The NFIB‐ERO1A axis promotes breast cancer metastatic colonization of disseminated tumour cells

Zilli, Federica; Ramos, Pedro Marques; Maur, Priska Auf der; Jehanno, Charly; Sethi, Atul; Coissieux, Marie–May; Eichlisberger, Tobias; Sauteur, Loïc; Rouchon, Adelin; Bonapace, Laura; Couto, Joana; Rad, Roland; Jensen, Michael Rugaard; Banfi, Andrea; Stadler, Michael; Bentires‐Alj, Mohamed

doi:10.15252/emmm.202013162

Cited by 29 publications

(27 citation statements)

References 74 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…ERO1A, which is a protein involved in the oxidative protein folding of molecules involved in cancer progression, has been reported to be induced by hypoxia in HeLa cells ( 44 ). The expression levels of ERO1A have been reported to be upregulated in numerous types of cancer cells compared with normal cells, such as breast, pancreatic and colorectal cancer ( 19 , 17 , 22 ), which was consistent with the present findings that CC cells exhibited upregulated ERO1A expression compared with End1/E6E7 cells. Notably, transfection with the miR-582-5p mimic downregulated the expression levels of ERO1A in HeLa cells.…”

Section: Discussionsupporting

confidence: 93%

“…Endoplasmic reticulum oxidoreductase 1α (ERO1α; ERO1A) is an oxidase located in the endoplasmic reticulum, which promotes the formation of disulphide bonds in granulocyte-colony stimulating factor (15). Accumulating evidence has demonstrated the close association between upregulated expression levels of ERO1A and poor prognosis in multiple types of cancer, such as pancreatic cancer, cholangiocarcinoma and breast cancer (16)(17)(18)(19). In a previous study, knockdown of ERO1A expression reduced the proliferation, migration and tumorigenesis of CC cells by downregulating H 2 O 2 -associated epithelial-to-mesenchymal transition (20).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

circ‑ACACA promotes proliferation, invasion, migration and glycolysis of cervical cancer cells by targeting the miR‑582‑5p/ERO1A signaling axis

Huang

Li²

2021

Oncol Lett

View full text Add to dashboard Cite

Circular RNAs (circ) have been reported to serve crucial roles in the regulation of cancer occurrence and development. The present study aimed to investigate the role of circ-acetyl-CoA carboxylase α (ACACA) in the progression of cervical cancer (CC). The expression levels of circ-ACACA in several CC cell lines were first determined using reverse transcription-quantitative PCR. circ-ACACA expression was subsequently knocked down to evaluate its effects on the viability, proliferation, apoptosis, invasion and migration of CC cells using MTT, colony formation, TUNEL, transwell and wound healing assays, respectively. 13 C-labeling of intracellular metabolites and analysis of glucose consumption and lactate production were performed to determine the levels of glycolysis. In addition, the expression levels of endoplasmic reticulum oxidoreductase 1α (ERO1α; ERO1A) and glycolysis-related proteins were analyzed using western blotting. The binding interactions among circ-ACACA, microRNA (miR)-582-5p and ERO1A were validated using dual-luciferase reporter assays. Subsequently, rescue experiments were performed to determine the potential underlying mechanism by which circ-ACACA affected CC cell functions. The results revealed that circ-ACACA expression was significantly upregulated in CC cells and silencing of circ-ACACA significantly reduced the proliferation, invasion and migration, and promoted the apoptosis of CC cells. Knockdown of circ-ACACA markedly inhibited glycolysis in CC cells. However, the effects of silencing of circ-ACACA on CC cells were reversed following transfection with the miR-582-5p inhibitor or pcDNA3.1-ERO1A overexpression plasmid. In conclusion, to the best of our knowledge, the present study was the first to investigate the role of circ-ACACA in CC progression. The results suggested that circ-ACACA may promote CC tumorigenesis and glycolysis by targeting the miR-582-5p/ERO1A signaling axis. Therefore, circ-ACACA may be a promising biomarker for CC diagnosis and treatment.

show abstract

Section: Discussionsupporting

confidence: 93%

Section: Introductionmentioning

confidence: 99%

circ‑ACACA promotes proliferation, invasion, migration and glycolysis of cervical cancer cells by targeting the miR‑582‑5p/ERO1A signaling axis

Huang

Li²

2021

Oncol Lett

View full text Add to dashboard Cite

show abstract

“…Subsequently, we predicted the downstream targets of miR-603 using the miRDB database. 6 genes (NFIB [ 27 ], ZEB2 [ 28 ], TLR4 [ 29 ], KDM7A [ 30 ], LASP1 [ 31 ], and KIF2A [ 32 ]) related to BC were selected as candidate targets for further analysis among all predicted target genes. Moreover, only KIF2A was repressed in both miR-603-overexpressing HCC70 and MDA-MB-231 cells, so KIF2A was selected for subsequent investigation (Additional file 3 : Fig.…”

Section: Resultsmentioning

confidence: 99%

Circular RNA circ_IRAK3 contributes to tumor growth through upregulating KIF2A via adsorbing miR-603 in breast cancer

