RETRACTED: Silencing lncRNAs PVT1 Upregulates miR-145 and Confers Inhibitory Effects on Viability, Invasion, and Migration in EC

Shen, Shuxin; Li, Ke; Liu, Ying; Yang, Chengli; He, Chao; Wang, Hao-Rang

doi:10.1016/j.omtn.2019.11.030

Cited by 13 publications

(7 citation statements)

References 38 publications

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“…LncRNAs are a class of mRNA-like transcripts with a length of > 200 nucleotides that lack protein-coding ability. Accumulating evidence indicates that lncRNAs play important roles in various biological processes, including transcriptional modifications, cell proliferation, differentiation, epigenetic modulation, and immune system-modulated pathways [ 20 – 25 ]. For example, lncRNA SNHG1 enhances the differentiation of Treg cells to provoke immune escape in BC [ 26 ].…”

Section: Introductionmentioning

confidence: 99%

Molecular characterization of breast cancer: a potential novel immune-related lncRNAs signature

et al. 2020

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Background Accumulating evidence has demonstrated that immune-related lncRNAs (IRLs) are commonly aberrantly expressed in breast cancer (BC). Thus, we aimed to establish an IRL-based tool to improve prognosis prediction in BC patients. Methods We obtained IRL expression profiles in large BC cohorts (N = 911) from The Cancer Genome Atlas (TCGA) database. Then, in light of the correlation between each IRL and recurrence-free survival (RFS), we screened prognostic IRL signatures to construct a novel RFS nomogram via a Cox regression model. Subsequently, the performance of the IRL-based model was evaluated through discrimination, calibration ability, risk stratification ability and decision curve analysis (DCA). Results A total of 52 IRLs were obtained from TCGA. Based on multivariate Cox regression analyses, four IRLs (A1BG-AS1, AC004477.3, AC004585.1 and AC004854.2) and two risk parameters (tumor subtype and TNM stage) were utilized as independent indicators to develop a novel prognostic model. In terms of predictive accuracy, the IRL-based model was distinctly superior to the TNM staging system (AUC: 0.728 VS 0.673, P = 0.010). DCA indicated that our nomogram had favorable clinical practicability. In addition, risk stratification analysis showed that the IRL-based tool efficiently divided BC patients into high- and low-risk groups (P < 0.001). Conclusions A novel IRL-based model was constructed to predict the risk of 5-year RFS in BC. Our model can improve the predictive power of the TNM staging system and identify high-risk patients with tumor recurrence to implement more appropriate treatment strategies.

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Section: Introductionmentioning

confidence: 99%

Molecular characterization of breast cancer: a potential novel immune-related lncRNAs signature

et al. 2020

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“…The expression of miR‐145 was negatively correlated with lymph node metastasis of ESCC [ 40 ]. More interestingly, the down‐regulation of PVT1 may inhibit cell migration and invasion by promoting the expression of miR‐145 [ 41 , 42 ]. These reports further support the reliability of our ceRNA network and indicate that the expression relationship between PVT1 and miR‐145 may play a significant role in the ESCC.…”

Section: Discussionmentioning

confidence: 99%

Overexpression of cyclin‐dependent kinase 1 in esophageal squamous cell carcinoma and its clinical significance

