Downregulation of selenium-binding protein 1 is associated with poor prognosis in lung squamous cell carcinoma

Tan, Xing Fei; Liao, Li; Wu, Yanping; Li, Meixiang; Chen, Sihan; Mo, Wenjuan; Zhao, Qi; Huang, Lifang; Zeng, Gu-Qing

doi:10.1186/s12957-016-0832-6

Cited by 15 publications

(16 citation statements)

References 33 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In contrast with small cell lung cancer cells, the growth and division of NSCLC cells are much quicker, and their invasion to adjacent tissues and distant metastasis are much earlier [ 2 , 3 ]. More than half of the non-small cell lung tumors are diagnosed at advanced stages, so that the 5-year survival rate of NSCLC patients is lower than 15% [ 4–6 ]. The pathogenesis of NSCLC is not yet fully understood.…”

Section: Introductionmentioning

confidence: 99%

lncRNA Gm15290 promotes cell proliferation and invasion in lung cancer through directly interacting with and suppressing the tumor suppressormiR-615-5p

et al. 2018

View full text Add to dashboard Cite

Long non-coding RNAs (lncRNAs) have been involved in occurrence and progression of multiple cancers. In the present study, we investigated the role of lncRNA Gm15290 in the proliferation and invasion of non-small cell lung cancer (NSCLC) cells. First, we found that lncRNA Gm15290 was markedly up-regulated in tumor tissues from NSCLC patients and NSCLC cell lines, compared with adjacent normal tissues and normal lung cell line HBE respectively. Then, different concentrations of pcDNA-Gm15290 expression vector and Gm15290 siRNA were respectively transfected into A549 NSCLC cells. Our results showed that overexpression of Gm15290 significantly increased the proliferation and invasion of A549 cells and suppressed cell apoptosis. Knockdown of Gm15290 suppressed A549 cell proliferation and invasion and promoted cell apoptosis. Subsequently, we explored the underlying mechanism through which Gm15290 promoted cell proliferation and invasion. The output of RNA hybrid bioinformatic tool revealed that Gm15290 potentially interacted with tumor suppressor miR-615-5p which displayed an opposite expression pattern in the cell lines and a strong negative correlation with the levels of Gm15290 in NSCLC patients (r2 = 0.9677, P<0.0001). The results of RNA pull-down assays confirmed that Gm15290 directly bound with miR-615-5p. Gm15290 negatively regulated the expression of miR-615-5p and increased the protein levels of miR-615-5p target genes, including IGF2, AKT2, and SHMT2. Moreover, miR-615-5p mimic could antagonize the promoting effect of Gm15290 on cell proliferation and invasion.

show abstract

Section: Introductionmentioning

confidence: 99%

lncRNA Gm15290 promotes cell proliferation and invasion in lung cancer through directly interacting with and suppressing the tumor suppressormiR-615-5p

et al. 2018

View full text Add to dashboard Cite

show abstract

“…Previous studies have indicated that sodium selenite exhibited anti-proliferative activity by modulating various pathways including ERK activation (15)(16)(17)(18)(19). Sodium selenite could upregulate ERK expression at lower doses, while at higher doses it decreases ERK activation (27).…”

Section: Discussionmentioning

confidence: 99%

“…The anticancer mechanism of selenium in thyroid cancer, however, has not been fully elucidated (13,14). Previous studies have suggested that the possible mechanism of action of selenite included stimulation of the immune system, activation of natural killer cells, inhibition of angiogenesis, enhancement of damaged DNA fragment repair, and initiation of apoptosis in various cancers (15)(16)(17)(18)(19). Recent studies further demonstrated that selenite suppressed cell differentiation through inhibiting ERK activation in vascular smooth muscle cells (20,21).…”

mentioning

confidence: 99%

Sodium Selenite Enhanced the Anti-proliferative Effect of MEK-ERK Inhibitor in Thyroid Cancer Cells

Kim

Yang

Woo

et al. 2019

In Vivo

View full text Add to dashboard Cite

Background/Aim: MEK-ERK pathway plays major roles in the progression of thyroid cancer, while the use of MEK-ERK inhibitors has been limited by its toxicity. We investigated the effect of sodium selenite as an adjunct for MEK-ERK inhibitors to avoid the toxicity of ERK inhibitors. Materials and Methods: TPC1, 8505C and HTori-3 cells were treated with U0126 (MEK-ERK inhibitor) and cell viability was counted in the Neubauer chamber. The synergistic effects of sodium selenite and U0126 were also measured. The expression of ERK, pERK , and p90 RSK was determined by western blot. Results: Treatment with U0126 inhibited proliferation of TPC1 and 8505C cells in a dosedependent manner. When 5 μM sodium selenite was added to 1 μM U0126, relative cell survival further decreased. Decreased expression of p90 RSK indicated that sodium selenite down-regulated ERK signaling in thyroid cancer cells. Conclusion: The combination of U0126 and sodium selenite inhibited proliferation of thyroid cancer cells through ERK inhibition. Materials and Methods Cell culture. Human thyrocyte cell line HTori-3, human papillary thyroid cancer cell line TPC1, and human anaplastic thyroid cancer 185 This article is freely accessible online.

show abstract

“…Seleniumbinding proteins are known to play important roles in cancer prevention effects of selenium. Downregulation of SELENBP1 is associated with poor prognosis in NSCLC patients (Tan et al, 2016;Zeng et al, 2013). Overall, the proposed approach identifies more informative prognostic markers.…”

Section: Nsclc Datamentioning

confidence: 99%

“…They are TOP2A, ASPM, SELENBP1, MAD2L1, CDC20, PRC1, TYMS, and DLGAP5. Downregulation of SELENBP1 is associated with poor prognosis in NSCLC patients (Tan et al, 2016;Zeng et al, 2013). PRC1 (Protein regulator of Cytokinesis 1) has the highest correlation with PCLAF (r= 0.83).…”

Section: Nsclc Datamentioning

confidence: 99%

Robust network‐based regularization and variable selection for high‐dimensional genomic data in cancer prognosis

Ren

et al. 2019

Genetic Epidemiology

View full text Add to dashboard Cite

In cancer genomic studies, an important objective is to identify prognostic markers associated with patients' survival. Network‐based regularization has achieved success in variable selections for high‐dimensional cancer genomic data, because of its ability to incorporate the correlations among genomic features. However, as survival time data usually follow skewed distributions, and are contaminated by outliers, network‐constrained regularization that does not take the robustness into account leads to false identifications of network structure and biased estimation of patients' survival. In this study, we develop a novel robust network‐based variable selection method under the accelerated failure time model. Extensive simulation studies show the advantage of the proposed method over the alternative methods. Two case studies of lung cancer datasets with high‐dimensional gene expression measurements demonstrate that the proposed approach has identified markers with important implications.

show abstract

Downregulation of selenium-binding protein 1 is associated with poor prognosis in lung squamous cell carcinoma

Cited by 15 publications

References 33 publications

lncRNA Gm15290 promotes cell proliferation and invasion in lung cancer through directly interacting with and suppressing the tumor suppressormiR-615-5p

lncRNA Gm15290 promotes cell proliferation and invasion in lung cancer through directly interacting with and suppressing the tumor suppressormiR-615-5p

Sodium Selenite Enhanced the Anti-proliferative Effect of MEK-ERK Inhibitor in Thyroid Cancer Cells

Robust network‐based regularization and variable selection for high‐dimensional genomic data in cancer prognosis

Contact Info

Product

Resources

About