LncRNA, TUG1 regulates the oral squamous cell carcinoma progression possibly via interacting with Wnt/β-catenin signaling

Liang, Shuang; Zhang, Songzi; Wang, Peng; Yang, Chia-Han; Shang, Chao; Yang, Jianjun; Wang, Jun

doi:10.1016/j.gene.2017.01.024

Cited by 91 publications

(72 citation statements)

References 19 publications

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“…Epithelial-mesenchymal transition is one of the most crucial steps in metastatic tumor progression and enhances cells' migratory and invasive properties [31]. In oral squamous cell carcinomas, elevated expression of TUG1 promoted tumor cell growth, proliferation, and invasion by suppressing Wnt/bcatenin signaling [32]. Results of an investigation of cervical cancers suggested that TUG1 knockdown decreased the expression of epithelial-mesenchymal transition-related proteins Cellular Physiology and Biochemistry Cellular Physiology and Biochemistry [33].…”

Section: Discussionmentioning

confidence: 99%

The Long Noncoding RNA TUG1 Promotes Laryngeal Cancer Proliferation and Migration

Zhang

Wang

Cao

et al. 2018

Cell Physiol Biochem

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Background/Aims: Researchers have shown that long noncoding RNAs are closely associated with the pathogenesis of laryngeal squamous cell carcinoma (LSCC). However, the role of the long noncoding RNA taurine-upregulated gene 1 (TUG1) in the pathogenesis of LSCC remains unclear, although it is recognized as an oncogenic regulator for several types of squamous cell carcinoma. Methods: qRT-PCR was performed to measure the expression of TUG1 in LSCC tissues and cell lines. 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) was used to measure the effect of TUG1 on cell proliferation. Transwell assay and flow cytometry were employed to determine the effect of TUG1 on cell migration and invasion. Western-blot were performed to explore the relation of TUG1 and p53 mRNA. Results: Higher TUG1 expression in LSCC than in paired normal tumor-adjacent tissue specimens (N = 64) was observed using quantitative real-time polymerase chain reaction. Also, high TUG1 expression was positively associated with advanced T category, worse lymph node metastasis and late clinical stage. Furthermore, in vitro experiments demonstrated that silencing of TUG1 markedly inhibited proliferation, cell-cycle progression, migration, and invasion of LSCC cells, whereas depletion of TUG1 led to increased apoptosis. Conclusion: These findings demonstrated that upregulated TUG1 expression exerted oncogenic effects by promoting proliferation, migration, and invasion, and inhibiting apoptosis in LSCC cells.

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Section: Discussionmentioning

confidence: 99%

The Long Noncoding RNA TUG1 Promotes Laryngeal Cancer Proliferation and Migration

Zhang

Wang

Cao

et al. 2018

Cell Physiol Biochem

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“…The Wnt/β-catenin signaling pathway, which activates β-catenin to initiate the transcription of its specific downstream target genes [25], has been reported to be associated with numerous cancers [26,27,28,29]. Aberrant activation of the canonical Wnt pathway plays a significant role in human cervical cancer.…”

Section: Discussionmentioning

confidence: 99%

Sulfiredoxin May Promote Cervical Cancer Metastasis via Wnt/β-Catenin Signaling Pathway

Lan

Zhao

Fan

et al. 2017

IJMS

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The abnormal elevation of sulfiredoxin (Srx/SRXN1)—an antioxidant enzyme whose main function is to protect against oxidative stress—has been shown to be closely correlated with the progression of several types of cancer, including human cervical cancer. However, the molecular mechanism by which Srx promotes tumor progression, especially cancer metastasis in cervical cancer, has not been elucidated. Here, we show that Srx expression gradually increases during the progression of human cervical cancer and its expression level is closely correlated with lymph node metastasis. Our study also reveals a significant positive correlation between the expression of Srx and β-catenin in cervical cancer tissues. Loss-of-function studies demonstrate that Srx knockdown using a lentiviral vector-mediated specific shRNA decreases the migration and invasion capacity in HeLa (human papilloma virus 18 type cervical cancer cell line) and SiHa SiHa (cervical squamous cancer cell line). Notably, the exact opposite effects were observed in gain-of-function experiments in C-33A cells. Mechanistically, downregulation or upregulation of Srx leads to an altered expression of proteins associated with the Wnt/β-catenin signaling pathway. Furthermore, blockage of the Wnt/β-catenin signaling pathway contributed to attenuated Srx expression and resulted in significant inhibition of cell migration and invasion in cervical cancer cell lines. Combined, Srx might be an oncoprotein in cervical cancer, playing critical roles in activating the Wnt/β-catenin signaling pathway; it may therefore be a therapeutic target for cervical cancer.

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“…Recently study also showed that lncRNA PLIN2 act as a carcinogenic factor in the progression of chronic myeloid leukemia (CML) via interacting with the GSK3 and Wnt/β-catenin signaling pathways (9). Perhaps more encouragingly, lncRNA TUG1 was also reported to promote progression of OSCC by suppressing the level of Wnt/β-catenin signaling (10), which also indicates a new research direction about the role of TUG1 in SCLC.…”

mentioning

confidence: 88%

The role and potential mechanisms of long non-coding RNA in small cell lung cancer

Niu

Xue

et al. 2017

J. Thorac. Dis.

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LncRNA, TUG1 regulates the oral squamous cell carcinoma progression possibly via interacting with Wnt/β-catenin signaling

Cited by 91 publications

References 19 publications

The Long Noncoding RNA TUG1 Promotes Laryngeal Cancer Proliferation and Migration

The Long Noncoding RNA TUG1 Promotes Laryngeal Cancer Proliferation and Migration

Sulfiredoxin May Promote Cervical Cancer Metastasis via Wnt/β-Catenin Signaling Pathway

The role and potential mechanisms of long non-coding RNA in small cell lung cancer

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