Zhang

Chen

et al. 2021

FEBS Open Bio

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Cyclin-dependent kinase 1 (CDK1) plays a significant role in certain malignancies. However, it remains unclear whether CDK1 plays a role in esophageal squamous cell carcinoma (ESCC). The aim of this study was to analyze the expression and clinical value of CDK1 in ESCC. CDK1 protein in 151 ESCC tissues and 138 normal esophageal tissues was detected by immunohistochemistry. RNA-seq of eight pairs of ESCC and adjacent esophageal specimens was performed to evaluate the levels of CDK1 mRNA. Microarray and external RNA-seq data from 664 cases of ESCC and 1733 cases of control tissues were used to verify the difference in CDK1 expression between the two groups. A comprehensive analysis of all data was performed to evaluate the difference in CDK1 between ESCC tissues and control tissues. Further, functional enrichment analyses were performed based on differentially expressed genes (DEGs) of ESCC and coexpressed genes (CEGs) of CDK1. In addition, a lncRNA-miRNA-CDK1 network was constructed. The expression of CDK1 protein was obviously increased in ESCC tissues (3.540 AE 2.923 vs. 1.040 AE 1.632, P < 0.001). RNA-seq indicated that the mRNA level of CDK1 was also highly expressed in ESCC tissues (5.261 AE 0.703 vs. 2.229 AE 1.161, P < 0.0001). Comprehensive analysis revealed consistent up-regulation of CDK1 (SMD = 1.41; 95% CI 1.00-1.83). Further, functional enrichment analyses revealed that the functions of these genes were mainly concentrated in the cell cycle. A triple regulatory network of PVT1-hsa-miR-145-5p/hsa-miR-30c-5p-CDK1 was constructed using in silico analysis. In summary, overexpression of CDK1 is closely related to ESCC tumorigenesis.Esophageal cancer is one of the most common malignant tumors in the world and is the seventh highest cause of cancer-related death [1]. There are approximately 19,260 new cases and 15,530 deaths each year [1]. Esophageal squamous cell carcinoma (ESCC) is the main subtype of esophageal cancer, accounting for 90% of all esophageal cancers [2]. Thus far, the main treatment method for ESCC is a combined treatment of radiotherapy, chemotherapy, and surgery [3]. The emergence of drug resistance in molecular targeted Abbreviations CDKs, cyclin-dependent kinases; CDK1, cyclin-dependent kinase 1; CEGs, co-expressed genes; DEGs, differentially expressed genes; ESCC, esophageal squamous cell carcinoma.

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“…Cytoplasmic lncRNAs that mostly localize and function in the cytoplasm act as decoys for miRNAs and proteins to affect gene modulation [30,31]. Several studies reveal that lncRNAs are sponges of many miRNAs, exerting the same function as ceRNAs in tumorigenesis [32,33].…”

Section: Discussionmentioning

confidence: 99%

LncRNA LINC00337 Sponges miR-1285-3p to Promote Proliferation and Metastasis of Lung Adenocarcinoma Cells Through Up-Regulating YTHDF1

Zhang

et al. 2020

Preprint

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Background: Emerging studies have attested that long noncoding RNAs (lncRNAs) predominantly functioned in carcinogenesis of multiple developing human tumors. The current research aimed at probing the underlying participation and mechanisms of LINC00337 in lung adenocarcinoma.Methods: Here we analyzed TCGA and GTEx datasets and chose LINC00337 as research object. Cell proliferation, cell apoptosis, cell cycle, and invasion were detected in gain and loss experiment of LINC00337 both in vitro and in vivo. Moreover, RNA pull-down, luciferase reporter assays, western blotting analysis, rescue experiment were performed to investigate underlying molecular mechanisms of LINC00337 function. Results: LINC00337 was remarkably increased in lung adenocarcinoma. Also, LINC00337 knock-down was unraveled to repress cell invasion and proliferation as well as cell cycle, and gear up apoptosis in lung adenocarcinoma in vitro and in vivo. With respect to mechanism, LINC00337 knock-down boosted miR-1285-3p to be expressed and then restrained YTHDF1 to be expressed post-transcriptionally. Crucially, both miR-1285-3p decrement and YTHDF1 overexpression successfully countered the influence on cell proliferation, invasion and apoptosis caused by LINC00337 shRNA.Conclusions: These results suggest that LINC00337 acted as an oncogenic lncRNA, targeting miR-1285-3p and regulating YTHDF1 expression, to promote the progression of lung adenocarcinoma.

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RETRACTED: Silencing lncRNAs PVT1 Upregulates miR-145 and Confers Inhibitory Effects on Viability, Invasion, and Migration in EC

Cited by 13 publications

References 38 publications

Molecular characterization of breast cancer: a potential novel immune-related lncRNAs signature

Molecular characterization of breast cancer: a potential novel immune-related lncRNAs signature

Overexpression of cyclin‐dependent kinase 1 in esophageal squamous cell carcinoma and its clinical significance

LncRNA LINC00337 Sponges miR-1285-3p to Promote Proliferation and Metastasis of Lung Adenocarcinoma Cells Through Up-Regulating YTHDF1

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