scholarly journals Circular RNA circGTIC1 drives gastric TIC self-renewal to initiate gastric tumorigenesis and metastasis

2019 ◽  
Author(s):  
Liyan Wang ◽  
Bin Li ◽  
Xuhua Xiao ◽  
Xiaoyuan Yi ◽  
Feifei He
Keyword(s):  
Gastric Cancer ◽  
Chromatin Remodeling ◽  
Circular Rna ◽  
The Self ◽  
Gastric Tumor ◽  
Dependent Manner ◽  
Tumor Initiating Cells ◽  
Self Renewal ◽  
Chromatin Remodeling Complex ◽  
The World

AbstractGastric cancer is one of the most serious cancers all over the world. Gastric tumor initiating cells (TIC) account for gastric tumorigenesis and metastasis. Here we identified circGTIC1 as a highly expressed circRNA in gastric cancer and gastric TICs. circGTIC1 knockout inhibited the self-renewal of gastric TICs and metastasis, and its overexpression activated gastric TICs. circGTIC1 drove the expression of Sox8 and exerted its role via Sox8-dependent manner. circGTIC1 associated with Ino80 chromatin remodeling complex, and recruited Ino80 complex to Sox8 promoter, finally initiated Sox8 expression. Our work revealed a novel circRNA to regulate gastric tumorigenesis and gastric TICs, adding a new layer for gastric TIC regulation and circRNA functions. CircGTIC1 plays a central role in gastric TIC self-renewal and metastasis. circGTIC1 drives the expression of Sox8 through recruiting Ino80 complex to Sox8 promoter. circGTIC1-Ino80-Sox8 axis can be used for gastric tumor and gastric TIC targeting. Our work revealed a novel circRNA to regulate gastric tumorigenesis and gastric TICs, adding a new layer for gastric TIC regulation and circRNA functions

scholarly journals Efg1-mediated Recruitment of NuA4 to Promoters Is Required for Hypha-specific Swi/Snf Binding and Activation inCandida albicans

2008 ◽  
Vol 19 (10) ◽  
pp. 4260-4272 ◽  
Author(s):  
Yang Lu ◽  
Chang Su ◽  
Xuming Mao ◽  
Prashna Pala Raniga ◽  
Haoping Liu ◽  
...  
Keyword(s):  
Chromatin Remodeling ◽  
Transcriptional Activation ◽  
Chromatin Immunoprecipitation ◽  
Pathogenic Fungus ◽  
Dependent Manner ◽  
Hyphal Development ◽  
Chromatin Remodeling Complex ◽  
A Subunit ◽  
Human Pathogenic Fungus ◽  
Incandida Albicans

Efg1 is essential for hyphal development and virulence in the human pathogenic fungus Candida albicans. How Efg1 regulates gene expression is unknown. Here, we show that Efg1 interacts with components of the nucleosome acetyltransferase of H4 (NuA4) histone acetyltransferase (HAT) complex in both yeast and hyphal cells. Deleting YNG2, a subunit of the NuA4 HAT module, results in a significant decrease in the acetylation level of nucleosomal H4 and a profound defect in hyphal development, as well as a defect in the expression of hypha-specific genes. Using chromatin immunoprecipitation, Efg1 and the NuA4 complex are found at the UAS regions of hypha-specific genes in both yeast and hyphal cells, and Efg1 is required for the recruitment of NuA4. Nucleosomal H4 acetylation at the promoters peaks during initial hyphal induction in an Efg1-dependent manner. We also find that Efg1 bound to the promoters of hypha-specific genes is critical for recruitment of the Swi/Snf chromatin remodeling complex during hyphal induction. Our data show that the recruitment of the NuA4 complex by Efg1 to the promoters of hypha-specific genes is required for nucleosomal H4 acetylation at the promoters during hyphal induction and for subsequent binding of Swi/Snf and transcriptional activation.

scholarly journals PGD2/PTGDR2 Signaling Restricts the Self-Renewal and Tumorigenesis of Gastric Cancer

Stem Cells ◽  
2018 ◽  
Vol 36 (7) ◽  
pp. 990-1003 ◽  
Author(s):  
Bin Zhang ◽  
Qingli Bie ◽  
Peipei Wu ◽  
Jie Zhang ◽  
Benshuai You ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
The Self ◽  
Self Renewal

IL-13 secreted by ILC2s promotes the self-renewal of intestinal stem cells through circular RNA circPan3

2019 ◽  
Vol 20 (2) ◽  
pp. 183-194 ◽  
Author(s):  
Pingping Zhu ◽  
Xiaoxiao Zhu ◽  
Jiayi Wu ◽  
Luyun He ◽  
Tiankun Lu ◽  
...  
Keyword(s):  
Stem Cells ◽  
Circular Rna ◽  
The Self ◽  
Intestinal Stem Cells ◽  
Self Renewal

The TGF- β Family Member Growth Differentiation Factor 15 (GDF15) Regulates the Self-Renewal of Multiple Myeloma Cancer Stem Cells

