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Article ; Online: A nomogram for predicting short-term prognosis in severely traumatized patients with acute respiratory failure.

Lu, Han / Qiu, Yuyao / Sun, Xuling / Zhao, Yuan

2024

Language	English
Publishing date	2024-04-10
Publishing country	Netherlands
Document type	Letter
ZDB-ID	1068461-x
ISSN	0219-3108 ; 1015-9584
ISSN (online)	0219-3108
ISSN	1015-9584
DOI	10.1016/j.asjsur.2024.03.198
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Article ; Online: TRIB3 Interacts with STAT3 to Promote Cancer Angiogenesis.

Chen, Qian-Zhi / Chen, Yan / Li, Xia / Liu, Hao / Sun, Xu-Ling

Current medical science

2022 Volume 42, Issue 5, Page(s) 932–940

Abstract: Objective: Vascular endothelial growth factor A (VEGFA) is a key regulator of angiogenesis, which is a hallmark of cancer that promotes cancer growth and metastasis. It is of great significance to find new intervention targets and related regulatory ... ...

Abstract	Objective: Vascular endothelial growth factor A (VEGFA) is a key regulator of angiogenesis, which is a hallmark of cancer that promotes cancer growth and metastasis. It is of great significance to find new intervention targets and related regulatory mechanisms of VEGFA related angiogenesis for the treatment of tumors. This study focuses on the role of tribbles pseudokinase 3 (TRIB3)/signal transducer and activator of transcription 3 (STAT3)/VEGFA signaling axis in colon cancer angiogenesis. Methods: This study investigated the expression level of TRIB3 in colon cancer through database analysis and tissue microarray analysis. The effect of TRIB3 on proliferation, migration and tube formation ability of human umbilical vein endothelial cells (HUVECs) was further confirmed by CCK8 assay, scratch-wound assay/migration assay and tube formation assay respectively. The regulatory relationship of TRIB3/VEGFA signaling axis was identified by qPCR and Western blotting, which was further confirmed through animal experiments, and the specific regulatory mechanism was explored by immunoprecipitation (IP) and chromatin immunoprecipitation (ChIP) with colon cancer cell lines. Results: TRIB3 was increased in colon cancer tissues compared to normal tissues, and elevated TRIB3 expression indicated a poor prognosis in colon cancer patients. Moreover, it was found that silencing TRIB3 could inhibit cancer angiogenesis, whereas overexpressing TRIB3 promoted cancer angiogenesis in vitro and in vivo. Mechanistically, TRIB3 physically interacted with STAT3 and enhanced STAT3-mediated transcriptional activity. Furthermore, the function of TRIB3 in cancer angiogenesis was through cooperating with STAT3 to increase the VEGFA expression. Conclusion: Our study provides insights into cancer angiogenesis and offers a potential therapeutic strategy for TRIB3-overexpressed cancer.
MeSH term(s)	Animals ; Humans ; Vascular Endothelial Growth Factor A/genetics ; Vascular Endothelial Growth Factor A/metabolism ; STAT3 Transcription Factor/genetics ; STAT3 Transcription Factor/metabolism ; Neovascularization, Pathologic/genetics ; Human Umbilical Vein Endothelial Cells/metabolism ; Colonic Neoplasms/genetics ; Repressor Proteins/metabolism ; Protein Serine-Threonine Kinases/genetics ; Cell Cycle Proteins/metabolism
Chemical Substances	Vascular Endothelial Growth Factor A ; STAT3 Transcription Factor ; TRIB3 protein, human ; Repressor Proteins ; Protein Serine-Threonine Kinases (EC 2.7.11.1) ; Cell Cycle Proteins ; STAT3 protein, human
Language	English
Publishing date	2022-10-17
Publishing country	China
Document type	Journal Article
ZDB-ID	2931065-9
ISSN	2523-899X ; 2096-5230
ISSN (online)	2523-899X
ISSN	2096-5230
DOI	10.1007/s11596-022-2655-8
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Book: Ying-Han wangluo jishu cidian

