Long non-coding RNA PHACTR2-AS1 promotes tongue squamous cell carcinoma metastasis by regulating Snail

2020 ◽  
Vol 168 (6) ◽  
pp. 651-657 ◽  
Author(s):  
Fenqian Yuan ◽  
Zhiguo Miao ◽  
Wen Chen ◽  
Fanggeng Wu ◽  
Chao Wei ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Cell Biology ◽  
Tongue Squamous Cell Carcinoma ◽  
Migration And Invasion ◽  
Mesenchymal Transition ◽  
Non Coding Rna ◽  
Long Non Coding Rna

Abstract Long non-coding RNA is an endogenous non-coding RNA that has currently been proved to be an important player in cancer cell biology. In the present study, we investigated the biological role of PHACTR2-AS1 in tongue squamous cell carcinoma (TSCC). PHACTR2-AS1 was preferentially localized in the cytoplasm, and was notably upregulated in TSCC tissues. High PHACTR2-AS1 was correlated with tumour differentiation, metastatic clinical features, relapse and shortened survival time. Depletion of PHACTR2-AS1 did not affect TSCC cell viability and colony formation ability, whereas substantially inhibited cell migration and invasion in vitro and lung metastasis in vivo. Mechanistically, PHACTR2-AS1 could sponge miR-137 to increase Snail expression, resulting in triggering epithelial–mesenchymal transition process, thereby promoting TSCC cell metastasis. Taken together, our data for the first time elucidate the metastasis-promoting role of PHACTR2-AS1 in TSCC, hinting a new therapeutic target for metastatic TSCC patients.

Long non-coding RNA HOTTIP is correlated with progression and prognosis in tongue squamous cell carcinoma

Tumor Biology ◽  
2015 ◽  
Vol 36 (11) ◽  
pp. 8805-8809 ◽  
Author(s):  
Hua Zhang ◽  
Lei Zhao ◽  
Ying-Xue Wang ◽  
Mian Xi ◽  
Shi-Liang Liu ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Tongue Squamous Cell Carcinoma ◽  
Non Coding Rna ◽  
Long Non Coding Rna

scholarly journals Long non-coding RNA CRNDE promote the progression of tongue squamous cell carcinoma through regulating the PI3K/AKT/mTOR signaling pathway

RSC Advances ◽  
2019 ◽  
Vol 9 (37) ◽  
pp. 21381-21390
Author(s):  
Zhongheng Yang ◽  
Weizhi Chen
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Signaling Pathway ◽  
Squamous Cell ◽  
Colorectal Neoplasia ◽  
Tongue Squamous Cell Carcinoma ◽  
Mtor Signaling Pathway ◽  
Non Coding Rna ◽  
Non Coding Rnas ◽  
Long Non Coding Rna

Long non-coding RNAs (lnRNAs) colorectal neoplasia differentially expressed (CRNDE) has been identified as a crucial regulator involved in tongue squamous cell carcinoma (TSCC).

scholarly journals MicroRNA-625 inhibits cell invasion and epithelial–mesenchymal transition by targeting SOX4 in laryngeal squamous cell carcinoma

2019 ◽  
Vol 39 (1) ◽  
Author(s):  
Yuan Li ◽  
Chenjuan Tao ◽  
Lili Dai ◽  
Caixia Cui ◽  
Chaohui Chen ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Laryngeal Squamous Cell Carcinoma ◽  
Critical Role ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Mesenchymal Transition ◽  
Expression Levels

AbstractIntroduction: Laryngeal squamous cell carcinoma (LSCC) is a highly aggressive malignant cancer, but the molecular mechanisms underlying its development and progression remain largely elusive. The purpose of the present study is to investigate the expression profile and functional role of microRNA-625 (miR-625) in LSCC.Materials and methods: LSCC tissues and adjacent normal tissues were collected from 86 LSCC patients. The expression levels of miR-625 and SOX4 mRNA in tissues and cells were detected by RT-qPCR analysis. The expression levels of SOX4 and EMT-related proteins were detected by western blot analysis. In vitro cell proliferation, migration, and invasion were detected by MTT assay, colony formation assay, wound healing assay, and transwell invasion assay, respectively. Dual-luciferase reporter assay was performed to verify the binding relationship between miR-625 and the 3′-UTR of SOX4.Results: The results demonstrated that miR-625 is significantly down-regulated in clinical LSCC tissues, and its low expression may be closely associated with unfavorable clinicopathological characteristics of LSCC patients. Overexpression of miR-625 significantly suppressed the proliferation, migration, invasion, and EMT of LSCC cells. Furthermore, SOX4 was validated as a direct target of miR-625 in LSCC cells, and rescue experiments suggested that restoration of SOX4 blocked the tumor suppressive role of miR-625 in LSCC cells.Conclusions: Taken together, these findings highlighted a critical role of miR-625 in the pathogenesis of LSCC, and restoration of miR-625 could be considered as a potential therapeutic strategy against this fatal disease.

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