Knockdown of ribosomal protein S15A induces human glioblastoma cell apoptosis

Zhang, Chen; Fu, Jiqiang; Xue, Fei; Ryu, BoMi; Zhang, Ting; Zhang, Shuili; Sun, Jui Sheng; Xu, Xinxin; Zhang, Shen; Zheng, Longpo; Chen, Xianzhen

doi:10.1186/s12957-016-0891-8

Cited by 22 publications

(25 citation statements)

References 27 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Previous studies have revealed that RPS15A is aberrantly overexpressed in various types of cancer, 14,17,24 and its expression could promote cell proliferation, tumour angiogenesis and inhibit cell cycle arrest and apoptosis. 15,16,[24][25][26][27][28] However, the potential effect of RPS15A on cell The initial stage of metastatic progression is essentially dependent on EMT. 3,5 Nevertheless, a more in-depth understanding of the factors promoting EMT in GC and GC metastasis is urgently needed in order to identify specific biomarkers for improving GC prognosis and treatment.…”

Section: Discussionmentioning

confidence: 99%

RPS15A promotes gastric cancer progression via activation of the Akt/IKK‐β/NF‐κB signalling pathway

Liu

et al. 2019

J Cellular Molecular Medi

View full text Add to dashboard Cite

This study aimed to investigate the clinical significance, potential biological function and underlying mechanism of RPS15A in gastric cancer (GC) progression. RPS15A expression was detected in 40 pairs of GC tissues and matched normal gastric mucosae (MNGM) using qRT‐PCR analysis. Immunohistochemistry assay was conducted using a tissue microarray including 186 primary GC samples to characterize the clinical significance of RPS15A. A series of in vitro and in vivo assays were performed to elucidate the biological function of RPS15A in GC development and underlying molecular mechanisms. The expression of RPS15A was significantly up‐regulated in GC samples compared to MNGM, and its expression was closely related to TNM stage, tumour size, differentiation, lymph node metastasis and poor patient survival. Ectopic expression of RPS15A markedly enhanced the proliferation and metastasis of GC cells both in vitro and in vivo. RPS15A overexpression also promoted the epithelial‐mesenchymal transition (EMT) phenotype formation of GC cells. Investigations of underlying mechanisms found that RPS15A activated the NF‐κB signalling pathway by inducing the nuclear translocation and phosphorylation of the p65 NF‐κB subunit, transactivation of NF‐κB reporter and up‐regulating target genes of this pathway. In addition, RPS15A overexpression activated, while RPS15A knockdown inhibited the Akt/IKK‐β signalling axis in GC cells. And both Akt inhibitor LY294002 and IKK inhibitor Bay117082 neutralized the p65 and p‐p65 nuclear translocation induced by RPS15A overexpression. Collectively, our findings suggest that RPS15A activates the NF‐κB pathway through Akt/IKK‐β signalling axis, and consequently promotes EMT and GC metastasis. This newly identified RPS15A/Akt/IKK‐β/NF‐κB signalling pathway may be a potential therapeutic target to prevent GC progression.

show abstract

Section: Discussionmentioning

confidence: 99%

RPS15A promotes gastric cancer progression via activation of the Akt/IKK‐β/NF‐κB signalling pathway

Liu

et al. 2019

J Cellular Molecular Medi

View full text Add to dashboard Cite

show abstract

“…High expression of RPS15A in hepatocellular carcinoma promotes tumour angiogenesis by inducing the expression of fibroblast growth factor 18 . Moreover, knockdown of RPS15A represses the growth of osteosarcoma, glioma, acute myeloid leukaemia, breast cancer, and kidney cancer . Notably, RPS15A has been reported to be highly expressed in NSCLC .…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‐147b suppresses the proliferation and invasion of non‐small‐cell lung cancer cells through downregulation of Wnt/β‐catenin signalling via targeting of RPS15A