Sun, Xuling

An English-Chinese dictionary of networking

2006

Title variant	An English-Chinese dictionary of networking
Author's details	Ed.: Xuling Sun
Language	English ; Chinese
Size	535 S.
Edition	1. Aufl., Nachdr.
Publisher	Qinghua Daxue
Publishing place	Tsinghua
Document type	Book
ISBN	7302123578 ; 9787302123576
Database	Library catalogue of the German National Library of Science and Technology (TIB), Hannover

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Article ; Online: PIK3R3 inhibits cell senescence through p53/p21 signaling.

Chen, Qianzhi / Sun, Xuling / Luo, Xuelai / Wang, Jing / Hu, Junbo / Feng, Yongdong

Cell death & disease

2020 Volume 11, Issue 9, Page(s) 798

Abstract: Cellular senescence is a stress response of human cells that removes potentially harmful cells by initiating cell cycle arrest. Inducing senescence of tumor cells may be an effective tumor-inhibiting strategy. In this study we found that PIK3R3 could ... ...

Abstract	Cellular senescence is a stress response of human cells that removes potentially harmful cells by initiating cell cycle arrest. Inducing senescence of tumor cells may be an effective tumor-inhibiting strategy. In this study we found that PIK3R3 could inhibit the cell senescence of colorectal cancer cells and promote cell proliferation through the p53/p21 signal pathway. PIK3R3 could bind to p53 and inhibit the binding of p53 to the p21 gene promoter region, and thus affecting the transcriptional activity of p21 gene. Our study has provided new evidence of the role of PIK3R3 in p53 regulation and inhibition of PIK3R3 may be one of the potential targets of tumor therapy.
MeSH term(s)	Animals ; Cellular Senescence ; Cyclin-Dependent Kinase Inhibitor p21/metabolism ; Humans ; Mice ; Mice, Nude ; Phosphatidylinositol 3-Kinases/metabolism ; Signal Transduction ; Tumor Suppressor Protein p53/metabolism
Chemical Substances	Cyclin-Dependent Kinase Inhibitor p21 ; Tumor Suppressor Protein p53 ; PIK3R3 protein, human (EC 2.7.1.137)
Language	English
Publishing date	2020-09-24
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2541626-1
ISSN	2041-4889 ; 2041-4889
ISSN (online)	2041-4889
ISSN	2041-4889
DOI	10.1038/s41419-020-02921-z
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Article ; Online: EZH2-triggered methylation of SMAD3 promotes its activation and tumor metastasis.

Huang, Changsheng / Hu, Fuqing / Song, Da / Sun, Xuling / Liu, Anyi / Wu, Qi / She, Xiaowei / Chen, Yaqi / Chen, Lisheng / Hu, Fayong / Xu, Feng / Luo, Xuelai / Feng, Yongdong / Yang, Xiangping / Hu, Junbo / Wang, Guihua

The Journal of clinical investigation

2022 Volume 132, Issue 5

Abstract: SMAD3 plays a central role in cancer metastasis, and its hyperactivation is linked to poor cancer outcomes. Thus, it is critical to understand the upstream signaling pathways that govern SMAD3 activation. Here, we report that SMAD3 underwent methylation ... ...

