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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: MiR-363-3p inhibits the epithelial-to-mesenchymal transition and suppresses metastasis in colorectal cancer by targeting Sox4

Hu, Fayong / Min, Jiang / Cao, Xiaonian / Liu, Liang / Ge, Zongqing / Hu, Junbo / Li, Xiaolan

Biochemical and biophysical research communications. 2016,

2016

Abstract: Epithelial-to-mesenchymal transition (EMT) plays an essential role in cancer invasion and metastasis and is associated with tumor recurrence in colorectal cancer (CRC). However, the mechanism that contributes to EMT have not been fully understood in CRC. ...

Abstract	Epithelial-to-mesenchymal transition (EMT) plays an essential role in cancer invasion and metastasis and is associated with tumor recurrence in colorectal cancer (CRC). However, the mechanism that contributes to EMT have not been fully understood in CRC. In the present study, we showed that miR-363-3p was frequently down-regulated in CRC tissue specimens with lymph node metastasis. Moreover, we demonstrated that down-regulation of miR-363-3p promoted CRC cell migration and invasion, and induced EMT in vitro and in vivo, revealing that miR-363-3p playes a potential tumor-suppressive role in CRC. Analysis of the underlying mechanisms revealed that miR-363-3p could regulate Sox4 expression by directly targeting its 3'untranslated region. Down-regulation of miR-363-3p increased Sox4 expression and induced EMT, while overexpression of miR-363-3p decreased Sox4 expression. Taken together, our findings indicate that miR-363-3p is involved in CRC metastasis and functions as a tumor suppressor via negatively regulating Sox4. Therefore, the up-regulation of miR-363-3p in human CRC may have therapeutic benefits.
Keywords	cell movement ; colorectal neoplasms ; humans ; lymph nodes ; metastasis
Language	English
Size	p. .
Publishing place	Elsevier Inc.
Document type	Article
Note	Pre-press version
ZDB-ID	205723-2
ISSN	0006-291X ; 0006-291X
ISSN (online)	0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2016.04.055
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: MiR-363-3p inhibits the epithelial-to-mesenchymal transition and suppresses metastasis in colorectal cancer by targeting Sox4.

Hu, Fayong / Min, Jiang / Cao, Xiaonian / Liu, Liang / Ge, Zongqing / Hu, Junbo / Li, Xiaolan

Biochemical and biophysical research communications

2016 Volume 474, Issue 1, Page(s) 35–42

Abstract	Epithelial-to-mesenchymal transition (EMT) plays an essential role in cancer invasion and metastasis and is associated with tumor recurrence in colorectal cancer (CRC). However, the mechanism that contributes to EMT have not been fully understood in CRC. In the present study, we showed that miR-363-3p was frequently down-regulated in CRC tissue specimens with lymph node metastasis. Moreover, we demonstrated that down-regulation of miR-363-3p promoted CRC cell migration and invasion, and induced EMT in vitro and in vivo, revealing that miR-363-3p playes a potential tumor-suppressive role in CRC. Analysis of the underlying mechanisms revealed that miR-363-3p could regulate Sox4 expression by directly targeting its 3'untranslated region. Down-regulation of miR-363-3p increased Sox4 expression and induced EMT, while overexpression of miR-363-3p decreased Sox4 expression. Taken together, our findings indicate that miR-363-3p is involved in CRC metastasis and functions as a tumor suppressor via negatively regulating Sox4. Therefore, the up-regulation of miR-363-3p in human CRC may have therapeutic benefits.
MeSH term(s)	Animals ; Cell Line, Tumor ; Cell Movement/genetics ; Colorectal Neoplasms/genetics ; Colorectal Neoplasms/pathology ; Colorectal Neoplasms/secondary ; Down-Regulation ; Epithelial-Mesenchymal Transition/genetics ; Genes, Tumor Suppressor ; Humans ; Lymphatic Metastasis ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; MicroRNAs/genetics ; Neoplasm Invasiveness/genetics ; SOXC Transcription Factors/genetics ; Tumor Cells, Cultured
Chemical Substances	MIRN363 microRNA, human ; MicroRNAs ; SOX4 protein, human ; SOXC Transcription Factors
Language	English
Publishing date	2016--20
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	205723-2
ISSN	1090-2104 ; 0006-291X ; 0006-291X
ISSN (online)	1090-2104 ; 0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2016.04.055
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Article ; Online: Human colorectal cancer-derived mesenchymal stem cells promote colorectal cancer progression through IL-6/JAK2/STAT3 signaling.

Zhang, Xiaochao / Hu, Fayong / Li, Geng / Li, Guodong / Yang, Xi / Liu, Liang / Zhang, Rongsheng / Zhang, Bixiang / Feng, Yongdong

Cell death & disease

2018 Volume 9, Issue 2, Page(s) 25

Abstract: Mesenchymal stem cells (MSCs) have been reported to localize in colorectal carcinomas, and participate in the formation of the tumor microenvironment. They have recently been isolated from colorectal cancer tissues, and are implicated in the growth, ... ...

