scholarly journals Ribosome assembly factor URB1 contributes to colorectal cancer proliferation through transcriptional activation of ATF4

2020 ◽  
Vol 112 (1) ◽  
pp. 101-116
Author(s):  
Tao Wang ◽  
Lai‐Yuan Li ◽  
Yi‐Feng Chen ◽  
Si‐Wu Fu ◽  
Zhi‐Wei Wu ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Transcriptional Activation ◽  
Ribosome Assembly ◽  
Cancer Proliferation ◽  
Assembly Factor

scholarly journals RAPTOR promotes colorectal cancer proliferation by inducing mTORC1 and upregulating ribosome assembly factor URB1

2019 ◽  
Vol 9 (4) ◽  
pp. 1529-1543 ◽  
Author(s):  
Tao Wang ◽  
Wei‐Sheng Zhang ◽  
Zheng‐Xia Wang ◽  
Zhi‐Wei Wu ◽  
Bin‐Bin Du ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Ribosome Assembly ◽  
Cancer Proliferation ◽  
Assembly Factor

scholarly journals Oncogenic lncRNA ZNF561-AS1 is essential for colorectal cancer proliferation and survival through regulation of miR-26a-3p/miR-128-5p-SRSF6 axis

2021 ◽  
Vol 40 (1) ◽  
Author(s):  
Zizhen Si ◽  
Lei Yu ◽  
Haoyu Jing ◽  
Lun Wu ◽  
Xidi Wang
Keyword(s):  
Colorectal Cancer ◽  
Rna Binding ◽  
Xenograft Model ◽  
Luciferase Reporter ◽  
Cancer Proliferation ◽  
Mouse Xenograft ◽  
Mouse Xenograft Model

Abstract Background Long non-coding RNAs (lncRNA) are reported to influence colorectal cancer (CRC) progression. Currently, the functions of the lncRNA ZNF561 antisense RNA 1 (ZNF561-AS1) in CRC are unknown. Methods ZNF561-AS1 and SRSF6 expression in CRC patient samples and CRC cell lines was evaluated through TCGA database analysis, western blot along with real-time PCR. SRSF6 expression in CRC cells was also examined upon ZNF561-AS1 depletion or overexpression. Interaction between miR-26a-3p, miR-128-5p, ZNF561-AS1, and SRSF6 was examined by dual luciferase reporter assay, as well as RNA binding protein immunoprecipitation (RIP) assay. Small interfering RNA (siRNA) mediated knockdown experiments were performed to assess the role of ZNF561-AS1 and SRSF6 in the proliferative actives and apoptosis rate of CRC cells. A mouse xenograft model was employed to assess tumor growth upon ZNF561-AS1 knockdown and SRSF6 rescue. Results We find that ZNF561-AS1 and SRSF6 were upregulated in CRC patient tissues. ZNF561-AS1 expression was reduced in tissues from treated CRC patients but upregulated in CRC tissues from relapsed patients. SRSF6 expression was suppressed and enhanced by ZNF561-AS1 depletion and overexpression, respectively. Mechanistically, ZNF561-AS1 regulated SRSF6 expression by sponging miR-26a-3p and miR-128-5p. ZNF561-AS1-miR-26a-3p/miR-128-5p-SRSF6 axis was required for CRC proliferation and survival. ZNF561-AS1 knockdown suppressed CRC cell proliferation and triggered apoptosis. ZNF561-AS1 depletion suppressed the growth of tumors in a model of a nude mouse xenograft. Similar observations were made upon SRSF6 depletion. SRSF6 overexpression reversed the inhibitory activities of ZNF561-AS1 in vivo, as well as in vitro. Conclusion In summary, we find that ZNF561-AS1 promotes CRC progression via the miR-26a-3p/miR-128-5p-SRSF6 axis. This study reveals new perspectives into the role of ZNF561-AS1 in CRC.

scholarly journals Transcriptional activation of FN1 and IL11 by HMGA2 promotes the malignant behavior of colorectal cancer