Abstract	SMAD3 plays a central role in cancer metastasis, and its hyperactivation is linked to poor cancer outcomes. Thus, it is critical to understand the upstream signaling pathways that govern SMAD3 activation. Here, we report that SMAD3 underwent methylation at K53 and K333 (K53/K333) by EZH2, a process crucial for cell membrane recruitment, phosphorylation, and activation of SMAD3 upon TGFB1 stimulation. Mechanistically, EZH2-triggered SMAD3 methylation facilitated SMAD3 interaction with its cellular membrane localization molecule (SARA), which in turn sustained SMAD3 phosphorylation by the TGFB receptor. Pathologically, increased expression of EZH2 expression resulted in the accumulation of SMAD3 methylation to facilitate SMAD3 activation. EZH2-mediated SMAD3 K53/K333 methylation was upregulated and correlated with SMAD3 hyperactivation in breast cancer, promoted tumor metastasis, and was predictive of poor survival outcomes. We used 2 TAT peptides to abrogate SMAD3 methylation and therapeutically inhibit cancer metastasis. Collectively, these findings reveal the complicated layers involved in the regulation of SMAD3 activation coordinated by EZH2-mediated SMAD3 K53/K333 methylation to drive cancer metastasis.
MeSH term(s)	Breast Neoplasms/pathology ; Cell Line, Tumor ; Enhancer of Zeste Homolog 2 Protein/genetics ; Enhancer of Zeste Homolog 2 Protein/metabolism ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; Methylation ; Phosphorylation ; Signal Transduction ; Smad3 Protein/genetics ; Smad3 Protein/metabolism
Chemical Substances	SMAD3 protein, human ; Smad3 Protein ; EZH2 protein, human (EC 2.1.1.43) ; Enhancer of Zeste Homolog 2 Protein (EC 2.1.1.43)
Language	English
Publishing date	2022-01-27
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3067-3
ISSN	1558-8238 ; 0021-9738
ISSN (online)	1558-8238
ISSN	0021-9738
DOI	10.1172/JCI152394
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Article: SIX4 promotes metastasis through STAT3 activation in breast cancer.

Sun, Xuling / Ma, Jin / Chen, Qianzhi / Hou, Zhenlin / Luo, Xuelai / Wang, Guihua / Wang, Jing / Hu, Junbo / Cao, Zhixin

American journal of cancer research

2020 Volume 10, Issue 1, Page(s) 224–236

Abstract: Sine oculis homeobox homolog 4 (SIX4), a member of the SIX family, play important role in the development and construction of vertebrate tissues and organs. There is very little known about the function of SIX4 in cancer cells. Herein, we investigated ... ...

Abstract	Sine oculis homeobox homolog 4 (SIX4), a member of the SIX family, play important role in the development and construction of vertebrate tissues and organs. There is very little known about the function of SIX4 in cancer cells. Herein, we investigated whether SIX4 promote cancer metastasis in addition to its direct role in breast cancer cells. Our study showed that the expression of SIX4 was profoundly increased in breast cancer tissues, and the high expression of SIX4 correlated strongly with distant metastasis and poor prognosis. Functional experiments demonstrated that SIX4 obviously promoted the cell migration and invasion of breast cancer cells, and up-regulated the expression of EMT mesenchymal marker, down-regulated the epithelial molecules by Snai1 induction
Language	English
Publishing date	2020-01-01
Publishing country	United States
Document type	Journal Article
ZDB-ID	2589522-9
ISSN	2156-6976
ISSN	2156-6976
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Article ; Online: SIX4 activates Akt and promotes tumor angiogenesis.

Sun, Xuling / Hu, Fuqing / Hou, Zhenlin / Chen, Qianzhi / Lan, Jingqin / Luo, Xuelai / Wang, Guihua / Hu, Junbo / Cao, Zhixin

Experimental cell research

2019 Volume 383, Issue 1, Page(s) 111495

Abstract: Angiogenesis plays important roles in solid tumors progression. Growth factors such as vascular endothelial growth factors (VEGFs) can induce angiogenesis and hypoxia promotes the expression of VEGFs through activating hypoxia-inducible factor 1 (HIF-1α). ...