Blood ◽  
2011 ◽  
Vol 118 (21) ◽  
pp. 2954-2954
Author(s):  
Toshihiko Tanno ◽  
Akil Merchant ◽  
Jasmin R. Agarwal ◽  
Qiuju Wang ◽  
William Matsui
Keyword(s):  
Stem Cells ◽  
Multiple Myeloma ◽  
Bone Marrow ◽  
Cancer Stem Cells ◽  
The Self ◽  
Disease Stage ◽  
Dependent Manner ◽  
Self Renewal ◽  
Growth Differentiation Factor 15 ◽  
Differentiation Factor

Abstract Abstract 2954 Multiple myeloma (MM) cancer stem cells (CSCs) possess both enhanced tumorigenic potential and relative drug resistance suggesting they play a major role in disease relapse and progression. Therefore, a better understanding of the processes regulating MM CSCs may lead to the development of novel therapies that prevent tumor regrowth and improve long-term outcomes. Normal stem cells are tightly regulated by factors within the local microenvironment that include both soluble factors and direct contact with accessory cells. However, external factors regulating MM CSCs have not been identified. Recent studies have demonstrated that stromal cells in the MM bone marrow microenvironment secrete growth differentiation factor 15 (GDF15), a member of the TGF-b family. We initially studied the role of this cytokine in the pathogenesis of MM by examining circulating GDF15 levels in MM patients. Compared to healthy volunteers, we found that median GDF15 levels were significantly increased in MM patients (821 vs. 390 pg/ml; n=16; p<0.05) and increased with disease stage (Stage II=585 pg/ml, Stage III=1, 004 pg/ml). To examine the functional effects of GDF15 on MM cells, we cultured human MM cell lines (NCI-H929, RPMI 8226) with recombinant GDF15 and found that it induced the expansion of isolated CD138neg MM CSCs in a dose-dependent manner but had little impact on the growth of CD138+ plasma cells (Fig). Furthermore, GDF15 enhanced clonogenic myeloma growth as evidenced by increased colony formation that was maintained during serial replating, a surrogate for self-renewal. This effect appeared to be GDF15 specific since it could be blocked using anti-GDF15 antibody. Similarly, GDF15 treatment increased the in vitro clonogenic growth of MM CSCs from primary clinical bone marrow specimens. We also investigated the down-stream cellular pathways potentially mediating the effects of GDF15 and found that it activates the AKT signaling pathway known to improve the self-renewal of embryonic (ES) and normal hematopoietic stem cells. GDF15 also induced expression of the SOX2 transcription factor known to be upregulated in CD138neg MM CSCs. Since SOX2 is required for the self-renewal of ES cells and the generation of induced pluripotent stem (iPS) cells, its induction by GDF15 may also increase the self-renewal of MM CSCs. GDF15 is the first soluble factor identified that regulates MM CSCs, and its effects are mediated by the activation of highly conserved self-renewal programs. Disclosures: No relevant conflicts of interest to declare.

scholarly journals The Osa-Containing SWI/SNF Chromatin-Remodeling Complex Is Required in the Germline Differentiation Niche for Germline Stem Cell Progeny Differentiation

Genes ◽  
2021 ◽  
Vol 12 (3) ◽  
pp. 363
Author(s):  
Xiaolong Hu ◽  
Mengjie Li ◽  
Xue Hao ◽  
Yi Lu ◽  
Lei Zhang ◽  
...  
Keyword(s):  
Stem Cell ◽  
Bmp Signaling ◽  
Germline Stem Cell ◽  
Dependent Manner ◽  
Self Renewal ◽  
Cellular Processes ◽  
Lineage Differentiation ◽  
Chromatin Remodeling Complex ◽  
Germline Differentiation ◽  
Drosophila Ovary

The Drosophila ovary is recognized as a powerful model to study stem cell self-renewal and differentiation. Decapentaplegic (Dpp) is secreted from the germline stem cell (GSC) niche to activate Bone Morphogenic Protein (BMP) signaling in GSCs for their self-renewal and is restricted in the differentiation niche for daughter cell differentiation. Here, we report that Switch/sucrose non-fermentable (SWI/SNF) component Osa depletion in escort cells (ECs) results in a blockage of GSC progeny differentiation. Further molecular and genetic analyses suggest that the defective germline differentiation is partially attributed to the elevated dpp transcription in ECs. Moreover, ectopic Engrailed (En) expression in osa-depleted ECs partially contributes to upregulated dpp transcription. Furthermore, we show that Osa regulates germline differentiation in a Brahma (Brm)-associated protein (BAP)-complex-dependent manner. Additionally, the loss of EC long cellular processes upon osa depletion may also partly contribute to the germline differentiation defect. Taken together, these data suggest that the epigenetic factor Osa plays an important role in controlling EC characteristics and germline lineage differentiation.

Sign in / Sign up

Export Citation Format

Share Document