Ning

Pang

Shao

et al. 2019

Clin Exp Pharma Physio

View full text Add to dashboard Cite

| INTRODUC TI ONLung cancer, 85% of which is non-small-cell lung cancer (NSCLC), is the leading cause of cancer-related death in both males and females worldwide. 1 Most lung cancer patients are diagnosed at an advanced stage, and therefore have an extremely low 5-year survival rate. 2 Although great advances have been made in cancer therapeutic strategies over the past decade, the high recurrence rate still poses a high risk of decreased patient survival. 3 Therefore, elucidation of the elaborate molecular mechanism underlying NSCLC cell proliferation and metastasis is urgently needed to identify key molecular targets that can aid in the development of an effective target therapy. AbstractDeregulation of microRNAs (miRNAs) leads to malignant growth and aggressive invasion during cancer occurrence and progression. miR-147b has emerged as one of the cancer-related miRNAs that are dysregulated in multiple cancers. Yet, the relevance of miR-147b in non-small-cell lung cancer (NSCLC) remains unclear. In the present study, we aimed to report the biological function and signalling pathways mediated by miR-147b in NSCLC. Our results demonstrate that miR-147b expression is significantly downregulated in NSCLC tissues and cell lines. Overexpression of miR-147b decreased the proliferative ability, colony-forming capability, and invasive potential of NSCLC cells. Notably, our study identified ribosomal protein S15A (RPS15A), an oncogene in NSCLC, as a target gene of miR-147b. Our results showed that miR-147b negatively modulates RPS15A expression in NSCLC cells. An inverse correlation between miR-147b and RPS15A was evidenced in NSCLC specimens. Moreover, miR-147b overexpression downregulated the activation of Wnt/β-catenin signalling via targeting of RPS15A. Overexpression of RPS15A partially reversed the miR-147bmediated antitumour effect in NSCLC cells. Collectively, these findings reveal that miR-147b restricts the proliferation and invasion of NSCLC cells by inhibiting RPS15A-induced Wnt/β-catenin signalling and suggest that the miR-147b/RPS15A/ Wnt/β-catenin axis is an important regulatory mechanism for malignant progression of NSCLC. K E Y W O R D Scancer, miR-147b, non-small-cell lung cancer, ribosomal protein S15A, Wnt

show abstract

“…The knockdown of ribosomal protein S15A induces human glioblastoma cell apoptosis [28]. Also, NAA 10 inhibits apoptosis [29], and the de ciency of NAA10 expression can induce cell cycle arrest and apoptosis [30].…”

Section: Discussionmentioning

confidence: 99%

The Whole Cell Proteome-based Study on The Mechanism of Apoptosis Induced by Soybean Agglutinin on IPEC-J2

Pan¹,

Liu²,

Farouk³

et al. 2020

Preprint

View full text Add to dashboard Cite

Background: Soybean agglutinin (SBA), a major anti-nutritional factor in soybean, may induce abnormal health and metabolism of intestinal cells, resulting in the reduction of the production performance of animals. The anti-nutritional mechanisms of SBA are not fully understood, in terms of the cell life activities and metabolism of intestinal cells. This research aims to find the effects of SBA on the cell cycle, apoptosis and proteomic, and furtherly to get more findings for verifying the mechanism of SBA anti-nutritional characters.Methods: The IPEC-J2 cell line was cultured with the medium containing 0.0, 0.5 or 2.0 mg/mL SBA, respectively, for 24 h. The percentage of the cells at different cell cycle phases (G0/G1 phase, S phase and G2 phase) and cell apoptosis rates were measured with flow cytometry. The expressions of Cyclin D1, active p21, Bcl-2, and Bax were determined by western blotting. The activity of caspase-3 (Casp-3) and caspase-9 (Casp-9) were tested with ELISA. The whole-cell quantitative proteome were detected by TMT/iTRAQ Labeling, HPLC fractionation and LC-MS/MS Analysis. The functions and characteristics of the differential expressed proteins in the proteome results were analyzed from the aspects of GO annotation and KEGG pathway. The relationship between the results of proteomics and apoptosis or cell cycle were analyzed and discussed.Results: The percentage of the cells at G0/G1 phase, cell apoptosis rates, expressions of Bax and p21, and the activities of Casp-3 and Casp-9 were increased, cyclin D1 and Bcl-2 expression were declined with the increased of the SBA treatment levels (p<0.05). The proteomic measurements showed that a numbers of differentially expressed proteins, caused by SBA treatment, were mainly enriched in the DNA replication, base excision repair, nucleus excision repair, mismatch repair, ubiquitin-mediated proteolysis pathway, cell structural-proteins, and structures and functions of mitochondria. Moreover, the differential expressed proteins enriched in AMP-activated protein kinase (AMPK) pathway and the process of synthesis and metabolism of proteins were only found in 2.0 mg/mL SBA treatment.Conclusion: The results of this experiment demonstrated that cell cycle arrest and apoptosis induced by SBA may be resulted from the downregulating the expression of the proteins related to DNA replication and repair, protein translation, signal-conducting relation, cell structure, and subcellular structure and function.

show abstract

Knockdown of ribosomal protein S15A induces human glioblastoma cell apoptosis

Cited by 22 publications

References 27 publications

RPS15A promotes gastric cancer progression via activation of the Akt/IKK‐β/NF‐κB signalling pathway

RPS15A promotes gastric cancer progression via activation of the Akt/IKK‐β/NF‐κB signalling pathway

MicroRNA‐147b suppresses the proliferation and invasion of non‐small‐cell lung cancer cells through downregulation of Wnt/β‐catenin signalling via targeting of RPS15A

The Whole Cell Proteome-based Study on The Mechanism of Apoptosis Induced by Soybean Agglutinin on IPEC-J2

Contact Info

Product

Resources

About