<scp>YY</scp>1 directly suppresses <scp>MYCT</scp>1 leading to laryngeal tumorigenesis and progress

Qu, Siyao; Sun, Yuanyuan; Li, Yunhui; Xu, Zhonghua; Fu, Wei

doi:10.1002/cam4.1073

Cited by 28 publications

(33 citation statements)

References 36 publications

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“…YY1 binds and inhibits the MYCT1 promoter and the effects of YY1 silencing were recovered by MYCT1 knockdown. These findings implicate YY1 as a potential target in laryngeal cancer …”

Section: Yy1 and Tumor Growthmentioning

confidence: 64%

The Yin and Yang of YY1 in tumor growth and suppression

Khachigian

2018

Intl Journal of Cancer

128

106

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Yin Yang-1 (YY1) is a zinc finger protein and member of the GLI-Kruppel family that can activate or inactivate gene expression depending on interacting partners, promoter context and chromatin structure, and may be involved in the transcriptional control of ∼10% of the total mammalian gene set. A growing body of literature indicates that YY1 is overexpressed in multiple cancer types and that increased YY1 levels correlate with poor clinical outcomes in many cancers. However, the role of YY1 in the promotion or suppression of tumor growth remains controversial and its regulatory effects may be tumor cell type dependent at least in experimental systems. The molecular mechanisms responsible for the apparently conflicting roles of YY1 are not yet fully elucidated. This review highlights recent advances in our understanding of regulatory insights involving YY1 function in a range of cancer types. For example, YY1's roles in tumor growth involve stabilization of hypoxia-inducible factor HIF-1α in a p53 independent manner, negative regulation of miR-9 transcription, control of MYCT1 transcription, a novel miR-193a-5p-YY1-APC axis, intracellular ROS and mitochondrial superoxide generation, p53 reduction and EGFR activation, control of genes associated with mitochondrial energy metabolism and miRNA regulatory networks involving miR-7, miR-9, miR-34a, miR-186, miR-381, miR-584-3p and miR-635. On the other hand, tumor suppressor roles of YY1 appear to involve YY1 stimulation of tumor suppressor BRCA1, increased Bax transcription and apoptosis involving cytochrome c release and caspase-3/-7 cleavage, induction of heme oxygenase-1, inhibition of pRb phosphorylation and p21 binding to cyclin D1 and cdk4, reduced expression of long noncoding RNA of SOX2 overlapping transcript, and MUC4/ErbB2/p38/MEF2C-dependent downregulation of MMP-10. YY1 expression is associated with that of cancer stem cell markers SOX2, BMI1 and OCT4 across many cancers suggesting multidynamic regulatory control and groups of cancers with distinct molecular signatures. Greater understanding of the mechanistic roles of YY1 will in turn lead to the development of more specific approaches to modulate YY1 expression and activity with therapeutic potential.

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“…YY1 binds and inhibits the MYCT1 promoter and the effects of YY1 silencing were recovered by MYCT1 knockdown. These findings implicate YY1 as a potential target in laryngeal cancer …”

Section: Yy1 and Tumor Growthmentioning

confidence: 64%

The Yin and Yang of YY1 in tumor growth and suppression

Khachigian

2018

Intl Journal of Cancer

128

106

View full text Add to dashboard Cite

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“…As a transcriptional regulator, YY1 is involved in multiple biological functions of cells, including embryonic formation, cell proliferation, apoptosis, DNA repair and differentiation via upregulating or downregulating different genes (16). It has been reported that YY1 is overexpressed and serves as oncogene in numerous tumor types, including breast, ovary, colon, prostate, gastric and laryngeal cancer (17)(18)(19)(20)(21). However, YY1 may serve an inhibitory role in pancreatic cancer (22).…”

Section: Discussionmentioning

confidence: 99%

“…As a key transcription factor, YY1 regulates its target gene transcription in a complex manner. YY1 can activate the transcription of oncogenes and tumor suppressors in different cancer tissues (14)(15)(16)(17)(18)(19)(20)(21)(22)(23). However, the mechanism regulating YY1 has not been well illustrated.…”

