S100A16 suppresses the proliferation, migration and invasion of colorectal cancer cells in part via the JNK/p38 MAPK pathway

Ou, Shiyu; Liao, Yan; Shi, Jie; Tang, Jing; Ye, Yanqing; Wu, Fengfei; Wang, Weidong; Fei, Jieying; Xie, Fang; Bai, Lan

doi:10.3892/mmr.2020.11803

Cited by 29 publications

(25 citation statements)

References 32 publications

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“…Given the enrichment in JUN/JUND binding at LTR10A, LTR10F and LTR8B elements, we treated hTSCs with SP600125, an inhibitor of c-Jun N-terminal kinases (JNKs) and performed RNAseq. JNK inhibition led to upregulation of genes involved in cell migration (Supplementary Figure 4A), which is in agreement with past observations in human trophoblast (He et al, 2019), but in contrast to what is commonly seen in most cancer cells (e.g., (Chen and Zhao, 2020;Ou et al, 2021)). Unexpectedly, genes lying within 5 kb of a JUN binding site were on average upregulated (Figure 3E), including known JNK-dependent targets such as MMP14 (Supplementary Figure 4B).…”

Section: Htsc-active Ervs Lie Close To Genes With Preferential Tropho...supporting

confidence: 92%

Regulation of human trophoblast gene expression by endogenous retroviruses

Frost

Amante

Okae

et al. 2022

Preprint

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The placenta is a fast-evolving organ with large morphological and histological differences across eutherians, but the genetic changes driving placental evolution have not been fully elucidated. Transposable elements, through their capacity to quickly generate genetic variation and affect host gene regulation, may have helped to define species-specific trophoblast gene expression programmes. Here, we assessed the contribution of transposable elements to human trophoblast gene expression as enhancers or promoters. Using epigenomic data from primary human trophoblast and trophoblast stem cell lines, we identified multiple endogenous retrovirus families with regulatory potential that lie close to genes with preferential expression in trophoblast. These largely primate-specific elements are associated with inter-species gene expression differences, and are bound by transcription factors with key roles in placental development. Using genetic editing we demonstrated that several elements act as transcriptional enhancers of important placental genes, such as CSF1R and PSG5. We also identified an LTR10A element that regulates ENG expression, affecting secretion of soluble ENG, with potential implications for preeclampsia. Our data show that transposons have made important contributions to human trophoblast gene regulation, and suggest that their activity may affect pregnancy outcomes.

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Section: Htsc-active Ervs Lie Close To Genes With Preferential Tropho...supporting

confidence: 92%

Regulation of human trophoblast gene expression by endogenous retroviruses

Frost

Amante

Okae

et al. 2022

Preprint

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“…Studies have found that S100A16 can inhibit the immune infiltration of CD8 + T cells through the focal adhesion-Ras-stimulated signaling pathway in pancreatic cancer [ 35 ]. The study of Ou et al [ 36 ] found that S100A16 inhibits activities of CRC cells through the JNK/p38 MAPK signaling pathway and subsequent EMT. DDK1 encodes secreted proteins and regulates protein-protein interactions [ 37 ].…”

Section: Discussionmentioning

confidence: 99%

A Risk-Assessing Signature Based on Hypoxia- and Immune-Related Genes for Prognosis of Lung Adenocarcinoma Patients

Wang¹,

Feng²,

Liu³

et al. 2022

Computational and Mathematical Methods in Medicine

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Lung Adenocarcinoma (LUAD) drastically influences human health. Tumor hypoxia and immunity impact hugely on the immunotherapeutic effect of LUAD patients. This study is aimed at exploring the prognostic markers associated with hypoxia and immunity in LUAD patients and evaluates their reliability. The relationship between hypoxia and immune-related genes and prognoses of LUAD patients was investigated by the univariate regression analysis. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) methods were used to reveal the enriched pathways and biological processes of prognosis-related genes. Univariate, LASSO, and multivariate Cox regression analyses were used to construct a prognostic signature and verify its independence. The reliability of the signature was evaluated by the Principal Component Analysis (PCA), the Kaplan-Meier (K-M) curve, and the receiver operating characteristic (ROC) curve. Gene set enrichment analysis (GSEA), tumor mutational burden (TMB), and single-sample GSEA (ssGSEA) further verified the performance of the signature. Finally, a prognostic signature for LUAD was constructed based on 7 hypoxia- and immune-related genes. According to riskScores acquired from the signature, the test set was divided into groups, where the prognosis of high-risk patients was poor. The feature genes had good reliability, and the riskScore could be used as an independent prognostic factor for LUAD patients. Meanwhile, high TMB scores and low immune scores were found in high-risk patients, and feature genes were enriched in signaling pathways such as cell cycle and p53 signaling pathway. In sum, a prognostic signature based on 7 hypoxia- and immune-related genes was constructed.

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“…Among these genes, we identified S100A16 using multiple criteria, including its association with glioma, functional validation, and overall survival analysis. S100A16 is involved in various tumors, such as colorectal cancer, bladder cancer, pancreatic cancer, lung adenocarcinoma, cervical cancer, leukemia, and gastric cancer [37][38][39][40][41][42][43]. According to the CGGA database, S100A16 closely correlates with the survival rate of patients with primary gliomas.…”

Section: Discussionmentioning

confidence: 99%

An inhibitor of BRD4, GNE987, inhibits the growth of glioblastoma cells by targeting C-Myc and S100A16

Yang

et al. 2022

Cancer Chemother Pharmacol

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Purpose Among children, glioblastomas (GBMs) are a relatively common type of brain tumor. BRD4 expression was elevated in GBM and negatively correlated with the prognosis of glioma. We investigated the anti-GBM effects of a novel BRD4 inhibitor GNE987. Methods We evaluated the anti-tumor effect of GNE987 in vitro and in vivo by Western blot, CCK8, flow cytometry detection, clone formation, the size of xenografts, and Ki67 immunohistochemical staining, and combined ChIP-seq with RNA-seq techniques to find its anti-tumor mechanism. Results In vitro experiments showed that GNE987 significantly degraded BRD4, inhibited the proliferation of GBM cells, blocked the cell cycle, and induced apoptosis. Similarly, in vivo experiments, GNE987 also inhibited GBM growth as seen from the size of xenografts and Ki67 immunohistochemical staining. Based on Western blotting, GNE987 can significantly reduce the protein level of C-Myc; meanwhile, we combined ChIP-seq with RNA-seq techniques to confirm that GNE987 downregulated the transcription of S100A16 by disturbing H3K27Ac. Furthermore, we validated that S100A16 is indispensable in GBM growth. Conclusion GNE987 may be effective against GBM that targets C-Myc expression and influences S100A16 transcription through downregulation of BRD4.

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S100A16 suppresses the proliferation, migration and invasion of colorectal cancer cells in part via the JNK/p38 MAPK pathway

Cited by 29 publications

References 32 publications

Regulation of human trophoblast gene expression by endogenous retroviruses

Regulation of human trophoblast gene expression by endogenous retroviruses

A Risk-Assessing Signature Based on Hypoxia- and Immune-Related Genes for Prognosis of Lung Adenocarcinoma Patients

An inhibitor of BRD4, GNE987, inhibits the growth of glioblastoma cells by targeting C-Myc and S100A16

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