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Article ; Online: Advances on the role of PTTG1 in the pathogenesis of tumors

WU Nianping / HUANG Huili / ZHOU Kuaile / ZHOU Cefan / TANG Jingfeng

Jichu yixue yu linchuang, Vol 43, Iss 9, Pp 1448-

2023 Volume 1452

Abstract: Pituitary tumor transforming gene 1(PTTG1) is an oncogene which isolated from the pituitary gland. PTTG1 was previously reported to bind and inhibit separase to affect sister chromatid separation and lead to chromosome aneuploidy, activate the DNA damage ...

Abstract	Pituitary tumor transforming gene 1(PTTG1) is an oncogene which isolated from the pituitary gland. PTTG1 was previously reported to bind and inhibit separase to affect sister chromatid separation and lead to chromosome aneuploidy, activate the DNA damage response pathway to induce p53-dependent senescence, and also transactivate some oncogenes and promote cell transformation and tumorigenesis in nude mice. It can also promote tumor growth and invasion by affecting Wnt/β-catenin, epithelial-mesenchymal transition(EMT), and TGFβ/SMAD3 pathways. This article provides ideas for the development of tumor therapeutic drugs targeting PTTG1.
Keywords	pituitary tumor transforming gene 1(pttg1)\|mechanism\|tumor ; Medicine ; R
Language	Chinese
Publishing date	2023-09-01T00:00:00Z
Publisher	Institute of Basic Medical Sciences and Peking Union Medical College Hospital, Chinese Academy of Medical Sciences / Peking Union Medical College.
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: RUNDC1 negatively mediates the fusion of autophagosomes with lysosomes via regulating SNARE complex assembly.

Zhang, Rui / Torraca, Vincenzo / Lyu, Hao / Xiao, Shuai / Guo, Dong / Zhou, Cefan / Tang, Jingfeng

Autophagy

2024 Volume 20, Issue 2, Page(s) 454–456

Abstract: Macroautophagy/autophagy is an essential pro-survival mechanism activated in response to nutrient deficiency. The proper fusion between autophagosomes and lysosomes is a critical step for autophagic degradation. We recently reported that RUNDC1 (RUN ... ...

Abstract	Macroautophagy/autophagy is an essential pro-survival mechanism activated in response to nutrient deficiency. The proper fusion between autophagosomes and lysosomes is a critical step for autophagic degradation. We recently reported that RUNDC1 (RUN domain containing 1) inhibits autolysosome formation via clasping the ATG14-STX17-SNAP29 complex to hinder VAMP8 binding. We showed that RUNDC1 colocalizes with LC3 and associates with mature autophagosomes in cell lines and the zebrafish model. We utilized liposome fusion and
MeSH term(s)	Animals ; Autophagosomes/metabolism ; Autophagy/physiology ; Zebrafish/metabolism ; Transcription Factors/metabolism ; Lysosomes/metabolism ; Membrane Fusion/physiology ; SNARE Proteins/metabolism
Chemical Substances	Transcription Factors ; SNARE Proteins
Language	English
Publishing date	2024-01-25
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2454135-7
ISSN	1554-8635 ; 1554-8627
ISSN (online)	1554-8635
ISSN	1554-8627
DOI	10.1080/15548627.2023.2274210
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Article ; Online: Inhibition of TRPP3 by calmodulin through Ca

Liu, Xiong / Wang, Yifang / Weng, Ziyi / Xu, Qinyi / Zhou, Cefan / Tang, JingFeng / Chen, Xing-Zhen

Cell insight

2023 Volume 2, Issue 2, Page(s) 100088

Abstract: Transient receptor potential (TRP) polycystin-3 (TRPP3) is a non-selective cation channel activated by ... ...

Abstract	Transient receptor potential (TRP) polycystin-3 (TRPP3) is a non-selective cation channel activated by Ca
Language	English
Publishing date	2023-02-09
Publishing country	Netherlands
Document type	Journal Article
ISSN	2772-8927
ISSN (online)	2772-8927
DOI	10.1016/j.cellin.2023.100088
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Article: Insights into the Roles of Epigenetic Modifications in Ferroptosis.

Kong, Jinghua / Lyu, Hao / Ouyang, Qian / Shi, Hao / Zhang, Rui / Xiao, Shuai / Guo, Dong / Zhang, Qi / Chen, Xing-Zhen / Zhou, Cefan / Tang, Jingfeng

Biology

2024 Volume 13, Issue 2

Abstract: Ferroptosis is a non-apoptotic mode of cell death driven by membrane lipid peroxidation and is characterized by elevated intracellular levels of ... ...

