scholarly journals Effect of the transcription factor YY1 on the development of pancreatic endocrine and exocrine tumors: a narrative review

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Qun Chen ◽  
Wu-Jun Wang ◽  
Yun-Xuan Jia ◽  
Hao Yuan ◽  
Peng-Fei Wu ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Clinical Manifestations ◽  
Causative Factor ◽  
Ductal Adenocarcinoma ◽  
Pancreatic Tumors ◽  
Therapeutic Effects ◽  
Degree Of Malignancy ◽  
Malignant Changes ◽  
Transcription Factor Yy1

AbstractPancreatic tumors are classified into endocrine and exocrine types, and the clinical manifestations in patients are nonspecific. Most patients, especially those with pancreatic ductal adenocarcinoma (PDAC), have lost the opportunity to receive for the best treatment at the time of diagnosis. Although chemotherapy and radiotherapy have shown good therapeutic results in other tumors, their therapeutic effects on pancreatic tumors are minimal. A multifunctional transcription factor, Yin-Yang 1 (YY1) regulates the transcription of a variety of important genes and plays a significant role in diverse tumors. Studies have shown that targeting YY1 can improve the survival time of patients with tumors. In this review, we focused on the mechanism by which YY1 affects the occurrence and development of pancreatic tumors. We found that a YY1 mutation is specific for insulinomas and has a role in driving the degree of malignancy. In addition, changes in the circadian network are a key causative factor of PDAC. YY1 promotes pancreatic clock progression and induces malignant changes, but YY1 seems to act as a tumor suppressor in PDAC and affects many biological behaviors, such as proliferation, migration, apoptosis and metastasis. Our review summarizes the progress in understanding the role of YY1 in pancreatic endocrine and exocrine tumors and provides a reasonable assessment of the potential for therapeutic targeting of YY1 in pancreatic tumors.

Transcriptional control of human papillomavirus type 18 oncogene expression in different cell lines: Role of transcription factor YY1

Virus Genes ◽  
1995 ◽  
Vol 11 (1) ◽  
pp. 53-58 ◽  
Author(s):  
Franziska Jundt ◽  
Ingrid Herr ◽  
Peter Angel ◽  
Harald Zur Hausen ◽  
Tobias Bauknecht
Keyword(s):  
Transcription Factor ◽  
Human Papillomavirus ◽  
Cell Lines ◽  
Transcriptional Control ◽  
Oncogene Expression ◽  
Transcription Factor Yy1

scholarly journals The morphological and functional characteristics of the pineal gland

2019 ◽  
Author(s):  
Bogdan Alexandru Gheban ◽  
Ioana Andreea Rosca ◽  
Maria Crisan
Keyword(s):  
Pineal Gland ◽  
Clinical Manifestations ◽  
Narrative Review ◽  
Therapeutic Effects ◽  
Endocrine Organ ◽  
Diagnostic Protocol ◽  
Search Terms ◽  
Physiological Information ◽  
The Brain

Introduction. The pineal gland is a photo-neuro-endocrine organ situated inside the brain, that secretes serotonin, melatonin and N,N-dymethyltriptamine. This narrative review will address the latest information gathered on this function of the gland as well as the unknown roles it may have. The different histological and pathological findings of the pineal gland have demonstrated a role in clinical manifestations of numerous endocrine, neurological and psychiatric pathologies. Materials. For this narrative review we used the NCBI website database PubMed. The search terms were “Pineal Gland” AND/OR “histology, melatonin, DMT, pathology”. Total number of articles included were 86. Results: We have reviewed physiological information of melatonin and DMT, anatomical, histological and histopathological information on the pineal gland and its role in endocrine, neurological and psychiatric pathology. Conclusion. The role of melatonin in immunity and its potential therapeutic effects show promising potential for further research. DMT seems to have a role in psychiatric pathology and potential therapeutic effects. Proper tumoral screening and diagnostic protocol are required.

