The Role of Transcription Factor YY1 in the Biology of Cancer

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.

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Abstract 4687: Oncogenic role of the transcription factor YY1 and its target Survivin in non-Hodgkin's lymphoma

10.1158/1538-7445.am2020-4687 ◽

2020 ◽

Author(s):

Silvia Vivarelli ◽

Luca Falzone ◽

Saverio Candido ◽

Benjamin Bonavida ◽

Massimo Libra

Keyword(s):

Transcription Factor ◽

Hodgkin’S Lymphoma ◽

Hodgkin's Lymphoma ◽

Non Hodgkin’S Lymphoma ◽

Non Hodgkin's Lymphoma ◽

Transcription Factor Yy1

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

Journal of Autoimmunity ◽

10.1016/j.jaut.2016.10.008 ◽

2017 ◽

Vol 77 ◽

pp. 67-75 ◽

Cited By ~ 21

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

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

Biological Chemistry ◽

10.1515/hsz-2020-0276 ◽

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.

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