MRPS16 facilitates tumor progression via the PI3K/AKT/Snail signaling axis

Wang, Zhen; Li, Junjun; Long, Xiaohong; Jiao, Liwu; Zhou, Minghui; Wu, Kang

doi:10.7150/jca.39671

Cited by 26 publications

(33 citation statements)

References 34 publications

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“…Based on microarray data analysis, they identified four ribosomal genes similar to MRPL17 as key genes for prognosis of lung cancer [ 18 ]. A recent study found that MRPS16 promoted the growth, migration, and invasion of glioma cells by activating PI3K/AKT nail axis, these processes can be eliminated by knocking down MRPS16 and similar trends are observable in U251 and A172 cells after deletion of MRPL42 [ 43 , 113 ]. However, the high expression of MRPL35 can predict the longer survival of glioblastoma multiforme [ 34 ].…”

Section: Mrps Associated With Cancersmentioning

confidence: 97%

Abnormal Expression of Mitochondrial Ribosomal Proteins and Their Encoding Genes with Cell Apoptosis and Diseases

Huang

Zhang

2020

IJMS

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Mammalian mitochondrial ribosomes translate 13 proteins encoded by mitochondrial genes, all of which play roles in the mitochondrial respiratory chain. After a long period of reconstruction, mitochondrial ribosomes are the most protein-rich ribosomes. Mitochondrial ribosomal proteins (MRPs) are encoded by nuclear genes, synthesized in the cytoplasm and then, transported to the mitochondria to be assembled into mitochondrial ribosomes. MRPs not only play a role in mitochondrial oxidative phosphorylation (OXPHOS). Moreover, they participate in the regulation of cell state as apoptosis inducing factors. Abnormal expressions of MRPs will lead to mitochondrial metabolism disorder, cell dysfunction, etc. Many researches have demonstrated the abnormal expression of MRPs in various tumors. This paper reviews the basic structure of mitochondrial ribosome, focuses on the structure and function of MRPs, and their relationships with cell apoptosis and diseases. It provides a reference for the study of the function of MRPs and the disease diagnosis and treatment.

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Section: Mrps Associated With Cancersmentioning

confidence: 97%

Abnormal Expression of Mitochondrial Ribosomal Proteins and Their Encoding Genes with Cell Apoptosis and Diseases

Huang

Zhang

2020

IJMS

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“…We performed the coimmunoprecipitation (co-IP) experiment as reported earlier (14,18). Supplementary Table S3 lists the details of the antibodies involved in this experiment.…”

Section: Coimmunoprecipitationmentioning

confidence: 99%

Hypoxic Glioma Stem Cell–Derived Exosomes Containing Linc01060 Promote Progression of Glioma by Regulating the MZF1/c-Myc/HIF1α Axis

et al. 2021

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Glioma stem cells (GSC) are a subpopulation of tumor cells with special abilities to proliferate and differentiate in gliomas. They are one of the main causes of tumor recurrence, especially under hypoxic conditions. Although long noncoding RNAs (lncRNA) are known to be involved in numerous biological processes and are implied in the occurrence of certain diseases, their role in tumor development and progression remains poorly understood. Here we explored the mechanisms by which lncRNA derived from hypoxic GSCs (H-GSC) cause glioma progression. Isolation and identification of the Linc01060 gene, the exosomes containing them, and the proteins from tumor cells regulating the gene allowed for studying the effects of Linc01060 on proliferation and glycometabolism. H-GSC exerted their effects by transferring exosomes to glioma cells, resulting in a significant increase in Linc01060 levels. Mechanistically, Linc01060 directly interacted with the transcription factor myeloid zinc finger 1 (MZF1) and enhanced its stability. Linc01060 facilitated nuclear translocation of MZF1 and promoted MZF1-mediated c-Myc transcriptional activities. In addition, c-Myc enhanced the accumulation of the hypoxia-inducible factor-1 alpha (HIF1a) at the posttranscriptional level. HIF1a bound the hormone response elements of the Linc01060 promoter, upregulating the transcription of Linc01060 gene. Clinically, Linc01060 was upregulated in glioma and was significantly correlated with tumor grade and poor clinical prognosis. Overall, these data show that secretion of Linc01060-containing exosomes from H-GSCs activates prooncogenic signaling pathways in glioma cells to promote disease progression.Significance: These findings suggest that inhibition of Linc01060containing exosomes or targeting the Linc01060/MZF1/c-Myc/ HIF1a axis may be an effective therapeutic strategy in glioma.

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“…By an unbias screening of biological mass spectrometry and further validation, we identified that ribosomal protein S16 (RPS16, the basic component of the 40 S ribosome) is a new substrate of USP1, responsible for proliferation and metastasis of HCC cells. RPS16 was previously considered to be an oncoprotein of breast cancer and gliomas by mediating resistance to doxorubicin or activating the PI3K/AKT/Snail pathway [ 20 , 21 ]. In this study, we revealed that USP1 interacts with RPS16, thereby deubiquitinating and stabilizing RPS16 via its DUB activity on C90 site.…”

Section: Introductionmentioning

confidence: 99%

USP1-dependent RPS16 protein stability drives growth and metastasis of human hepatocellular carcinoma cells

Liao

Shao

Liu

et al. 2021

J Exp Clin Cancer Res

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Background Hepatocellular carcinoma (HCC) remains a medical challenge due to its high proliferation and metastasis. Although deubiquitinating enzymes (DUBs) play a key role in regulating protein degradation, their pathological roles in HCC have not been fully elucidated. Methods By using biomass spectrometry, co-immunoprecipitation, western blotting and immunofluorescence assays, we identify ribosomal protein S16 (RPS16) as a key substrate of ubiquitin-specific peptidase 1 (USP1). The role of USP1-RPS16 axis in the progression of HCC was evaluated in cell cultures, in xenograft mouse models, and in clinical observations. Results We show that USP1 interacts with RPS16. The depletion of USP1 increases the level of K48-linked ubiquitinated-RPS16, leading to proteasome-dependent RPS16 degradation. In contrast, overexpression of USP1-WT instead of USP1-C90A (DUB inactivation mutant) reduces the level of K48-linked ubiquitinated RPS16, thereby stabilizing RPS16. Consequently, USP1 depletion mimics RPS16 deficiency with respect to the inhibition of growth and metastasis, whereas transfection-enforced re-expression of RPS16 restores oncogenic-like activity in USP1-deficient HCC cells. Importantly, the high expression of USP1 and RPS16 in liver tissue is a prognostic factor for poor survival of HCC patients. Conclusions These findings reveal a previously unrecognized role for the activation of USP1-RPS16 pathway in driving HCC, which may be further developed as a novel strategy for cancer treatment.

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MRPS16 facilitates tumor progression via the PI3K/AKT/Snail signaling axis

Cited by 26 publications

References 34 publications

Abnormal Expression of Mitochondrial Ribosomal Proteins and Their Encoding Genes with Cell Apoptosis and Diseases

Abnormal Expression of Mitochondrial Ribosomal Proteins and Their Encoding Genes with Cell Apoptosis and Diseases

Hypoxic Glioma Stem Cell–Derived Exosomes Containing Linc01060 Promote Progression of Glioma by Regulating the MZF1/c-Myc/HIF1α Axis

USP1-dependent RPS16 protein stability drives growth and metastasis of human hepatocellular carcinoma cells

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