2016 ◽  
Vol 37 (5) ◽  
pp. 511-521 ◽  
Author(s):  
Jingjing Wu ◽  
Yuhong Wang ◽  
Xi Xu ◽  
Hui Cao ◽  
Sana Sahengbieke ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Transcriptional Activation ◽  
Malignant Behavior

scholarly journals Septin ring assembly involves cycles of GTP loading and hydrolysis by Cdc42p

2002 ◽  
Vol 156 (2) ◽  
pp. 315-326 ◽  
Author(s):  
Amy S. Gladfelter ◽  
Indrani Bose ◽  
Trevin R. Zyla ◽  
Elaine S.G. Bardes ◽  
Daniel J. Lew
Keyword(s):  
Transcriptional Activation ◽  
Gtpase Activating Protein ◽  
Gtp Hydrolysis ◽  
Septin Ring ◽  
Turn On ◽  
Ring Assembly ◽  
Bud Emergence ◽  
Assembly Factor ◽  
Gtpase Cycle ◽  
Budding Yeast Cell Cycle

At the beginning of the budding yeast cell cycle, the GTPase Cdc42p promotes the assembly of a ring of septins at the site of future bud emergence. Here, we present an analysis of cdc42 mutants that display specific defects in septin organization, which identifies an important role for GTP hydrolysis by Cdc42p in the assembly of the septin ring. The mutants show defects in basal or stimulated GTP hydrolysis, and the septin misorganization is suppressed by overexpression of a Cdc42p GTPase-activating protein (GAP). Other mutants known to affect GTP hydrolysis by Cdc42p also caused septin misorganization, as did deletion of Cdc42p GAPs. In performing its roles in actin polarization and transcriptional activation, GTP-Cdc42p is thought to function by activating and/or recruiting effectors to the site of polarization. Excess accumulation of GTP-Cdc42p due to a defect in GTP hydrolysis by the septin-specific alleles might cause unphysiological activation of effectors, interfering with septin assembly. However, the recessive and dose-sensitive genetic behavior of the septin-specific cdc42 mutants is inconsistent with the septin defect stemming from a dominant interference of this type. Instead, we suggest that assembly of the septin ring involves repeated cycles of GTP loading and GTP hydrolysis by Cdc42p. These results suggest that a single GTPase, Cdc42p, can act either as a ras-like GTP-dependent “switch” to turn on effectors or as an EF-Tu–like “assembly factor” using the GTPase cycle to assemble a macromolecular structure.

scholarly journals Expression of PRDX6 Correlates with Migration and Invasiveness of Colorectal Cancer Cells

2018 ◽  
Vol 51 (6) ◽  
pp. 2616-2630 ◽  
Author(s):  
Wen-Shih Huang ◽  
Cheng-Yi Huang ◽  
Meng-Chiao Hsieh ◽  
Yi-Hung Kuo ◽  
Shui-Yi Tung ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Transcriptional Activation ◽  
Colorectal Adenomas ◽  
Tissue Array ◽  
Boyden Chamber ◽  
Node Positive ◽  
Proliferation Capacity ◽  
Twist 1 ◽  
Tissue Specimens

Background/Aims: Colorectal cancer (CRC) is the third most common type of cancer and the second leading cause of cancer-related deaths worldwide. PRDXs are antioxidant enzymes that play an important role in cell differentiation, proliferation and apoptosis and have diverse functions in malignancy development. However, the mechanism of aberrant overexpression of PRDX6 in CRC remains unclear. Methods: Boyden chamber assay, flow cytometry and a lentiviral shRNA targeting PRDX6 and transient transfection with pCMV-6-PRDX6 plasmid were used to examine the role of PRDX6 in the proliferation capacity and invasiveness of CRC cells. Immunohistochemistry (IHC) with tissue array containing 40 paraffin- embedded CRC tissue specimens and Western blot assays were used to detect target proteins. Results: PRDX6 was significantly up-expressed in different comparisons of metastasis of colorectal adenomas in node-positive CRC (P = 0.03). In in vitro HCT-116, PRDX6 silencing markedly suppressed CRC cell migration and invasiveness while also inducing cell cycle arrest as well as the generation of reactive oxygen species (ROS); specific overexpression of PRDX6 had the opposite effect. Mechanistically, the PRDX6 inactivation displayed decreased levels of PRDX6, N-cadherin, β-catenin, Vimentin, Slug, Snail and Twist-1 through the activation of the PI3K/ AKT/p38/p50 pathways, but they were also significantly inhibited by PRDX6 transfectants. There was also increased transcriptional activation of dimethylation of histone H3 lysine 4 (H3K4me3) of PRDX6 promoter via the activation of the PI3K/Akt/NFkB pathways. Conclusion: Our findings demonstrated that PRDX6 expression plays a characteristic growth-promoting role in CRC metastasis. This study suggests that PRDX6 may serve as a biomarker of node-positive status and may have a role as an important endogenous regulator of cancer cell tumorigenicity in CRC. PRDX6 may also be an effective therapeutic target.