Abstract	Angiogenesis plays important roles in solid tumors progression. Growth factors such as vascular endothelial growth factors (VEGFs) can induce angiogenesis and hypoxia promotes the expression of VEGFs through activating hypoxia-inducible factor 1 (HIF-1α). However, the regulation of HIF-1α still not been fully understood. Here, we demonstrate that the Sine Oculis Homeobox Homolog 4 (SIX4) is up-regulated in colorectal cancer (CRC) and high expression of SIX4 predicts a poor prognosis. Overexpression of SIX4 enhances tumor growth and angiogenesis in vitro and in vivo, while knockdown of SIX4 inhibits tumor growth and angiogenesis. Furthermore, we show that SIX4 increases the expression of VEGF-A by coordinating with the HIF-1α. Mechanically, we explore that SIX4 up-regulates the expression of HIF-1α depending on Akt activation. Collectively, we demonstrate that SIX4 is functional in regulating tumor angiogenesis and SIX4 might be used as anti-angiogenic therapy in CRC.
MeSH term(s)	Animals ; Apoptosis ; Biomarkers, Tumor/genetics ; Biomarkers, Tumor/metabolism ; Cell Proliferation ; Colorectal Neoplasms/blood supply ; Colorectal Neoplasms/metabolism ; Colorectal Neoplasms/pathology ; Female ; Gene Expression Regulation, Neoplastic ; Homeodomain Proteins/genetics ; Homeodomain Proteins/metabolism ; Humans ; Lymphatic Metastasis ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Middle Aged ; Neovascularization, Pathologic/metabolism ; Neovascularization, Pathologic/pathology ; Prognosis ; Proto-Oncogene Proteins c-akt/genetics ; Proto-Oncogene Proteins c-akt/metabolism ; Signal Transduction ; Survival Rate ; Trans-Activators/genetics ; Trans-Activators/metabolism ; Tumor Cells, Cultured ; Wound Healing ; Xenograft Model Antitumor Assays
Chemical Substances	Biomarkers, Tumor ; Homeodomain Proteins ; SIX4 protein, human ; Trans-Activators ; AKT1 protein, human (EC 2.7.11.1) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1)
Language	English
Publishing date	2019-07-10
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1493-x
ISSN	1090-2422 ; 0014-4827
ISSN (online)	1090-2422
ISSN	0014-4827
DOI	10.1016/j.yexcr.2019.111495
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Article ; Online: PRMT5 methylating SMAD4 activates TGF-β signaling and promotes colorectal cancer metastasis.

Liu, Anyi / Yu, Chengxin / Qiu, Cheng / Wu, Qi / Huang, Changsheng / Li, Xun / She, Xiaowei / Wan, Kairui / Liu, Lang / Li, Mao / Wang, Zhihong / Chen, Yaqi / Hu, Fuqing / Song, Da / Li, Kangdi / Zhao, Chongchong / Deng, Haiteng / Sun, Xuling / Xu, Feng /

Lai, Senyan / Luo, Xuelai / Hu, Junbo / Wang, Guihua

Oncogene

2023 Volume 42, Issue 19, Page(s) 1572–1584

Abstract: Perturbations in transforming growth factor-β (TGF-β) signaling can lead to a plethora of diseases, including cancer. Mutations and posttranslational modifications (PTMs) of the partner of SMAD complexes contribute to the dysregulation of TGF-β signaling. ...