Abstract	Mesenchymal stem cells (MSCs) have been reported to localize in colorectal carcinomas, and participate in the formation of the tumor microenvironment. They have recently been isolated from colorectal cancer tissues, and are implicated in the growth, invasion, and metastasis of cancer cells. However, the roles and detailed mechanisms associated with human colorectal cancer-derived MSCs (CC-MSCs) have not been fully addressed. In this study, we found that CC-MSCs increased the migration and invasion of colorectal cancer cells and promoted the tumorigenesis of colorectal cancer through epithelial-to-mesenchymal transition (EMT) in vitro. We also found that CC-MSCs enhanced the growth and metastasis of colorectal cancer in vivo. Mechanistically, we determined that interleukin-6 (IL-6) was the most highly expressed cytokine in the CC-MSC conditioned medium, and promoted the progression of colorectal cancer cells through IL-6/JAK2/STAT3 signaling, which activated PI3K/AKT signaling. We used anti-IL-6 antibody to target IL-6. Collectively, these results reveal that the IL-6 secreted by CC-MSCs enhances the progression of colorectal cancer cells through IL-6/JAK2/STAT3 signaling, and could provide a novel therapeutic or preventive target.
MeSH term(s)	Cell Line, Tumor ; Colorectal Neoplasms/genetics ; Colorectal Neoplasms/metabolism ; Colorectal Neoplasms/pathology ; Disease Progression ; Humans ; Interleukin-6/metabolism ; Mesenchymal Stem Cells/metabolism ; STAT3 Transcription Factor/metabolism ; Signal Transduction
Chemical Substances	Interleukin-6 ; STAT3 Transcription Factor
Language	English
Publishing date	2018-01-18
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/s41419-017-0176-3
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: IL-6 regulates autophagy and chemotherapy resistance by promoting BECN1 phosphorylation.

Hu, Fuqing / Song, Da / Yan, Yumeng / Huang, Changsheng / Shen, Chentao / Lan, Jingqin / Chen, Yaqi / Liu, Anyi / Wu, Qi / Sun, Li / Xu, Feng / Hu, Fayong / Chen, Lisheng / Luo, Xuelai / Feng, Yongdong / Huang, Shengyou / Hu, Junbo / Wang, Guihua

Nature communications

2021 Volume 12, Issue 1, Page(s) 3651

Abstract: Extracellular cytokines are enriched in the tumor microenvironment and regulate various important properties of cancers, including autophagy. However, the precise molecular mechanisms underlying the link between autophagy and extracellular cytokines ... ...

Abstract	Extracellular cytokines are enriched in the tumor microenvironment and regulate various important properties of cancers, including autophagy. However, the precise molecular mechanisms underlying the link between autophagy and extracellular cytokines remain to be elucidated. In the present study, we demonstrate that IL-6 activates autophagy through the IL-6/JAK2/BECN1 pathway and promotes chemotherapy resistance in colorectal cancer (CRC). Mechanistically, IL-6 triggers the interaction between JAK2 and BECN1, where JAK2 phosphorylates BECN1 at Y333. We demonstrate that BECN1 Y333 phosphorylation is crucial for BECN1 activation and IL-6-induced autophagy by regulating PI3KC3 complex formation. Furthermore, we investigate BECN1 Y333 phosphorylation as a predictive marker for poor CRC prognosis and chemotherapy resistance. Combination treatment with autophagy inhibitors or pharmacological agents targeting the IL-6/JAK2/BECN1 signaling pathway may represent a potential strategy for CRC cancer therapy.
Language	English
Publishing date	2021-06-15
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-021-23923-1
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Article ; Online: miR-19a contributes to gefitinib resistance and epithelial mesenchymal transition in non-small cell lung cancer cells by targeting c-Met.

Cao, Xiaonian / Lai, Senyan / Hu, Fayong / Li, Guodong / Wang, Guihua / Luo, Xuelai / Fu, Xiangning / Hu, Junbo

Scientific reports

2017 Volume 7, Issue 1, Page(s) 2939

Abstract: Gefitinib, an epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor, is used as a first-line treatment for advanced non-small cell lung cancer (NSCLC). However, most NSCLC patients inevitably develop gefitinib resistance, and the mechanisms ... ...