scholarly journals Structural Analysis Reveals Features of Ribosome Assembly Factor Nsa1/WDR74 Important for Localization and Interaction with Rix7/NVL2

Structure ◽  
2017 ◽  
Vol 25 (5) ◽  
pp. 762-772.e4 ◽  
Author(s):  
Yu-Hua Lo ◽  
Erin M. Romes ◽  
Monica C. Pillon ◽  
Mack Sobhany ◽  
Robin E. Stanley
Keyword(s):  
Structural Analysis ◽  
Ribosome Assembly ◽  
Assembly Factor

scholarly journals miR-125 inhibits colorectal cancer proliferation and invasion by targeting TAZ

2019 ◽  
Vol 39 (12) ◽  
Author(s):  
Meiyuan Yang ◽  
Xiaoli Tang ◽  
Zheng Wang ◽  
Xiaoqing Wu ◽  
Dong Tang ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cancer Progression ◽  
Underlying Mechanism ◽  
Cell Counting ◽  
Binding Motif ◽  
Cancer Proliferation ◽  
Qrt Pcr ◽  
Sirna Knockdown ◽  
Proliferation And Invasion ◽  
Hct116 Cells

Abstract Colorectal cancer (CRC) is the third most common malignant tumor worldwide and is a serious threat to human health. MicroRNAs (miRNAs) play a key role in oncogenesis and cancer progression. MiRNA-125 (miR-125) is an important miRNA that is dysregulated in several kinds of cancers. Thus, we investigated the expression and effects of miR-125 and Transcriptional co-activator with PDZ-binding motif (TAZ) for a better understanding of the underlying mechanism of tumor progression in CRC, which may provide an emerging biomarker for diagnosis and treatment of CRC. We measured the expression levels of miR-125 in CRC tissues, adjacent tissues, and cell lines (e.g. HCT116, SW480, FHC) by quantitative real-time polymerase chain reaction (qRT-PCR). The effect of miR-125 on proliferation and invasion in CRC cells was detected by Cell Counting Kit-8 (CCK-8), clone formation assay, and transwell assay. Western blotting and qRT-PCR were used to investigate the expression of TAZ after knocking down miR-125 in HCT116 cells or overexpressing miR-125 in SW480 cells. MiR-125 was significantly down-regulated in CRC compared with pericarcinomatous tissue from 18 patients. An miR-125 inhibitor promoted CRC cell proliferation and invasion, while miR-125 mimic had the opposite effect. Moreover, we found that TAZ was an miR-125 target and the siRNA knockdown of TAZ could reverse the effect of the miR-125 inhibitor on proliferation and invasion in HCT116 cells. The present study shows that miR-125 suppresses CRC proliferation and invasion by targeting TAZ.

scholarly journals microRNA-182 targets special AT-rich sequence-binding protein 2 to promote colorectal cancer proliferation and metastasis

2014 ◽  
Vol 12 (1) ◽  
pp. 109 ◽  
Author(s):  
Min-Hui Yang ◽  
Jiang Yu ◽  
Dong-Mei Jiang ◽  
Wen-Lu Li ◽  
Shuang Wang ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Binding Protein ◽  
Cancer Proliferation ◽  
Proliferation And Metastasis
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