Downregulation of RPN2 induces apoptosis and inhibits migration and invasion in colon carcinoma

Bi, Chongyao; Jiang, Baofei

doi:10.3892/or.2018.6434

Cited by 21 publications

(22 citation statements)

References 41 publications

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“…5), suggesting the activation of STAT3 by enhanced RPN2 expression. Consistent with our study, the activation of STAT3 by RPN2 was found in other types of cancers, including colon carcinoma, hepatocellular carcinoma (Huang et al, 2019;Bi & Jiang, 2018). RPN2 was reported to regulate colon cancer cell proliferation through mediating the glycosylation of EGFR, which affectes the EGFR/ERK signaling pathways (Li et al, 2017).…”

Section: Discussionsupporting

confidence: 88%

Overexpression of RPN2 suppresses radiosensitivity of glioma cells by activating STAT3 signal transduction

Ran

Song

et al. 2020

Mol Med

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Background: Radiation therapy is the primary method of treatment for glioblastoma (GBM). Therefore, the suppression of radioresistance in GBM cells is of enormous significance. Ribophorin II (RPN2), a protein component of an N-oligosaccharyl transferase complex, has been associated with chemotherapy drug resistance in multiple cancers, including GBM. However, it remains unclear whether this also plays a role in radiation therapy resistance in GBM. Methods: We conducted a bioinformatic analysis of RPN2 expression using the UCSC Cancer Genomics Browser and GEPIA database and performed an immunohistochemical assessment of RPN2 expression in biopsy specimens from 34 GBM patients who had received radiation-based therapy. We also studied the expression and function of RPN2 in radiation-resistant GBM cells. Results: We found that RPN2 expression was upregulated in GBM tumors and correlated with poor survival. The expression of RPN2 was also higher in GBM patients with tumor recurrence, who were classified to be resistant to radiation therapy. In the radiation-resistant GBM cells, the expression of RPN2 was also higher than in the parental cells. Depletion of RPN2 in resistant cells can sensitize these cells to radiation-induced apoptosis, and overexpression of RPN2 had the reverse effect. Myeloid cell leukemia 1 (MCL1) was found to be the downstream target of RPN2, and contributed to radiation resistance in GBM cells. Furthermore, STAT3 was found to be the regulator of MCL1, which can be activated by RPN2 dysregulation. Conclusion: Our study has revealed a novel function of RPN2 in radiation-resistant GBM, and has shown that MCL1 depletion or suppression could be a promising method of therapy to overcome the resistance promoted by RPN2 dysregulation.

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Section: Discussionsupporting

confidence: 88%

Overexpression of RPN2 suppresses radiosensitivity of glioma cells by activating STAT3 signal transduction

Ran

Song

et al. 2020

Mol Med

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“…Next, targets of miR-378e were explored and here we first confirmed RPN2 as a functional target of miR-378e in glioma. Accruing studies suggested RPN2 as an oncogene in multiple cancers, including breast cancer, colon carcinoma, nasopharyngeal carcinoma and esophageal cancer [30][31][32][33]. Hence, we hypothesized that RPN2 might be also as a carcinogenic gene in glioma.…”

Section: Discussionmentioning

confidence: 95%

CircNFIX promotes progression of glioma through regulating miR-378e/RPN2 axis

Ding

You

et al. 2019

J Exp Clin Cancer Res

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Background: Circular RNA nuclear factor I X (circNFIX) has been reported to play an important role in glioma progression. However, the mechanism by which circNFIX participates in glioma progression remains poorly understood.Methods: GERIA online were used to analyze the abnormally expressed genes in glioma tissues. The expression levels of circNFIX, microRNA (miR)-378e and Ribophorin-II (RPN2) were measured by quantitative real-time polymerase chain reaction or western blot. Cell cycle distribution, apoptosis, glycolysis, migration and invasion were determined by flow cytometry, special kit and trans-well assays, respectively. The target association between miR-378e and circNFIX or RPN2 was confirmed by luciferase reporter assay, RNA immunoprecipitation and pull-down. Xenograft model was established to investigate the role of circNFIX in vivo.Results: The expression of circNFIX was enhanced in glioma tissues and cells compared with matched controls and high expression of circNFIX indicated poor outcomes of patients. Knockdown of circNFIX led to arrest of cell cycle, inhibition of glycolysis, migration and invasion and promotion of apoptosis in glioma cells. circNFIX was a sponge of miR-378e. miR-378e overexpression suppressed cell cycle process, glycolysis, migration and invasion but promoted apoptosis. miR-378e silence abated the suppressive role of circNFIX knockdown in glioma progression. RPN2 as a target of miR-378e was positively regulated via circNFIX by competitively sponging miR-378e. Silencing circNFIX decreased glioma xenograft tumor growth by regulating miR-378e/RPN2 axis. Conclusion: Knockdown of circNFIX inhibits progression of glioma in vitro and in vivo by increasing miR-378e and decreasing RPN2, providing a novel mechanism for understanding the pathogenesis of glioma.

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“…Previous studies have also demonstrated that MMP-9 expression was positively-correlative with the phosphorylation of STAT3 and NFkB p65 [42, 43]. A previous study also suggested that phosphorylation levels of STAT3 and Janus kinase (JAK)2 were inhibited by RPN2 siRNA [44]. However, there is no report correlating p65 and RPN2.…”

Section: Discussionmentioning

confidence: 99%

RPN2 promotes metastasis of hepatocellular carcinoma cell and inhibits autophagy via STAT3 and NF-κB pathways

Huang¹,

Jian

Gao

et al. 2019

Aging

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This study aimed to investigate the function and the molecular mechanism of Ribophorin II (RPN2) in regulating Hepatocellular carcinoma (HCC) cell growth, metastasis, and autophagy. Quantitative real-time PCR (qPCR), western blotting analysis, and immunofluorescence assay were utilized to detect the RPN2 expression in HCC cell lines and specimens of HCC patients. We discovered that RPN2 expression was upregulated in HCC cell lines and tissues of HCC patients, which correlated with the low histological grade and low survival rate. Enhanced RPN2 expression stimulated cell proliferation, metastasis, invasion, and epithelial-mesenchymal transition (EMT), and decreased Microtubule-associated protein light chain 3B (LC3B) synthesis and reduced the expression of p62 protein. Further studies suggested that matrix metalloproteinase 9 (MMP-9) was partially upregulated by RPN2 via Nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) p65. Interestingly, we found that phosphorylated RPN2 activated the signal transducer and activator of transcription 3 (STAT3) in HCC cells. It was also accountable for RPN2-stimulated elevated expression of MMP-9 and for invading HCC cells. It can be concluded that over-expression of RPN2 in HCC aggravated the malignant progression into cancerous cells. This research provided new evidences that RPN2 could facilitate tumor invasion by increasing the expression of MMP-9 in HCC cells.

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Downregulation of RPN2 induces apoptosis and inhibits migration and invasion in colon carcinoma

Cited by 21 publications

References 41 publications

Overexpression of RPN2 suppresses radiosensitivity of glioma cells by activating STAT3 signal transduction

Overexpression of RPN2 suppresses radiosensitivity of glioma cells by activating STAT3 signal transduction

CircNFIX promotes progression of glioma through regulating miR-378e/RPN2 axis

RPN2 promotes metastasis of hepatocellular carcinoma cell and inhibits autophagy via STAT3 and NF-κB pathways

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