Abstract	Ferroptosis is a non-apoptotic mode of cell death driven by membrane lipid peroxidation and is characterized by elevated intracellular levels of Fe
Language	English
Publishing date	2024-02-15
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2661517-4
ISSN	2079-7737
ISSN	2079-7737
DOI	10.3390/biology13020122
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Article ; Online: Sense and anti-sense: Role of FAM83A and FAM83A-AS1 in Wnt, EGFR, PI3K, EMT pathways and tumor progression.

Zhao, Chenshu / Li, Xiaowen / Zhang, Rui / Lyu, Hao / Xiao, Shuai / Guo, Dong / Ali, Declan William / Michalak, Marek / Chen, Xing-Zhen / Zhou, Cefan / Tang, Jingfeng

Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie

2024 Volume 173, Page(s) 116372

Abstract: An increasing number of studies have shown that FAM83A, a member of the family with sequence similarity 83 (FAM83), which consists of eight members, is a key tumor therapeutic target involved in multiple signaling pathways. It has been reported that ... ...

Abstract	An increasing number of studies have shown that FAM83A, a member of the family with sequence similarity 83 (FAM83), which consists of eight members, is a key tumor therapeutic target involved in multiple signaling pathways. It has been reported that FAM83A plays essential roles in the regulation of Wnt/β-catenin, EGFR, MAPK, EMT, and other signaling pathways and physiological processes in models of pancreatic cancer, lung cancer, breast cancer, and other malignant tumors. Moreover, the expression of FAM83A could be significantly affected by multiple noncoding RNAs that are dysregulated in malignant tumors, the dysregulation of which is essential for the malignant process. Among these noncoding RNAs, the most noteworthy is the antisense long noncoding (Lnc) RNA of FAM83A itself (FAM83A-AS1), indicating an outstanding synergistic carcinogenic effect between FAM83A and FAM83A-AS1. In the present study, the specific mechanisms by which FAM83A and FAM83A-AS1 cofunction in the Wnt/β-catenin and EGFR signaling pathways were reviewed in detail, which will guide subsequent research. We also described the applications of FAM83A and FAM83A-AS1 in tumor therapy and provided a certain theoretical basis for subsequent drug target development and combination therapy strategies.
MeSH term(s)	Humans ; beta Catenin/genetics ; beta Catenin/metabolism ; Phosphatidylinositol 3-Kinases/metabolism ; Cell Movement/genetics ; Lung Neoplasms/pathology ; ErbB Receptors/genetics ; ErbB Receptors/metabolism ; RNA, Long Noncoding/genetics ; Wnt Signaling Pathway/genetics ; Cell Proliferation/genetics ; Gene Expression Regulation, Neoplastic ; Cell Line, Tumor ; Neoplasm Proteins/metabolism
Chemical Substances	beta Catenin ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; ErbB Receptors (EC 2.7.10.1) ; RNA, Long Noncoding ; EGFR protein, human (EC 2.7.10.1) ; FAM83A protein, human ; Neoplasm Proteins
Language	English
Publishing date	2024-03-02
Publishing country	France
Document type	Journal Article ; Review
ZDB-ID	392415-4
ISSN	1950-6007 ; 0753-3322 ; 0300-0893
ISSN (online)	1950-6007
ISSN	0753-3322 ; 0300-0893
DOI	10.1016/j.biopha.2024.116372
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Article: The TRPV6 Calcium Channel and Its Relationship with Cancer.

Wang, Yifang / Deng, Xiaoling / Zhang, Rui / Lyu, Hao / Xiao, Shuai / Guo, Dong / Ali, Declan William / Michalak, Marek / Zhou, Cefan / Chen, Xing-Zhen / Tang, Jingfeng

Biology

2024 Volume 13, Issue 3

Abstract: Transient receptor potential vanilloid-6 (TRPV6) is a cation channel belonging to the TRP superfamily, specifically the vanilloid subfamily, and is the sixth member of this subfamily. Its presence in the body is primarily limited to the skin, ovaries, ... ...

Abstract	Transient receptor potential vanilloid-6 (TRPV6) is a cation channel belonging to the TRP superfamily, specifically the vanilloid subfamily, and is the sixth member of this subfamily. Its presence in the body is primarily limited to the skin, ovaries, kidney, testes, and digestive tract epithelium. The body maintains calcium homeostasis using the TRPV6 channel, which has a greater calcium selectivity than the other TRP channels. Several pieces of evidence suggest that it is upregulated in the advanced stages of thyroid, ovarian, breast, colon, and prostate cancers. The function of TRPV6 in regulating calcium signaling in cancer will be covered in this review, along with its potential applications as a cancer treatment target.
Language	English
Publishing date	2024-03-05
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2661517-4
ISSN	2079-7737
ISSN	2079-7737
DOI	10.3390/biology13030168
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Article ; Online: Identification of Wnt/β-Catenin- and Autophagy-Related lncRNA Signature for Predicting Immune Efficacy in Pancreatic Adenocarcinoma