scholarly journals Back to the drawing board: Re-thinking the role of GLI1 in pancreatic carcinogenesis

F1000Research ◽  
2014 ◽  
Vol 3 ◽  
pp. 238 ◽  
Author(s):  
Tara L. Hogenson ◽  
Matthias Lauth ◽  
Marina Pasca diMagliano ◽  
Martin E. Fernandez-Zapico
Keyword(s):  
Clinical Trials ◽  
Transcription Factor ◽  
Drug Therapy ◽  
Ductal Adenocarcinoma ◽  
Pancreatic Carcinogenesis ◽  
Promising Target ◽  
Drawing Board ◽  
Late Stages ◽  
Central Effector

Aberrant activation of the transcription factor GLI1, a central effector of the Hedgehog (HH) pathway, is associated with several malignancies, including pancreatic ductal adenocarcinoma (PDAC), one of most deadly human cancers. GLI1 has been described as an oncogene in PDAC, making it a promising target for drug therapy. Surprisingly, clinical trials targeting HH/GLI1 axis in advanced PDAC were unsuccessful, leaving investigators questioning the mechanism behind these failures. Recent evidence suggests the loss of GLI1 in the later stages of PDAC may actually accelerate disease. This indicates GLI1 may play a dual role in PDAC, acting as an oncogene in the early stages of disease and a tumor-suppressor in the late stages.

scholarly journals Comprehensive analysis of abnormal expression, prognostic value and oncogenic role of the hub gene FN1 in pancreatic ductal adenocarcinoma via bioinformatic analysis and in vitro experiments

PeerJ ◽  
2021 ◽  
Vol 9 ◽  
pp. e12141
Author(s):  
Xiaohua Lei ◽  
Guodong Chen ◽  
Jiangtao Li ◽  
Wu Wen ◽  
Jian Gong ◽  
...  
Keyword(s):  
Gene Expression ◽  
Pancreatic Ductal Adenocarcinoma ◽  
Bioinformatic Analysis ◽  
Ductal Adenocarcinoma ◽  
Therapeutic Effects ◽  
Hub Genes ◽  
Poor Overall Survival ◽  
Geo Dataset

Background Pancreatic ductal adenocarcinoma (PDAC) is one of the most commonly diagnosed cancers with a poor prognosis worldwide. Although the treatment of PDAC has made great progress in recent years, the therapeutic effects are still unsatisfactory. Methods. In this study, we identified differentially expressed genes (DEGs) between PDAC and normal pancreatic tissues based on four Gene Expression Omnibus (GEO) datasets (GSE15471, GSE16515, GSE28735 and GSE71729). A protein–protein interaction (PPI) network was established to evaluate the relationship between the DEGs and to screen hub genes. The expression levels of the hub genes were further validated through the Gene Expression Profiling Interactive Analysis (GEPIA), ONCOMINE and Human Protein Atlas (HPA) databases, as well as the validation GEO dataset GSE62452. Additionally, the prognostic values of the hub genes were evaluated by Kaplan–Meier plotter and the validation GEO dataset GSE62452. Finally, the mechanistic roles of the most remarkable hub genes in PDAC were examined through in vitro experiments. Results We identified the following nine hub genes by performing an integrated bioinformatics analysis: COL1A1, COL1A2, FN1, ITGA2, KRT19, LCN2, MMP9, MUC1 and VCAN. All of the hub genes were significantly upregulated in PDAC tissues compared with normal pancreatic tissues. Two hub genes (FN1 and ITGA2) were associated with poor overall survival (OS) rates in PDAC patients. Finally, in vitro experiments indicated that FN1 plays vital roles in PDAC cell proliferation, colony formation, apoptosis and the cell cycle. Conclusions In summary, we identified two hub genes that are associated with the expression and prognosis of PDAC. The oncogenic role of FN1 in PDAC was first illustrated by performing an integrated bioinformatic analysis and in vitro experiments. Our results provide a fundamental contribution for further research aimed finding novel therapeutic targets for overcoming PDAC.

