scholarly journals LncRNA NORAD facilitates oral squamous cell carcinoma progression by sponging miR-577 to enhance TPM4

2022 ◽  
Vol 17 (1) ◽  
Author(s):  
Change Qi ◽  
Jianwei Liu ◽  
Pengnv Guo ◽  
Yali Xu ◽  
Jing Hu ◽  
...  

Abstract Background Long non-coding RNAs (lncRNAs) have been reported to be vital factors to affect the expression of genes and proteins. Also, it has been proved that the abnormal expression or mutation of lncRNAs stands as a signal of metastasis and proliferation of cancer. Nevertheless, the majority of lncRNAs still need to be explored in abundant cancers especially in oral squamous cell carcinoma (OSCC). Methods RT-qPCR assays were applied to test the expression of RNAs. Mechanism assays were performed to verify the combination among NORAD, TPM4 and miR-577. Also, functional assays were conducted to verify the function of RNAs on OSCC cells. Results LncRNA NORAD was highly expressed in OSCC tissues and cells. NORAD silencing repressed the biological behaviors of OSCC cells. MiR-577 was found in OSCC with low expression, and RIP assays illustrated that NORAD, miR-577 and TPM4 coexisted in RNA-induced silencing complexes. Rescue assays proved that the overexpression of TPM4 could recover the effect of NORAD silencing on OSCC progression. Conclusions It was revealed that NORAD functioned as a tumor promoter to sponge miR-577 thus elevating TPM4 in OSCC, which indicated that NORAD was worthy to be studied as a target for the treatment of OSCC.

Cancers ◽  
2021 ◽  
Vol 13 (23) ◽  
pp. 5944
Author(s):  
Jianfei Tang ◽  
Xiaodan Fang ◽  
Juan Chen ◽  
Haixia Zhang ◽  
Zhangui Tang

Oral squamous cell carcinoma (OSCC) is a type of malignancy with high mortality, leading to poor prognosis worldwide. However, the molecular mechanisms underlying OSCC carcinogenesis have not been fully understood. Recently, the discovery and characterization of long non-coding RNAs (lncRNAs) have revealed their regulatory importance in OSCC. Abnormal expression of lncRNAs has been broadly implicated in the initiation and progress of tumors. In this review, we summarize the functions and molecular mechanisms regarding these lncRNAs in OSCC. In addition, we highlight the crosstalk between lncRNA and tumor microenvironment (TME), and discuss the potential applications of lncRNAs as diagnostic and prognostic tools and therapeutic targets in OSCC. Notably, we also discuss lncRNA-targeted therapeutic techniques including CRISPR-Cas9 as well as immune checkpoint therapies to target lncRNA and the PD-1/PD-L1 axis. Therefore, this review presents the future perspectives of lncRNAs in OSCC therapy, but more research is needed to allow the applications of these findings to the clinic.


Oral Oncology ◽  
2006 ◽  
Vol 42 (4) ◽  
pp. 381-390 ◽  
Author(s):  
Sen-Tien Tsai ◽  
Kai-Ying Yang ◽  
Ying-Tai Jin ◽  
Yen-Chun Lin ◽  
Mei-Tzu Chang ◽  
...  

2013 ◽  
Vol 416 ◽  
pp. 100-106 ◽  
Author(s):  
Richa Garg ◽  
Vaishali Kapoor ◽  
Manasi Mittal ◽  
Manoj K. Singh ◽  
Nootan K. Shukla ◽  
...  

2019 ◽  
Vol 47 (4) ◽  
pp. 1758-1765 ◽  
Author(s):  
Zhifeng Yang ◽  
Zili Liu ◽  
Lingqiu Meng ◽  
Shuyan Ma

Objective The aim of this study was to identify important pathways regulated by a set of long non-coding RNAs (lncRNAs) in oral squamous cell carcinoma (OSCC). Methods A lncRNA-mediated competitive endogenous RNA network (LMCN) was constructed using information on microRNA (miRNA)–mRNA interactions and lncRNA–miRNA intersections from the E-GEOD-37991 transcription profiling data in the ArrayExpress database. A random walk with restart ranking algorithm was then applied to evaluate the influences of protein-coding genes regulated by competitive lncRNAs. Pathway enrichment scores were calculated based on the propagation scores of protein-coding genes. Finally, permutation tests were used to estimate the significance of the pathways. Results We obtained lncRNA–mRNA interactions based on miRNAs common to both miRNA–mRNA interactions and lncRNA–miRNA intersections, and used interactions with a z-score > 0.7 to construct a LMCN. Ten lncRNAs were identified as source nodes in the LMCN, and nine pathways with enrichment scores >0.8, including ‘Cell cycle’, ‘Endocytosis’, and ‘Pathways in cancer’, were significantly enriched by these source nodes. Conclusions Nine significant pathways regulated by a set of competitive lncRNAs were identified in OSCC, which may play important roles in the development of OSCC via the cell cycle and endocytosis.


2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Long Li ◽  
Hai-Chao Liu ◽  
Cheng Wang ◽  
Xiqiang Liu ◽  
Feng-Chun Hu ◽  
...  

Abnormal expression ofβ-catenin contributes to tumor development, progression, and metastasis in various cancers. However, little is known about the relationship between abnormal expression ofβ-catenin and cisplatin chemotherapy in oral squamous cell carcinoma (OSCC). The present study aimed to investigate the effect ofβ-catenin on OSCC cisplatin resistance and evaluated the drug susceptibility of stable cell lines withβ-catenin knockin and knockdown. In this study, we found that higher expression level ofβ-catenin can be observed in CDDP-treated cell lines as compared with the control group. Furthermore, the expression levels ofβ-catenin increased in both a concentration- and time-dependent manner with the cisplatin treatment. More importantly, the nuclear translocation ofβ-catenin could also be observed by confocal microscope analysis. Stable cell lines with CTNNB1 knockin and knockdown were established to further investigate the potential role and mechanism ofβ-catenin in the chemoresistance of OSCC in vitro and in vivo. Our findings indicated that overexpression ofβ-catenin promoted cisplatin resistance in OSCC in vitro and in vivo. We confirmed that GSK-3β, C-myc, Bcl-2, P-gp, and MRP-1 were involved inβ-catenin-mediated drug resistance. Our findings indicate that the Wnt/β-catenin signaling pathway may play important roles in cisplatin resistance in OSCC.


2020 ◽  
Vol 20 (1) ◽  
pp. 939-946
Author(s):  
Tingting Miao ◽  
Qingzong Si ◽  
Yuan Wei ◽  
Ruihong Fan ◽  
Junjie Wang ◽  
...  

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