Lyu, Hao / Zhang, Jiahui / Wei, Qian / Huang, Yuan / Zhang, Rui / Xiao, Shuai / Guo, Dong / Chen, Xing-Zhen / Zhou, Cefan / Tang, Jingfeng

Biology (Basel). 2023 Feb. 16, v. 12, no. 2

2023

Abstract: Pancreatic cancer is one of the tumors with a poor prognosis. Therefore, it is significant and urgent to explore effective biomarkers for risk stratification and prognosis prediction to promote individualized treatment and prolong the survival of ... ...

Abstract	Pancreatic cancer is one of the tumors with a poor prognosis. Therefore, it is significant and urgent to explore effective biomarkers for risk stratification and prognosis prediction to promote individualized treatment and prolong the survival of patients with PAAD. In this study, we identified Wnt/β-catenin- and autophagy-related long non-coding RNAs (lncRNAs) and demonstrated their role in predicting immune efficacy for PAAD patients. The univariate and multivariate Cox proportional hazards analyses were used to construct a prognostic risk model based on six autophagy- and Wnt/β-catenin-related lncRNAs (warlncRNAs): LINC01347, CASC8, C8orf31, LINC00612, UCA1, and GUSBP11. The high-risk patients were significantly associated with poor overall survival (OS). The receiver operating characteristic (ROC) curve analysis was used to assess the predictive accuracy of the prognostic risk model. The prediction efficiency was supported by the results of an independent validation cohort. Subsequently, a prognostic nomogram combining warlncRNAs with clinical indicators was constructed and showed a good predictive efficiency for survival risk stratification. Furthermore, functional enrichment analysis demonstrated that the signature according to warlncRNAs is closely linked to malignancy-associated immunoregulatory pathways. Correlation analysis uncovered that warlncRNAs’ signature was considerably associated with immunocyte infiltration, immune efficacy, tumor microenvironment score, and drug resistance.
Keywords	adenocarcinoma ; biomarkers ; drug resistance ; immunomodulation ; models ; nomogram ; pancreatic neoplasms ; prediction ; prognosis ; risk ; risk assessment
Language	English
Dates of publication	2023-0216
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article ; Online
ZDB-ID	2661517-4
ISSN	2079-7737
ISSN	2079-7737
DOI	10.3390/biology12020319
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: ILKAP Promotes the Metastasis of Hepatocellular Carcinoma Cells by Inhibiting β-Catenin Degradation and Enhancing the WNT Signaling Pathway.

Zhang, Rui / Yuan, Jinglei / Liu, Shicheng / Torraca, Vincenzo / Liao, Zhiquan / Wu, Yueyan / Tan, Hongfei / Yao, Xia / Hou, Xueyang / Lyu, Hao / Xiao, Shuai / Guo, Dong / Ali, Declan William / Michalak, Marek / Chen, Xing-Zhen / Zhou, Cefan / Tang, Jingfeng

Advanced biology

2024 , Page(s) e2300117

Abstract: The incidence of Hepatocellular carcinoma (HCC) and HCC-related deaths have remarkably increased over the recent decades. It has been reported that β-catenin activation can be frequently observed in HCC cases. This study identified the integrin-linked ... ...

Abstract	The incidence of Hepatocellular carcinoma (HCC) and HCC-related deaths have remarkably increased over the recent decades. It has been reported that β-catenin activation can be frequently observed in HCC cases. This study identified the integrin-linked kinase-associated phosphatase (ILKAP) as a novel β-catenin-interacting protein. ILKAP is localized both in the nucleus and cytoplasm and regulates the WNT pathway in different ways. First, it is demonstrated that ILKAP activates the WNT pathway in HCC cells by increasing the protein level of β-catenin and other proteins associated with the WNT signaling, such as c-Myc and CyclinD1. Next, it is shown that ILKAP promotes the metastasis of HCC both in vitro and in vivo in a zebrafish xenograft model. It is also found that ILKAP dephosphorylates the GSK3β and CK1, contributing to the reduced ubiquitination of β-catenin. Furthermore, it is identified that ILKAP functions by mediating binding between TCF4 and β-catenin to enhance expression of WNT target genes. Taken together, the study demonstrates a critical function of ILKAP in metastasis of HCC, since ILKAP is crucial for the activation of the WNT pathway via stabilization of β-catenin and increased binding between TCF4 and β-catenin.
Language	English
Publishing date	2024-02-20
Publishing country	Germany
Document type	Journal Article
ISSN	2701-0198
ISSN (online)	2701-0198
DOI	10.1002/adbi.202300117
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Article ; Online: Membrane Curvature: The Inseparable Companion of Autophagy.