A critical role of transcription factor YY1 in rheumatoid arthritis by regulation of interleukin-6

2017 ◽  
Vol 77 ◽  
pp. 67-75 ◽  
Author(s):  
Jinpiao Lin ◽  
Yujue He ◽  
Junmin Chen ◽  
Zhiyong Zeng ◽  
Bin Yang ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Transcription Factor ◽  
Interleukin 6 ◽  
Critical Role ◽  
Transcription Factor Yy1

PCAT1 induced by transcription factor YY1 promotes cholangiocarcinoma proliferation, migration and invasion by sponging miR-216a-3p to up-regulate oncogene BCL3

2020 ◽  
Vol 0 (0) ◽  
Author(s):  
Dongsheng Sun ◽  
Yuqiao Zhao ◽  
Weina Wang ◽  
Canghai Guan ◽  
Zengtao Hu ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Western Blot ◽  
Binding Capacity ◽  
Tumor Formation ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Protein Levels ◽  
Transcription Factor Yy1 ◽  
Emt Markers

AbstractThis study was designed to illustrate the function and role of PCAT1 in CCA. The relative expression was confirmed by RT-qPCR and western blot. The biological function of PCAT1 was evaluated by CCK8, EdU, colony formation, wound healing, transwell, and subcutaneous tumor formation assays. Protein levels of EMT markers were measured by western blot. The binding relationship was predicted by JASPAR and starBase. The binding of YY1 to PCAT1 promoter was assessed by ChIP and luciferase reporter. The binding capacity between miR-216a-3p and PCAT1 as well as BCL3 was assessed by luciferase reporter and AGO2-RIP assays. In this study, we found that PCAT1 was up-regulated in CCA tissues and cells, and the PCAT1 overexpression was associated with poor prognosis. Moreover, PCAT1 was assessed as an independent risk factor of prognosis for CCA patients. Amplified PCAT1 was found to promote tumor proliferation, migration, invasion and EMT process, whereas PCAT1 knockdown inhibited these malignant phenotypes. Mechanistically, PCAT1 was predominantly localized in the cytoplasm and competitively bound miR-216a-3p to increase BCL3 expression. In addition, PCAT1 was activated by transcription factor YY1. This study revealed that PCAT1 acted as an oncogene in CCA, and the YY1/PCAT1/miR-216a-3p/BCL3 axis exhibited critical functions in CCA progression.

scholarly journals Back to the drawing board: Re-thinking the role of GLI1 in pancreatic carcinogenesis

F1000Research ◽  
2016 ◽  
Vol 3 ◽  
pp. 238
Author(s):  
Tara L. Hogenson ◽  
Matthias Lauth ◽  
Marina Pasca diMagliano ◽  
Martin E. Fernandez-Zapico
Keyword(s):  
Clinical Trials ◽  
Transcription Factor ◽  
Drug Therapy ◽  
Ductal Adenocarcinoma ◽  
Pancreatic Carcinogenesis ◽  
Promising Target ◽  
Drawing Board ◽  
Late Stages ◽  
Central Effector

Aberrant activation of the transcription factor GLI1, a central effector of the Hedgehog (HH) pathway, is associated with several malignancies, including pancreatic ductal adenocarcinoma (PDAC), one of most deadly human cancers. GLI1 has been described as an oncogene in PDAC, making it a promising target for drug therapy. Surprisingly, clinical trials targeting HH/GLI1 axis in advanced PDAC were unsuccessful, leaving investigators questioning the mechanism behind these failures. Recent evidence suggests the loss of GLI1 in the later stages of PDAC may actually accelerate disease. This indicates GLI1 may play a dual role in PDAC, acting as an oncogene in the early stages of disease and a tumor-suppressor in the late stages.

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