Abstract	Gefitinib, an epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor, is used as a first-line treatment for advanced non-small cell lung cancer (NSCLC). However, most NSCLC patients inevitably develop gefitinib resistance, and the mechanisms underlying this resistance are not fully understood. In this study, we show that miR-19a is significantly down-regulated in gefitinib-resistant NSCLC cell lines compared with gefitinib-sensitive cell lines. In addition, the down-regulation of miR-19a suppressed the expression of epithelial markers but induced the expression levels of mesenchymal markers. A mechanistic analysis revealed that miR-19a regulated c-Met expression by directly targeting the c-Met 3'UTR. Overexpression of miR-19a decreased c-Met expression and re-sensitized gefitinib-resistant NSCLC cells in vitro and in vivo. Consistent with the in vitro findings, the miR-19a serum level was significantly decreased in NSCLC patients with acquired gefitinib resistance compared with the level observed prior to the acquisition of resistance in each patient, indicating that miR-19a expression may be a valuable biomarker for the prediction of acquired gefitinib resistance in a clinical setting. Our data demonstrate that the miR-19a/c-Met pathway plays a critical role in acquired resistance to gefitinib and that the manipulation of miR-19a might provide a therapeutic strategy for overcoming acquired gefitinib resistance.
MeSH term(s)	3' Untranslated Regions ; Animals ; Carcinoma, Non-Small-Cell Lung/diagnostic imaging ; Carcinoma, Non-Small-Cell Lung/genetics ; Carcinoma, Non-Small-Cell Lung/pathology ; Cell Line, Tumor ; Cell Movement/drug effects ; Cell Proliferation/drug effects ; Cell Survival/drug effects ; Cell Survival/genetics ; Disease Models, Animal ; Drug Resistance, Neoplasm/genetics ; Epithelial-Mesenchymal Transition/drug effects ; Epithelial-Mesenchymal Transition/genetics ; Gefitinib/pharmacology ; Gene Expression Regulation, Neoplastic/drug effects ; Genes, Reporter ; Humans ; Lung Neoplasms/diagnostic imaging ; Lung Neoplasms/genetics ; Lung Neoplasms/pathology ; Mice ; MicroRNAs/genetics ; Proto-Oncogene Proteins c-met/genetics ; Proto-Oncogene Proteins c-met/metabolism ; RNA Interference ; Signal Transduction ; Tomography, X-Ray Computed ; Xenograft Model Antitumor Assays
Chemical Substances	3' Untranslated Regions ; MIRN19 microRNA, human ; MicroRNAs ; MET protein, human (EC 2.7.10.1) ; Proto-Oncogene Proteins c-met (EC 2.7.10.1) ; Gefitinib (S65743JHBS)
Language	English
Publishing date	2017-06-07
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-017-01153-0
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: miR-124 modulates gefitinib resistance through SNAI2 and STAT3 in non-small cell lung cancer.

Hu, Fa-Yong / Cao, Xiao-Nian / Xu, Qin-Zi / Deng, Yu / Lai, Sen-Yan / Ma, Jing / Hu, Jun-Bo

Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban

2016 Volume 36, Issue 6, Page(s) 839–845

Abstract: Gefitinib is used as a first-line treatment for advanced non-small cell lung cancer (NSCLC). Unfortunately, most NSCLC patients inevitably develop gefitinib resistance during treatment. In addition to EGFR mutation status, the mechanisms involved are ... ...

Abstract	Gefitinib is used as a first-line treatment for advanced non-small cell lung cancer (NSCLC). Unfortunately, most NSCLC patients inevitably develop gefitinib resistance during treatment. In addition to EGFR mutation status, the mechanisms involved are largely unknown. In this study, we showed that miR-124, a tumor suppressor, was significantly down-regulated in gefitinib-resistant NSCLC patients and cell lines compared with gefitinib-sensitive patients and cell lines. In addition, the miR-124 depletion induced gefitinib resistance, and miR-124 overexpression sensitized gefitinib-resistant cells to gefitinib. Mechanistic analysis revealed that miR-124 decreased SNAI2 and STAT3 expression by directly targeting their 3'UTRs and that knocking down SNAI2 or STAT3 partly reversed the gefitinib resistance induced by miR-124 depletion. Our data demonstrate that the miR-124 plays a new critical role in acquired resistance to gefitinib and that the manipulation of miR-124 might provide a therapeutic strategy for reversing acquired gefitinib resistance.
MeSH term(s)	3' Untranslated Regions ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Carcinoma, Non-Small-Cell Lung/drug therapy ; Carcinoma, Non-Small-Cell Lung/genetics ; Carcinoma, Non-Small-Cell Lung/metabolism ; Cell Line, Tumor ; Drug Resistance, Neoplasm/genetics ; HEK293 Cells ; Humans ; Lung Neoplasms/drug therapy ; Lung Neoplasms/genetics ; Lung Neoplasms/metabolism ; MicroRNAs/genetics ; Quinazolines/pharmacology ; Quinazolines/therapeutic use ; STAT3 Transcription Factor/genetics ; STAT3 Transcription Factor/metabolism ; Snail Family Transcription Factors/genetics ; Snail Family Transcription Factors/metabolism
Chemical Substances	3' Untranslated Regions ; Antineoplastic Agents ; MIRN124 microRNA, human ; MicroRNAs ; Quinazolines ; SNAI2 protein, human ; STAT3 Transcription Factor ; STAT3 protein, human ; Snail Family Transcription Factors ; gefitinib (S65743JHBS)
Language	English
Publishing date	2016-12
Publishing country	China
Document type	Journal Article
ZDB-ID	2090603-1
ISSN	1993-1352 ; 1672-0733 ; 0257-716X
ISSN (online)	1993-1352
ISSN	1672-0733 ; 0257-716X
DOI	10.1007/s11596-016-1672-x
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Article ; Online: Expression of HAX-1 in colorectal cancer and its role in cancer cell growth.

