The histone deacetylase SIRT6 suppresses the expression of the RNA-binding protein PCBP2 in glioma

Chen, Xin; Hao, Bin; Liu, Ying; Dai, Dongwei; Han, Gangwen; Li, Yanan; Wu, Xi; Zhou, Xiao‐Ping; Yue, Zhijian; Wang, Laixing; Cao, Yiqun; Liu, Jianmin

doi:10.1016/j.bbrc.2014.02.116

Cited by 31 publications

(19 citation statements)

References 27 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In a recent report, Chen et al showed that SIRT6 is downregulated in human glioma tissues and glioma cell lines (46). They also showed that SIRT6 inhibits PCBP2 expression by deacetylating H3K9 (46). However, this study did not mention the type and WHO grade of the glioma tissues.…”

Section: Discussionmentioning

confidence: 84%

See 1 more Smart Citation

SIRT6 suppresses glioma cell growth via induction of apoptosis, inhibition of oxidative stress and suppression of JAK2/STAT3 signaling pathway activation

et al. 2015

View full text Add to dashboard Cite

Sirtuin 6 (SIRT6) is a member of the mammalian NAD+‑dependent deacetylase sirtuin family that acts to maintain genomic stability and to repress genes. SIRT6 has recently been reported to be a tumor suppressor that controls cancer metabolism, although this effect of SIRT6 is still in dispute. Moreover, the role of SIRT6 in glioma is largely unknown. In the present study, we found that overexpression of SIRT6 using an adenovirus inhibited glioma cell growth and induced marked cell injury in two glioma cell lines (U87‑MG and T98G). Fluorescent terminal deoxyribonucleotidyl transferase (TdT)‑mediated biotin‑16‑dUTP nick‑end labelling (TUNEL) assay showed that SIRT6 overexpression induced obvious apoptosis in the T98G glioma cells. Immunoblotting and immunofluorescent staining demonstrated that SIRT6 overexpression promoted the mitochondrial-to‑nuclear translocation of apoptosis‑inducing factor (AIF), a potent apoptosis inducer. Moreover, we found that SIRT6 overexpression largely reduced oxidative stress and suppressed the activation of the JAK2/STAT3 signaling pathway in glioma cells. Finally, we showed that SIRT6 mRNA and protein levels in human glioblastoma multiforme tissues were significantly lower than the levels in peritumor tissues. In summary, our data suggest that SIRT6 suppresses glioma cell growth via induction of apoptosis, inhibition of oxidative stress and inhibition of the activation of the JAK2/STAT3 signaling pathway. These results indicate that SIRT6 may be a promising therapeutic target for glioma treatment.

show abstract

Section: Discussionmentioning

confidence: 84%

“…Notably, neural-specific SIRT6-knockout mice show attenuated somatic growth and obesity (45). In a recent report, Chen et al showed that SIRT6 is downregulated in human glioma tissues and glioma cell lines (46). They also showed that SIRT6 inhibits PCBP2 expression by deacetylating H3K9 (46).…”

Section: Discussionmentioning

confidence: 99%

SIRT6 suppresses glioma cell growth via induction of apoptosis, inhibition of oxidative stress and suppression of JAK2/STAT3 signaling pathway activation

et al. 2015

View full text Add to dashboard Cite

show abstract

“…28 PCBP2 has been downregulated in glioma cell lines (T98G, U87MG, A172, U251, and CCF-STG1) and has been shown as a target in the treatment of cancer. 29 However, upregulation of BAX, EI24, PEA15, CYFIP2, DKK1, TFPI2, ABCA1, FEZ1, CLDN1, IGFBP7, TP53INP1, FAS, TNFRSF10B, TP53I3, CDKN1A, and This indicates that silver nitrate may affect same genes targeted by cisplatin as well. According to immunocytochemical and microarray results, silver nitrate has no effects on Bcl-2 and Bax expression levels.…”