Abstract	Perturbations in transforming growth factor-β (TGF-β) signaling can lead to a plethora of diseases, including cancer. Mutations and posttranslational modifications (PTMs) of the partner of SMAD complexes contribute to the dysregulation of TGF-β signaling. Here, we reported a PTM of SMAD4, R361 methylation, that was critical for SMAD complexes formation and TGF-β signaling activation. Through mass spectrometric, co-immunoprecipitation (Co-IP) and immunofluorescent (IF) assays, we found that oncogene protein arginine methyltransferase 5 (PRMT5) interacted with SMAD4 under TGF-β1 treatment. Mechanically, PRMT5 triggered SMAD4 methylation at R361 and induced SMAD complexes formation and nuclear import. Furthermore, we emphasized that PRMT5 interacting and methylating SMAD4 was required for TGF-β1-induced epithelial-mesenchymal transition (EMT) and colorectal cancer (CRC) metastasis, and SMAD4 R361 mutation diminished PRMT5 and TGF-β1-induced metastasis. In addition, highly expressed PRMT5 or high level of SMAD4 R361 methylation indicated worse outcomes in clinical specimens analysis. Collectively, our study highlights the critical interaction of PRMT5 and SMAD4 and the roles of SMAD4 R361 methylation for controlling TGF-β signaling during metastasis. We provided a new insight for SMAD4 activation. And this study indicated that blocking PRMT5-SMAD4 signaling might be an effective targeting strategy in SMAD4 wild-type CRC.
MeSH term(s)	Humans ; Cell Line, Tumor ; Colorectal Neoplasms/pathology ; Protein-Arginine N-Methyltransferases/genetics ; Protein-Arginine N-Methyltransferases/metabolism ; Signal Transduction ; Smad4 Protein/genetics ; Smad4 Protein/metabolism ; Transforming Growth Factor beta/metabolism ; Transforming Growth Factor beta1/metabolism ; Neoplasm Metastasis
Chemical Substances	PRMT5 protein, human (EC 2.1.1.319) ; Protein-Arginine N-Methyltransferases (EC 2.1.1.319) ; Smad4 Protein ; SMAD4 protein, human ; Transforming Growth Factor beta ; Transforming Growth Factor beta1
Language	English
Publishing date	2023-03-29
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	639046-8
ISSN	1476-5594 ; 0950-9232
ISSN (online)	1476-5594
ISSN	0950-9232
DOI	10.1038/s41388-023-02674-x
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Article ; Online: The combination therapy of high-intensity focused ultrasound with radiotherapy in locally advanced pancreatic carcinoma.

Li, Yu-Jiang / Huang, Gui-Lin / Sun, Xu-Ling / Zhao, Xin-Chun / Li, Zhi-Gang

World journal of surgical oncology

2016 Volume 14, Page(s) 60

Abstract: Background: The aim of the present study is to evaluate the effectiveness of the combined application of high-intensity focused ultrasound (HIFU) and radiotherapy in the treatment of locally advanced pancreatic carcinoma (LAPC).: Methods: A total ... ...

Abstract	Background: The aim of the present study is to evaluate the effectiveness of the combined application of high-intensity focused ultrasound (HIFU) and radiotherapy in the treatment of locally advanced pancreatic carcinoma (LAPC). Methods: A total number of sixteen patients with LAPC started treatment beginning with HIFU and radiotherapy 1 week after the HIFU treatment. Evaluation of the effectiveness of treatment was performed using main clinical symptoms, serum levels of CA-19-9, Response Evaluation Criteria in Solid Tumors (RECIST) guidelines, and the Kaplan-Meier method for estimating median overall survival (OS). The occurrence of adverse reactions was recorded. Results: The main clinical symptoms including abdominal pain and lower back pain were alleviated, and the mean visual analog scale (VAS) pain score declined from 5.1 points to just 3.3 points immediately after the HIFU treatment. The median pain relief time was 5.6 months after radiotherapy, serum CA-19-9 levels began to decrease significantly 1 week after the HIFU treatment, from 102.1 to 60.8 U/ml, and the median continuous decline time was 4.3 months after radiotherapy. Partial response (PR) was observed in seven of sixteen patients, with stable disease (SD) in four patients, and progressive disease (PD) in the remaining five patients at 6 months after radiotherapy. Serum levels of amylopsin and lipase were not elevated to abnormal levels. The median OS was 14 months. No serious adverse reactions occurred. Conclusions: Treatment with both HIFU and radiotherapy can quickly improve symptoms and the quality of life and prolong survival lengths. This combination might be a promising therapeutic treatment for patients with LAPC.
MeSH term(s)	Aged ; Combined Modality Therapy ; Female ; Follow-Up Studies ; High-Intensity Focused Ultrasound Ablation ; Humans ; Male ; Middle Aged ; Neoplasm Staging ; Pancreatic Neoplasms/pathology ; Pancreatic Neoplasms/therapy ; Prognosis ; Radiotherapy ; Pancreatic Neoplasms
Language	English
Publishing date	2016-02-29
Publishing country	England
Document type	Journal Article
ZDB-ID	2118383-1
ISSN	1477-7819 ; 1477-7819
ISSN (online)	1477-7819
ISSN	1477-7819
DOI	10.1186/s12957-016-0809-5
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Article ; Online: Inhibition of SIRT2 limits tumour angiogenesis via inactivation of the STAT3/VEGFA signalling pathway.

