Browsing by Subject "Long non-coding RNA"

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    Involvement of lncRNA dysregulation in gastric cancer
    (Universidad de Murcia. Departamento de Biología Celular e Histología, 2016) Sun, Ming; Nie, Feng-qi; Wang, Zhao-xia; De, Wei
    y. Benefiting from the fast development of sequencing technique and bioinformatics methods, more and more new long non-coding RNAs (lncRNAs) are discovered and identified. lncRNAs were firstly thought to be transcription noise that from genome desert without biological function; however, as the discovery of lncRNA XIST and HOTAIR uncovers the emerging roles of lncRNAs in development and tumorigenesis. In the past decades, accumulating evidence have indicated that lncRNAs involve in a wide range of biological functions, such as X-chromosome inactivation, reprogramming stem cell pluripotency, regulation of the immune response and carcinogenesis. Although lots of studies have demonstrated that dysregulation of lncRNAs involve in diverse diseases including cancers, the underlying molecular mechanisms of lncRNAs are not well documented. Interestingly, our previous studies and others’ have shown that numerous of lncRNAs expression was misregulated in gastric cancer. In this review, we will focus on the dysregulated lncRNAs and their biological function and underlying pathways or mechanisms in GC. Finally, we will discuss the potential roles of lncRNAs acting as biomarkers or therapeutic targets in GC patients.
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    Long non-coding RNA C20orf56 as a predictor of response to neoadjuvant CCRT and survival rates of rectal cancers
    (2026) Cheng-Fa Yeh; Ching-Chieh Yang; Yi-Kai Kao; Pin-Chun Chen; Po-Wen Yang; Sung-Wei Lee; Yu-Feng Tian; Yu-Hsuan Kuo; Li-Ching Wu; Chien-Feng Li; Yi-Che Chang Chien; I-Wei Chang; Chih-I Chen; Biología Celular e Histología; Universidad de Murcia, Departamento de Biología Celular e Histología
    Introduction. Colorectal cancer is the third most prevalent malignancy and the second leading cause of cancer mortality worldwide. Neoadjuvant concurrent chemoradiotherapy (CCRT) improves survival and increases curative surgery rates in rectal cancer. C20orf56, a long non-coding RNA (lncRNA), plays diverse roles in cancer, but its association with neoadjuvant CCRT response and prognosis in rectal cancer remains unexplored. Materials and Methods. Tumor samples from 343 rectal cancer patients who received neoadjuvant CCRT followed by surgery were analyzed for C20orf56 expression via in situ hybridization. Associations between C20orf56 expression and clinicopathological parameters were evaluated with the χ² test. Survival outcomes were assessed using the Kaplan-Meier method and compared by log-rank tests, while multivariate analysis was conducted using a Cox proportional hazards model. Additionally, an independent cohort of responders and non-responders (n=8 per group) was used to validate C20orf56 transcript levels by real-time RT-PCR. Results. A transcriptomic analysis (GSE35452) identified C20orf56 as differentially expressed between responders and non-responders. Decreased expression of C20orf56 showed significant correlations with less advanced post-treatment tumor invasiveness, negative post-treatment nodal metastasis, absence of vascular invasion and perineural invasion, and improved response to neoadjuvant CCRT (all p≤0.024). Diminished expression of C20orf56 was associated not only with favorable disease-specific survival (DSS), local recurrence-free survival (LRFS), and metastasis-free survival (MeFS) (all p<0.0001) in univariate analysis but also functioned as an independent predictor signifying enhanced clinical outcomes, including DSS, LRFS, and MeFS (all p<0.001). In the real-time RT-PCR analysis, the transcriptomic levels were significantly lower in the responder group compared with the non-responder group (p=0.007). Conclusion. C20orf56 may play a significant role in rectal cancer progression and response to neoadjuvant CCRT, serving as a novel prognostic factor.
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    Long non-coding RNA XIST promotes the malignant features of oral squamous cell carcinoma (OSCC) cells through regulating miR-133a-5p/VEGFB
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2023) Wu, Kankui; Wu, Mengxuan; Wu, Wancui; Liu, Wenzhe
    Objective. Oral squamous cell carcinoma (OSCC) represents a frequently seen oral cavity malignancy, and the mechanisms of its occurrence and development remain unclear. The present work examined the expression and biological function of long non-coding RNA (lncNRA) XIST (X-inactive specific transcript) in OSCC cells and tissues. Study design. A total number of 50 OSCC and paired non-carcinoma tissue samples were collected in this study. Gene expression levels in cancer tissues and cells were quantified by RT-qPCR. In addition, gain- and loss-of-function experiments were conducted to investigate the biological roles of XIST as well as its downstream targets in OSCC cells. Results. XIST was upregulated in OSCC cells and tissues, which predicted a poorer prognostic outcome in OSCC patients. Silencing XIST inhibited the growth and invasion of OSCC cells and triggered apoptosis. miR133a-5p was identified as a downstream target of XIST, which was downregulated in OSCC tissues. miR-133a5p mediated the effect of XIST by targeting VEGFB. VEGFB overexpression rescued the inhibitory effects of XIST silencing on cell growth, invasion and migration. Conclusion. Taken together, the above data indicates that XIST serves as an oncogenic factor to enhance the growth and invasion of
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    Long non-coding RNA-KCNQ1OT1 mediates miR-423-5p/microfibril-associated protein 2 axis in colon adenocarcinoma
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2021) Yin, Xunhai; Jiang, Amín; Ma, Zhibin; Lu, Xi; Li, Dongyue; Chen, Yingying
    Backgrounds. Long non-coding RNAs (lncRNAs) function as competing endogenous RNAs (ceRNAs) that contribute to carcinogenesis. Herein, we plan to explore whether lncRNA KCNQ1OT1 modulated miR-423-5p/microfibril-associated protein 2 (MFAP2) signaling axis is implicated in the progression of human colon adenocarcinoma. Material and methods. Clinical specimens were collected for histologic examination and gene expression analysis. In vitro experimental measurements, including CCK8, transwell and TUNEL staining, were performed to evaluate cell proliferation, migration and apoptosis. Results. up-regulation of KCNQ1OT1 and MFAP2 and down-regulation of miR-423-5p in COAD tissues were substantiated by The Cancer Genome Atlas (TCGA) database and our clinical specimens. In vitro experimental measurements exhibited that knockdown of KCNQ1OT1 facilitated miR-423-5p expression and inhibited MFAP2 expression, simultaneously. Transfection of si-KCNQ1OT1, miR-423-5p mimics or si-MFAP2 had the ability to repress malignant phenotypes of COAD cells. Intriguingly, overexpression of MFAP2 restrained si-KCNQ1OT1- or miR-423-5p mimics-induced the inhibition of cell proliferation and migration and elevation of the apoptotic proportion of COAD cells. Conclusions. KCNQ1OT1 serves as a molecular sponge of miR-423-5p to accelerate the expression of MFAP2 that may be involved in the development of COAD. Our findings present a novel signaling axis KCNQ1OT1/miR-423-5p/MFAP2, which provides a theoretical basis and therapeutic target for the treatment of COAD.