Li, Xiaolan / Jiang, Jianwu / Yang, Rui / Xu, Xiangshang / Hu, Fayong / Liu, Anding / Tao, Deding / Leng, Yan / Hu, Junbo / Gong, Jianping / Luo, Xuelai

Molecular medicine reports

2015 Volume 12, Issue 3, Page(s) 4071–4078

Abstract: Colorectal cancer (CRC) is one of the most common types of cancer worldwide. Hematopoietic cell‑specific protein 1‑associated protein X‑1 (HAX‑1) has been found to be involved in several types of cancer. However, the role of HAX‑1 in CRC remains to be ... ...

Abstract	Colorectal cancer (CRC) is one of the most common types of cancer worldwide. Hematopoietic cell‑specific protein 1‑associated protein X‑1 (HAX‑1) has been found to be involved in several types of cancer. However, the role of HAX‑1 in CRC remains to be elucidated. The aim of the present study was to investigate whether the expression of HAX‑1 is associated with the progression of CRC, and to determine the effects of HAX‑1 on the apoptosis and proliferation of CRC cells. Tumor tissues and adjacent noncancerous tissues were collected from 60 patients with CRC, following the provision of informed consent. The expression levels of HAX‑1 and the association with clinical and pathological characteristics were then analyzed. The expression levels of HAX‑1 were significantly higher in the cancerous tissues from the patients with CRC, particularly in tissues of an advanced stage of cancer. In addition, HAX‑1 expression was associated with malignant progression and poor prognosis. Furthermore, SW480 CRC cells, overexpressing HAX‑1, exhibited increased resistance to camptothecin in vitro, and promoted proliferation in vitro and in vivo. By contrast, HAX‑1 knockdown significantly decreased the proliferation. In addition, the expression levels of ki‑67 and phosphorylated‑akt were inhibited following HAX‑1 knockdown. In conclusion, the expression levels of HAX‑1 were increased in cancerous tissue from patients with CRC, and were associated with progression of the disease. These results suggested that HAX‑1 may contribute to chemotherapy resistance and malignant progression in CRC.
MeSH term(s)	Adaptor Proteins, Signal Transducing/antagonists & inhibitors ; Adaptor Proteins, Signal Transducing/genetics ; Adaptor Proteins, Signal Transducing/metabolism ; Aged ; Animals ; Apoptosis ; Cell Line, Tumor ; Cell Proliferation ; Colorectal Neoplasms/diagnosis ; Colorectal Neoplasms/metabolism ; Colorectal Neoplasms/pathology ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; Immunohistochemistry ; Ki-67 Antigen/metabolism ; Male ; Mice ; Mice, Nude ; Middle Aged ; Prognosis ; RNA Interference ; RNA, Small Interfering/genetics ; RNA, Small Interfering/metabolism ; Transplantation, Heterologous
Chemical Substances	Adaptor Proteins, Signal Transducing ; HAX1 protein, human ; Ki-67 Antigen ; RNA, Small Interfering
Language	English
Publishing date	2015-09
Publishing country	Greece
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1791-3004
ISSN (online)	1791-3004
DOI	10.3892/mmr.2015.3905
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: MiR-363-3p inhibits the epithelial-to-mesenchymal transition and suppresses metastasis in colorectal cancer by targeting Sox4

Hu, Fayong / Jiang MinauthorGastrointestinal Surgery Department, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China / Xiaonian CaoauthorCancer Research Institute, Tongji Hospital, Huazhong University of Science and Technology, Wuhan, China / Liang LiuauthorCancer Research Institute, Tongji Hospital, Huazhong University of Science and Technology, Wuhan, China / Zongqing GeauthorCancer Research Institute, Tongji Hospital, Huazhong University of Science and Technology, Wuhan, China / Junbo HuauthorCancer Research Institute, Tongji Hospital, Huazhong University of Science and Technology, Wuhan, China / Xiaolan LiauthorCancer Research Institute, Tongji Hospital, Huazhong University of Science and Technology, Wuhan, China

Language	English
Document type	Article
Database	AGRIS - International Information System for the Agricultural Sciences and Technology

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