Complex integrated analysis of lncRNAs-miRNAs-mRNAs in oral squamous cell carcinoma

Li, Simin; Chen, Xiujie; Liu, Xiangqiong; Ye, Yu; Pan, Hongying; Haak, Rainer; Schmidt, Jana; Ziebolz, Dirk; Schmalz, Gerhard

doi:10.1016/j.oraloncology.2017.07.026

Cited by 90 publications

(79 citation statements)

References 43 publications

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“…RNA pull down confirmed the binding ability between PART1 and miR‐635. Except for miR‐129 in ESCC, miR‐133a, miR‐135b, miR‐196b, and miR‐193b in oral squamous cell carcinoma, to the best of our knowledge, we first found that miR‐635 was a new target miRNA for PART1. Moreover, in the present study, we demonstrated that PART1 promoted cell proliferation, migration, and invasion of NSCLC, while knockdown of PART1 performed the opposite effects on NSCLC progression.Other lncRNAs, such as MALAT1, HOTAIR, and UCA1, that were highly expressed in NSCLC, also promoted the progression and the inhibition of these lncRNAs suppressed the progression.…”

Section: Discussionmentioning

confidence: 82%

Long noncoding RNA PART1 promotes progression of non‐small cell lung cancer cells via JAK‐STAT signaling pathway

Zhu

Wang

et al. 2019

Cancer Medicine

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Non‐small cell lung cancer (NSCLC), the major type of lung cancer, becomes the greatest threat to the life of people. Growing evidence shows prostate androgen‐regulated transcript 1 (PART1) is considered as effective markers for prostate cancer, and has been shown to be associated with poor prognosis of NSCLC. However, the tumorigenic mechanism of PART1 in NSCLC remains to be investigated. In this study, we found that the expression of PART1 was robustly induced in NSCLC tissues and cell lines. Functional studies established that overexpression of PART1 could promote NSCLC cell proliferation, migration, and invasion, while interference of PART1 inhibited NSCLC progression. Our results also identified miR‐635 as a novel target of PART1, whose expression was inhibited by PART1 in NSCLC cell lines. Moreover, gain‐ and loss‐of‐function studies revealed that PART1 could sponge miR‐635 and increase the expression of Janus kinase (JAK) and signal transducer and activator of transcription proteins (STATs). Finally, we deciphered the molecular mechanism by which PART1 contributed to promotion of NSCLC cell progression via phosphorylation and activation of JAK‐STAT signaling pathway. The animal experiment further confirmed that interference of NSCLC could suppress in vivo tumorigenic ability of NSCLC with favorable pharmacological activity via inactivation of JAK‐STAT signaling pathway. In conclusion, our findings clarified the biologic significance of PART1/miR‐635/JAK‐STAT axis in NSCLC progression and provided novel evidence that PART1 may be a new potential therapeutic target for the treatment of NSCLC.

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Section: Discussionmentioning

confidence: 82%

Long noncoding RNA PART1 promotes progression of non‐small cell lung cancer cells via JAK‐STAT signaling pathway

Zhu

Wang

et al. 2019

Cancer Medicine

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“…Several studies acquired data from public transcriptome data sets. When analysing merged data from three data sets, the TCGA and 2 GEO datasets (GSE9844 (Ye et al., ) and GSE13601 (Estilo et al., )), multivariate Cox regression analysis identified three lncRNAs as independent prognostic markers for OS in OSCC patients ( p < 0.05), namely overexpressed C10orf91 (chromosome 10 open reading frame 91) andC2orf48 (chromosome 2 open reading frame 48) and underexpressed TTTY14 (testis‐specific transcript, Y‐linked 14) (Li et al., ). An univariate analysis of 42 OSCCs from the GSE3524 data set (Toruner et al., ) revealed that the overexpression of H19 was significantly related to poorer OS (Hong et al., ).…”