Liu, Lei / Tang, Yu / Zhou, Zijuan / Huang, Yuan / Zhang, Rui / Lyu, Hao / Xiao, Shuai / Guo, Dong / Ali, Declan William / Michalak, Marek / Chen, Xing-Zhen / Zhou, Cefan / Tang, Jingfeng

Cells

2023 Volume 12, Issue 8

Abstract: Autophagy is a highly conserved recycling process of eukaryotic cells that degrades protein aggregates or damaged organelles with the participation of autophagy-related proteins. Membrane bending is a key step in autophagosome membrane formation and ... ...

Abstract	Autophagy is a highly conserved recycling process of eukaryotic cells that degrades protein aggregates or damaged organelles with the participation of autophagy-related proteins. Membrane bending is a key step in autophagosome membrane formation and nucleation. A variety of autophagy-related proteins (ATGs) are needed to sense and generate membrane curvature, which then complete the membrane remodeling process. The Atg1 complex, Atg2-Atg18 complex, Vps34 complex, Atg12-Atg5 conjugation system, Atg8-phosphatidylethanolamine conjugation system, and transmembrane protein Atg9 promote the production of autophagosomal membranes directly or indirectly through their specific structures to alter membrane curvature. There are three common mechanisms to explain the change in membrane curvature. For example, the BAR domain of Bif-1 senses and tethers Atg9 vesicles to change the membrane curvature of the isolation membrane (IM), and the Atg9 vesicles are reported as a source of the IM in the autophagy process. The amphiphilic helix of Bif-1 inserts directly into the phospholipid bilayer, causing membrane asymmetry, and thus changing the membrane curvature of the IM. Atg2 forms a pathway for lipid transport from the endoplasmic reticulum to the IM, and this pathway also contributes to the formation of the IM. In this review, we introduce the phenomena and causes of membrane curvature changes in the process of macroautophagy, and the mechanisms of ATGs in membrane curvature and autophagosome membrane formation.
MeSH term(s)	Autophagy ; Cell Membrane/chemistry ; Cell Membrane/metabolism ; Proteolysis ; Protein Aggregates ; Autophagosomes/chemistry ; Autophagosomes/metabolism ; Autophagy-Related Proteins/chemistry ; Autophagy-Related Proteins/metabolism ; Protein Domains ; Lipid Bilayers ; Humans
Chemical Substances	Protein Aggregates ; Autophagy-Related Proteins ; Lipid Bilayers
Language	English
Publishing date	2023-04-11
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells12081132
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Cellular senescence: a double-edged sword in cancer therapy.

Xiao, Shuai / Qin, Dongmin / Hou, Xueyang / Tian, Lingli / Yu, Yeping / Zhang, Rui / Lyu, Hao / Guo, Dong / Chen, Xing-Zhen / Zhou, Cefan / Tang, Jingfeng

Frontiers in oncology

2023 Volume 13, Page(s) 1189015

Abstract: Over the past few decades, cellular senescence has been identified in cancer patients undergoing chemotherapy and radiotherapy. Senescent cells are generally characterized by permanent cell cycle arrest as a response to endogenous and exogenous stresses. ...

Abstract	Over the past few decades, cellular senescence has been identified in cancer patients undergoing chemotherapy and radiotherapy. Senescent cells are generally characterized by permanent cell cycle arrest as a response to endogenous and exogenous stresses. In addition to exiting the cell cycle process, cellular senescence also triggers profound phenotypic changes such as senescence-associated secretory phenotype (SASP), autophagy modulation, or metabolic reprograming. Consequently, cellular senescence is often considered as a tumor-suppressive mechanism that permanently arrests cells at risk of malignant transformation. However, accumulating evidence shows that therapy-induced senescence can promote epithelial-mesenchymal transition and tumorigenesis in neighboring cells, as well as re-entry into the cell cycle and activation of cancer stem cells, thereby promoting cancer cell survival. Therefore, it is particularly important to rapidly eliminate therapy-induced senescent cells in patients with cancer. Here we review the hallmarks of cellular senescence and the relationship between cellular senescence and cancer. We also discuss several pathways to induce senescence in tumor therapy, as well as strategies to eliminate senescent cells after cancer treatment. We believe that exploiting the intersection between cellular senescence and tumor cells is an important means to defeat tumors.
Language	English
Publishing date	2023-09-12
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2649216-7
ISSN	2234-943X
ISSN	2234-943X
DOI	10.3389/fonc.2023.1189015
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