Wang

et al. 2022

Cancer Cell Int

View full text Add to dashboard Cite

Background Breast cancer (BC) threatens the health of women around the world. Researchers have proved that hsa_circ_0005505 (circ_IRAK3) facilitates BC cell invasion and migration, but the regulatory mechanisms of circ_IRAK3 in BC remain mostly unknown. We aim to explore a new mechanism by which circ_IRAK3 promotes BC progression. Methods Levels of circ_IRAK3, microRNA (miR)-603, and kinesin family member 2A (KIF2A) mRNA in BC tissues and cells were examined by quantitative real-time polymerase chain reaction (qRT-PCR). The cell cycle progression, colony formation, and proliferation of BC cells were evaluated by flow cytometry, plate clone, or 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazoliumbromide (MTT) assays. The migration, invasion, and apoptosis of BC cells were determined by transwell or flow cytometry assays. Several protein levels were detected using western blotting. The targeting relationship between circ_IRAK3 or KIF2A and miR-603 was verified via dual-luciferase reporter assay. The role of circ_IRAK3 in vivo was verified by xenograft assay. Results We observed higher levels of circ_IRAK3 in BC tissues and cell lines than their respective controls. Functional experiments presented that circ_IRAK3 silencing induced BC cell apoptosis, curbed cell proliferation, migration, and invasion in vitro, and decreased tumor growth in vivo. Mechanistically, circ_IRAK3 could modulate kinesin family member 2A (KIF2A) expression through acting as a microRNA (miR)-603 sponge. miR-603 silencing impaired the effects of circ_IRAK3 inhibition on the malignant behaviors of BC cells. Also, the repressive effects of miR-603 mimic on the malignant behaviors of BC cells were weakened by KIF2A overexpression. Conclusions circ_IRAK3 exerted a promoting effect on BC progression by modulating the miR-603/KIF2A axis, providing a piece of novel evidence for circ_IRAK3 as a therapeutic target for BC.

show abstract

“…In vivo, ERO1-deficient breast cancer xenografts show reduced ability to generate lung metastases, together with a decreased vasculogenesis in the primary tumors, suggesting that ERO1 inhibition might represent a good tool to selectively impair angiogenesis of solid tumors and limit metastases [45] [52].…”

Section: Accepted Articlementioning

confidence: 99%

Regulation of redox signaling in HIF‐1‐dependent tumor angiogenesis

et al. 2021

View full text Add to dashboard Cite

Hypoxia-inducible factor-1 (HIF-1), Epithelial grow factor (EGF), Transforming growth factor (TGF), Vascular growth factor (VEGF), Nitric oxide synthase (NOS), Platelet derived growth factor (PDGF), reactive oxygen species (ROS), tumor micro-environment (TME), carcinoma-associated fibroblasts (CAFs), prolyl hydroxylases (PHD), VEGF receptors (VEGFR), plasminogen activator mitogen 1(PAI-1), angiopoietin (ANG-1 and ANG-2), matrix metalloproteinase (MMP-2 and MMP-9), lactate dehydrogenase-A (LDH-A), Carbonic anhydrase (CA IX), Dimethyloxalylglycine (DMOG), and cobalt chloride (CoCl 2 ), Gulonolactone oxidase (Gulo), Nitric oxide (NO), oxygen-dependent degradation (ODD), endoplasmic oxidoreduction 1 (ERO1), NADPH oxidases (NOXs), electron transport chain (ETC), flavin adenine dinucleotide (FAD), protein disulfide isomerase (PDI), Peroxiredoxin (PRDX4), Glutathione peroxidase (GPX8, unfolded protein response (UPR), Protein kinase R-like Accepted ArticleThis article is protected by copyright. All rights reserved endoplasmic reticulum kinase (PERK), Inositol-requiring enzyme 1 (IRE1), Activating transcription factor 6 (ATF6), CCAAT/enhancer-binding protein (C/EBP) homology protein (CHOP), The Cancer Genome Atlas (TCGA), NADPH oxidases (NOX), diphenyleneiodonium (DPI), adenosine triphosphate (ATP), Nicotinamide adenine dinucleotide phosphate (NADPH), Snitrosylation (SNO), Endoplasmic reticulum (ER), Binding immunoglobulin protein (BIP)

show abstract

The NFIB‐ERO1A axis promotes breast cancer metastatic colonization of disseminated tumour cells

Cited by 29 publications

References 74 publications

circ‑ACACA promotes proliferation, invasion, migration and glycolysis of cervical cancer cells by targeting the miR‑582‑5p/ERO1A signaling axis

circ‑ACACA promotes proliferation, invasion, migration and glycolysis of cervical cancer cells by targeting the miR‑582‑5p/ERO1A signaling axis

Circular RNA circ_IRAK3 contributes to tumor growth through upregulating KIF2A via adsorbing miR-603 in breast cancer

Regulation of redox signaling in HIF‐1‐dependent tumor angiogenesis

Contact Info

Product

Resources

About