Section: De Lncrnas and Clinicopathological Featuresmentioning

confidence: 99%

World Workshop on Oral Medicine VII: Clinical evidence of differential expression of lncRNAs in oral squamous cell carcinoma: A scoping review

et al. 2019

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Background Long non‐coding RNAs (lncRNAs) have important roles in regulating gene expression pertaining to cell proliferation, survival, migration and genomic stability. Dysregulated expression of lncRNAs is implicated in cancer initiation, progression and metastasis. Objectives To explore, map and summarize the extent of evidence from clinical studies investigating the differential expression of lncRNAs in oral/tongue squamous cell carcinoma. Methods PubMed, Scopus and Web of Science were used as search engines. Clinical, full‐length, English language studies were included. PRISMA‐ScR protocol was used to evaluate and present results. The present scoping review summarizes relationships of the differential expression of lncRNAs with the presence of tumour and with clinicopathological features including survival. Results Almost half of the investigated transcripts have been explored in more than one study, yet not always with consistent results. The collected data were also compared to the limited studies investigating oral epithelial dysplasia. Data are not easily comparable, first because of different methods used to define what differential expression is, and second because only a limited number of studies performed multivariate analyses to identify clinicopathological features associated with the differentially expressed lncRNAs. Conclusions Standard methods and more appropriate data analyses are needed in order to achieve reliable results from future studies.

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“…Growing evidence indicates that lncRNAs and mRNAs can cross-regulate each other by competing for shared miRNA response elements (MREs) [16,20]. Specifically, many lncRNAs act as sponges in the regulation of miRNA target genes involved in OSCC carcinogenesis [21,22]. miR-433, a well-characterized miRNA, was found to be a tumor suppressor in different neoplasms [23,24].…”

Section: Discussionmentioning

confidence: 99%

Linc01234 promotes cell proliferation and metastasis in oral squamous cell carcinoma via miR-433/PAK4 axis

Liu

Jian

et al. 2020

BMC Cancer

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Background: Increasing studies have demonstrated that long non-coding RNAs (lncRNAs) play an important role in tumor progression. However, the potential biological functions and clinical importance of Linc01234 in oral squamous cell carcinoma (OSCC) remain unclear. Methods: We evaluated the expression profile and prognostic value of Linc01234 in OSCC tissues by RT-qPCR. Then, functional in vitro experiments were performed to investigate the effects of Linc01234 on tumor growth, migration and invasion in OSCC. Mechanistically, RT-qPCR, bioinformatic analysis and dual luciferase reporter assays were performed to identify a competitive endogenous RNA (ceRNA) mechanism involving Linc01234, miR-433-3p and PAK4. Results: We found that Linc01234 was clearly upregulated in OSCC tissues and cell lines, and its level was positively associated with T stage, lymph node metastasis, differentiation and poor prognosis of patients with OSCC. Our results shown that Linc01234 inhibited cell proliferation and metastatic abilities in CAL27 and SCC25 cells following its knockdown. Mechanistic analysis indicated that Linc01234 may act as a ceRNA (competing endogenous RNA) of miR-433-3p to relieve the repressive effect of miR-433-3p on its target PAK4. Conclusions:Our results indicated that Linc01234 promotes OSCC progression through the Linc01234/miR-433/ PAK4 axis and might be a potential therapeutic target for OSCC.

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Complex integrated analysis of lncRNAs-miRNAs-mRNAs in oral squamous cell carcinoma

Cited by 90 publications

References 43 publications

Long noncoding RNA PART1 promotes progression of non‐small cell lung cancer cells via JAK‐STAT signaling pathway

Long noncoding RNA PART1 promotes progression of non‐small cell lung cancer cells via JAK‐STAT signaling pathway

World Workshop on Oral Medicine VII: Clinical evidence of differential expression of lncRNAs in oral squamous cell carcinoma: A scoping review

Linc01234 promotes cell proliferation and metastasis in oral squamous cell carcinoma via miR-433/PAK4 axis

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