTEN

et al. 2022

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“…In the present work, we identified that PRDX1 is a directly interacted protein of IRAK1. Overexpression and the oncogenic function of PRDX1 were demonstrated in many cancers, including breast cancer [ 56 ], non-small-cell lung carcinoma [ 57 ], pancreatic ductal adenocarcinoma (PDAC) [ 58 ], and colorectal cancer [ 59 ]. In the studies reported so far, the impact of PRDX1 on autophagy still remains largely elusive and poorly understood.…”

Section: Discussionmentioning

confidence: 99%

Radiation induces IRAK1 expression to promote radioresistance by suppressing autophagic cell death via decreasing the ubiquitination of PRDX1 in glioma cells

Sun

Zhao

et al. 2023

Cell Death Dis

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Radiotherapy is the standard adjuvant treatment for glioma patients; however, the efficacy is limited by radioresistance. The function of Interleukin-1 receptor associated kinase 1 (IRAK1) in tumorigenesis and radioresistance remains to be elucidated. IRAK1 expression and its correlation with prognosis were analyzed in glioma tissues. We found that glioma patients with overexpressed IRAK1 show a poor prognosis. Notably, ionizing radiation (IR) remarkably induces IRAK1 expression, which was decreased by STING antagonist H-151 treatment. JASPAR prediction, ChIP assays, and dual luciferase reporter assays indicated that transcription factor FOXA2, suppressed by STING inhibition, directly binds to the IRAK1 promoter region and activates its transcription. IRAK1 knockdown inhibits malignancy and enhances the radiosensitivity of glioma in vitro and in vivo. To explore the potential IRAK1 interacting targets mediating the radioresistance of glioma cells, IP/Co-IP, LC-MS/MS, GST pull-down, and ubiquitination analyses were conducted. Mechanistically, IRAK1 bound to PRDX1, a major member of antioxidant enzymes, and further prevents ubiquitination and degradation of PRDX1 mediated by E3 ubiquitin ligase HECTD3; Both the DOC and HECT domains of HECTD3 directly interacted with PRDX1 protein. Overexpression of PRDX1 reverses the radiotherapy sensitization effect of IRAK1 depletion by diminishing autophagic cell death. These results suggest the IRAK1-PRDX1 axis provides a potential therapeutic target for glioma patients.

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“…A graphical representation of the effects of the overexpression of antioxidant genes on the induction, prevention, promotion, or suppression of tumor processes (based on an analysis of 130 studies) [ 58 , 63 , 66 , 87 , 88 , 89 , 90 , 103 , 104 , 105 , 114 , 117 , 159 , 173 , 174 , 175 , 192 , 201 , 210 , 230 , 232 , 233 , 234 , 238 , 239 , 240 , 241 , 242 , 243 , 244 , 245 , 246 , 247 , 248 , 249 , 250 , 251 , 252 , 253 , 254 , 255 , 256 , 257 , 258 , 259 , 260 , 261 , 262 , 263 , 264 , …”

Section: Effects Of the Antioxidant Defense Genes Overexpression On C...mentioning

confidence: 99%

Effects of Antioxidant Gene Overexpression on Stress Resistance and Malignization In Vitro and In Vivo: A Review

et al. 2022

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Reactive oxygen species (ROS) are normal products of a number of biochemical reactions and are important signaling molecules. However, at the same time, they are toxic to cells and have to be strictly regulated by their antioxidant systems. The etiology and pathogenesis of many diseases are associated with increased ROS levels, and many external stress factors directly or indirectly cause oxidative stress in cells. Within this context, the overexpression of genes encoding the proteins in antioxidant systems seems to have become a viable approach to decrease the oxidative stress caused by pathological conditions and to increase cellular stress resistance. However, such manipulations unavoidably lead to side effects, the most dangerous of which is an increased probability of healthy tissue malignization or increased tumor aggression. The aims of the present review were to collect and systematize the results of studies devoted to the effects resulting from the overexpression of antioxidant system genes on stress resistance and carcinogenesis in vitro and in vivo. In most cases, the overexpression of these genes was shown to increase cell and organism resistances to factors that induce oxidative and genotoxic stress but to also have different effects on cancer initiation and promotion. The last fact greatly limits perspectives of such manipulations in practice. The overexpression of GPX3 and SOD3 encoding secreted proteins seems to be the “safest” among the genes that can increase cell resistance to oxidative stress. High efficiency and safety potential can also be found for SOD2 overexpression in combinations with GPX1 or CAT and for similar combinations that lead to no significant changes in H2O2 levels. Accumulation, systematization, and the integral analysis of data on antioxidant gene overexpression effects can help to develop approaches for practical uses in biomedical and agricultural areas. Additionally, a number of factors such as genetic and functional context, cell and tissue type, differences in the function of transcripts of one and the same gene, regulatory interactions, and additional functions should be taken into account.

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PRDX1 stimulates non-small-cell lung carcinoma to proliferate via the Wnt/β-Catenin signaling

Cited by 13 publications

References 24 publications

MicroRNA‑20a promotes non‑small cell lung cancer proliferation by upregulating PD‑L1 by targeting PTEN

MicroRNA‑20a promotes non‑small cell lung cancer proliferation by upregulating PD‑L1 by targeting PTEN

Radiation induces IRAK1 expression to promote radioresistance by suppressing autophagic cell death via decreasing the ubiquitination of PRDX1 in glioma cells

Effects of Antioxidant Gene Overexpression on Stress Resistance and Malignization In Vitro and In Vivo: A Review

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