Section: Discussionmentioning

confidence: 99%

miR‑544 inhibits the migration and invasion of anaplastic thyroid cancer by targeting Yin Yang‑1

Wang

Sun

2019

Oncol Lett

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Anaplastic thyroid cancer (ATC), with a mean survival time of 6 months, was reported in 2012 to account for 1-2% of all thyroid tumor cases in the US. Understanding the molecular mechanisms underlying carcinogenesis and progression in ATC would contribute to determining novel therapeutic targets. The aberrant expression of microRNA-544 (miR-544) has been demonstrated in various cancer types. However, its expression and biological function in human ATC remain largely unknown. Therefore, the present study investigated the expression, function and molecular mechanism of miR-544 in ATC. Results of reverse transcription-quantitative polymerase chain reaction demonstrated that the expression levels of miR-544 in 40 pairs of surgical specimens and human ATC cell lines were significantly decreased, compared with the normal thyroid tissues and cell line. Functional assays indicated that ectopic expression of miR-544 significantly decreased the viability, proliferation and metastasis of SW1736 cells, whereas miR-544 inhibitor significantly enhanced the viability, proliferation and metastasis of 8305C cells. Furthermore, the present study confirmed that the oncogene Yin Yang-1 (YY1) was a direct target of miR-544. It was further demonstrated that YY1 overexpression rescued the inhibitory effect of progression induced by miR-544 in ATC cells. Finally, in vivo study indicated that miR-544 suppressed the tumorigenicity of ATC cells. In conclusion, the present study demonstrated that miR-544 may function as a tumor suppressor in ATC and serve as a future therapeutic target for patients with ATC.

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“…In our previous work, we found that MYC and YY1 directly promote and inhibit the transcription activities of MYCT1 in Hep2 cells. 13 , 24 In addition to MYCT1, there are other targets of CREB. For example, CREB is a positive transcript factor by binding to the promoters of HULC and YAP in liver cancer.…”

Section: Discussionmentioning

confidence: 99%

CREB promotes laryngeal cancer cell migration via MYCT1/NAT10 axis

Zhang

Sun

et al. 2018

OTT

Self Cite

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PurposeCREB, MYCY1 and NAT10 are involved in cancer cell migration. However, the relationship between these three proteins and their role in laryngeal cancer cell migration remains unknown.MethodsTransient gene transfection was performed in laryngeal cancer cells. Bioinformatics analysis was used to predict the binding of CREB to MYCT1 promoter. Binding of CREB to the promoter of MYCT1 was monitored by luciferase reporter assay and chromatin immuno-precipitation method in vitro and in vivo, respectively. Real-time RT-PCR and Western bolt were applied to detect gene transcription and translation levels, respectively. Laryngeal cancer cell migration was assayed by transwell chamber experiment.ResultsCREB protein expression was significantly up-regulated in laryngeal cancer tissues and associated with cancer differentiation, tumor stage, and lymphatic metastasis. CREB inhibits MYCT1 expression by direct binding to its promoter. Meanwhile, MYCT1 has a negative impact on the NAT10 gene expression. Furthermore, CREB promotes NAT10 expression via down-regulating the MYCT1 gene expression. In addition, contrary to MYCT1, CREB and NAT10 enhanced laryngeal cancer cell migration. MYCT1 and NAT10 significantly rescued the effects of CREB and MYCT1 on Hep2 cell migration, respectively.ConclusionCREB promotes laryngeal cancer cell migration via MYCT1/NAT10 axis, suggesting that CREB might be a potential prognostic marker in laryngeal cancer.

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YY1 directly suppresses MYCT1 leading to laryngeal tumorigenesis and progress

Cited by 28 publications

References 36 publications

The Yin and Yang of YY1 in tumor growth and suppression

The Yin and Yang of YY1 in tumor growth and suppression

miR‑544 inhibits the migration and invasion of anaplastic thyroid cancer by targeting Yin Yang‑1

CREB promotes laryngeal cancer cell migration via MYCT1/NAT10 axis

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