Section: Discussionmentioning

confidence: 99%

The apoptotic and genomic studies on A549 cell line induced by silver nitrate

2017

View full text Add to dashboard Cite

Lung cancer is the leading cause of male cancer deaths worldwide. Metal-based anticancer drugs have evolved significantly during the past decades. Recently, silver ions have been investigated for their anticancer effects. We aimed to study the time-course cytotoxic effects of silver nitrate on A549 adenocarcinomic human alveolar basal epithelial cells to provide insights into the molecular-level understanding of growth suppression mechanism involved in apoptosis. The influences of silver nitrate were studied via MTT assay, flow cytometry, immunocytochemical, confocal and transmission electron microscopy, and microarray assays. Silver nitrate showed inhibitory effects against A549 cells in a dose-and time-dependent manner for 24, 48, and 72 h and induced apoptosis. The early and late apoptotic cells and depolarized mitochondrial membrane potential were determined by the half-maximal inhibitory concentration (IC 50 ) value of silver nitrate treated for 72 h. But cysteinyl aspartate proteinase-3 was not activated for 72 h. Furthermore, IC 50 value of silver nitrate also induced apoptosis according to immunocytochemical assays for 72 h. The downregulated CCNY, HNRNPL, ASF1B, PIAS4, HNRNPH1, EIF2C2, TAF15, FOXC1, LEP, and PCB2 genes administered with silver nitrate IC 50 were identified as apoptosis-leading genes. Silver nitrate may be a suitable therapeutic agent against lung cancer.

show abstract

“…74,75 In glioma and gastric carcinoma, PCBP2 interacts with tumor suppressors, such as FHL3, SIRT6, and miR-34a, and thus, its elevation supports tumor cell growth. 76,77 HNRPA1 is a member of a family of RNA-binding proteins that are involved in a variety of functions, such as the regulation of transcription, mRNA metabolism, and translation. 78 hnRNPA1 may activate epithelial-to-mesenchymal transitions by interaction with the serine-arginine-rich splicing factor 1 (SRSF1) that regulates oncogenic alternative splicing.…”

Section: Discussionmentioning

confidence: 99%

Proteomic identification of potential biomarkers for cervical squamous cell carcinoma and human papillomavirus infection

Song

Tulake

et al. 2017

Tumour Biol.

View full text Add to dashboard Cite

It is known that high-risk human papillomavirus infection is the main etiological factor in cervical carcinogenesis. However, human papillomavirus screening is not sufficient for early diagnosis. In this study, we aimed to identify potential biomarkers common to cervical carcinoma and human papillomavirus infection by proteomics for human papillomavirus-based early diagnosis and prognosis. To this end, we collected 76 cases of fresh cervical tissues and 116 cases of paraffin-embedded tissue slices, diagnosed as cervical squamous cell carcinoma, cervical intraepithelial neoplasia II-III, or normal cervix from ethnic Uighur and Han women. Human papillomavirus infection by eight oncogenic human papillomavirus types was detected in tissue DNA samples using a quantitative polymerase chain reaction. The protein profile of cervical specimens from human papillomavirus 16-positive squamous cell carcinoma and human papillomavirus-negative normal controls was analyzed by proteomics and bioinformatics. The expression of candidate proteins was further determined by quantitative reverse transcriptase-polymerase chain reaction and immunohistochemistry. We identified 67 proteins that were differentially expressed in human papillomavirus 16-positive squamous cell carcinoma compared to normal cervix. The quantitative reverse transcriptase-polymerase chain reaction analysis verified the upregulation of ASAH1, PCBP2, DDX5, MCM5, TAGLN2, hnRNPA1, ENO1, TYPH, CYC, and MCM4 in squamous cell carcinoma compared to normal cervix (p < 0.05). In addition, the transcription of PCBP2, MCM5, hnRNPA1, TYPH, and CYC was also significantly increased in cervical intraepithelial neoplasia II-III compared to normal cervix. Immunohistochemistry staining further confirmed the overexpression of PCBP2, hnRNPA1, ASAH1, and DDX5 in squamous cell carcinoma and cervical intraepithelial neoplasia II-III compared to normal controls (p < 0.05). Our data suggest that the expression of ASAH1, PCBP2, DDX5, and hnRNPA1, and possibly MCM4, MCM5, CYC, ENO1, and TYPH, is upregulated during cervical carcinogenesis and potentially associated with human papillomavirus infection. Further validation studies of the profile will contribute to establishing auxiliary diagnostic markers for human papillomavirus-based cancer prognosis. KeywordsCervical carcinoma, isobaric tags for relative and absolute quantitation, proteomics, human papillomavirus infection, cervical specimen Date

show abstract

The histone deacetylase SIRT6 suppresses the expression of the RNA-binding protein PCBP2 in glioma

Cited by 31 publications

References 27 publications

SIRT6 suppresses glioma cell growth via induction of apoptosis, inhibition of oxidative stress and suppression of JAK2/STAT3 signaling pathway activation

SIRT6 suppresses glioma cell growth via induction of apoptosis, inhibition of oxidative stress and suppression of JAK2/STAT3 signaling pathway activation

The apoptotic and genomic studies on A549 cell line induced by silver nitrate

Proteomic identification of potential biomarkers for cervical squamous cell carcinoma and human papillomavirus infection

Contact Info

Product

Resources

About