Hu, Fuqing / Sun, Xuling / Li, Geng / Wu, Qi / Chen, Yaqi / Yang, Xi / Luo, Xuelai / Hu, Junbo / Wang, Guihua

Cell death & disease

2018 Volume 10, Issue 1, Page(s) 9

Abstract: Mounting evidence has demonstrated that angiogenesis plays an important role in tumour progression. However, the key regulators in tumour angiogenesis remain unclear. Recently, emerging reports have indicated that SIRT2 plays critical roles in ... ...

Abstract	Mounting evidence has demonstrated that angiogenesis plays an important role in tumour progression. However, the key regulators in tumour angiogenesis remain unclear. Recently, emerging reports have indicated that SIRT2 plays critical roles in proliferation, metastasis and tumourigenesis in diverse tumours. However, the function of SIRT2 in tumour angiogenesis and the mechanism underlying the regulation of angiogenesis by SIRT2 are still unknown. Here, we found that SIRT2 was upregulated in colorectal cancer tissues compared to that in normal samples and that the elevated SIRT2 was associated with poor prognosis in patients with colorectal cancer. In addition, a series of in vitro and in vivo experiments were performed to demonstrate the role of SIRT2 in tumour angiogenesis. We showed that silencing SIRT2 significantly suppressed tumour angiogenesis. Mechanistically, the knockdown of SIRT2 inhibited STAT3 phosphorylation, causing decreased secretion of VEGFA. Notably, we found that SIRT2 directly interacted with STAT3 and affected the phosphorylation of STAT3 and the translocation of phosphorylated STAT3 to the nucleus. Importantly, a series of rescue experiments suggested that the function of SIRT2 in tumour angiogenesis depends on the STAT3/VEGFA signalling pathway. Our findings provide insight into the important role of SIRT2 in colon tumour angiogenesis and suggest that SIRT2/STAT3/VEGFA might be a novel prognostic biomarker and a potential therapeutic target for patients with colorectal cancer.
MeSH term(s)	Cell Line, Tumor ; Colorectal Neoplasms/blood supply ; Colorectal Neoplasms/metabolism ; Colorectal Neoplasms/pathology ; Colorectal Neoplasms/therapy ; Human Umbilical Vein Endothelial Cells ; Humans ; Neoplasm Proteins/antagonists & inhibitors ; Neoplasm Proteins/metabolism ; Neovascularization, Pathologic/metabolism ; Neovascularization, Pathologic/therapy ; STAT3 Transcription Factor/metabolism ; Signal Transduction ; Sirtuin 2/antagonists & inhibitors ; Sirtuin 2/metabolism ; Vascular Endothelial Growth Factor A/metabolism
Chemical Substances	Neoplasm Proteins ; STAT3 Transcription Factor ; STAT3 protein, human ; VEGFA protein, human ; Vascular Endothelial Growth Factor A ; SIRT2 protein, human (EC 3.5.1.-) ; Sirtuin 2 (EC 3.5.1.-)
Language	English
Publishing date	2018-12-18
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2541626-1
ISSN	2041-4889 ; 2041-4889
ISSN (online)	2041-4889
ISSN	2041-4889
DOI	10.1038/s41419-018-1260-z
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