Identification of long noncoding RNA RP11-89K21.1 and RP11-357H14.17 as prognostic signature of endometrial carcinoma via integrated bioinformatics analysis

Background. Redox plays an essential role in the pathogeneses and progression of tumors, which could be regulated by long noncoding RNA (lncRNA). We aimed to develop and verify a novel redox-related lncRNA-based prognostic signature for clear cell renal cell carcinoma (ccRCC). Materials and Methods. A total of 530 ccRCC patients from The Cancer Genome Atlas (TCGA) were included in this study. All the samples were randomly split into training and test group at a 1 : 1 ratio. Then, we screened differentially expressed redox-related lncRNAs and constructed a novel prognostic signature from the training group using the least absolute shrinkage and selection operation (LASSO) and COX regression. Next, to verify the accuracy of the signature, we conducted risk and survival analysis, as well as the construction of ROC curve, nomogram, and calibration curves in the training group, test group, and all samples. Finally, the redox gene-redox-related lncRNA interaction network was constructed, and gene set enrichment analysis (GSEA) was performed to investigate the status of redox-related functions between high/low-risk groups. Results. A nine-redox-related lncRNA signature consisted of AC025580.3, COLCA1, AC027601.2, DLEU2, AC004918.3, AP006621.2, AL031670.1, SPINT1-AS1, and LAMA5-AS1 was significantly associated with overall survival in ccRCC patients. The signature proved efficient, and thus, a nomogram was successfully assembled. In addition, the GSEA results demonstrated that two major redox-related functions were enhanced in the high-risk group ccRCC patients. Conclusions. Our findings robustly demonstrate that the nine-redox-related lncRNA signature could serve as an efficient prognostic indicator for ccRCC.

Download Full-text

Prognostic Value of Long Noncoding RNA NORAD in Various cancers: a meta-analysis

10.1101/2020.07.09.20150185 ◽

2020 ◽

Author(s):

Qin Yang ◽

Zheng Zhang ◽

Yuan-Yuan Gong ◽

Zhi-Ran Li ◽

Hua-Zhu Zhang ◽

...

Keyword(s):

Risk Factor ◽

Long Noncoding Rna ◽

Noncoding Rna ◽

Bioinformatics Analysis ◽

Meta Analysis ◽

Disease Free Survival ◽

Cancer Prognosis ◽

Clinicopathological Parameters ◽

Survival Outcomes ◽

Free Survival

Abstract Objective: Accumulating studies reported that noncoding RNA activated by DNA damage (NORAD) was correlated with poor survival outcomes for patients in different cancers. However, the effects of NORAD on cancer prognosis were controversial. Therefore, a meta-analysis was carried out to elucidate this issue. Methods: Literature search was performed to collect eligible relevant publications until June 2020. The pooled hazard ratios (HRs) or odds ratios (ORs) with 95% confidence intervals (CIs) were calculated to assess the association of NORAD with prognosis and clinical features in diverse cancers. In addition, bioinformatics analysis was also utilized to validate the results of the meta-analysis. Results: Fourteen relevant articles involving 867 patients were enrolled in the present study. The pooled results showed that elevated expression of NORAD was a risk factor for overall survival (HR = 1.46, 95% CI: 1.06-2.01, P = 0.020), disease-free survival (HR = 1.74, 95% CI: 1.18-2.57, P = 0.005) and recurrence-free survival. Besides, overexpression of NORAD significantly correlated with lymph node metastasis and T stage. Additionally, bioinformatics analysis further strengthened and complemented the results of the present study. Conclusion: Our results showed that NORAD was a risk factor for survival outcomes and clinicopathological parameters in cancer patients. These findings indicated that NORAD may be a promising candidate for prognosis prediction and potential therapeutic target in diverse cancers. Key words: Long noncoding RNA, NORAD, prognosis, cancer, meta-analysis

Download Full-text

Identification and Function Analysis of a Five-Long Noncoding RNA Prognostic Signature for Endometrial Cancer Patients

DNA and Cell Biology ◽

10.1089/dna.2019.4944 ◽

2019 ◽

Vol 38 (12) ◽

pp. 1480-1498 ◽

Cited By ~ 7

Author(s):

Hong Tang ◽

Zhixi Wu ◽

Yuan Zhang ◽

Tingting Xia ◽

Dong Liu ◽

...

Keyword(s):

Endometrial Cancer ◽

Cancer Patients ◽

Long Noncoding Rna ◽

Noncoding Rna ◽

Function Analysis ◽

Prognostic Signature ◽

And Function

Download Full-text

Long Noncoding RNA HOXB-AS1 Is Upregulated in Endometrial Carcinoma and Sponged miR-149-3p to Upregulate Wnt10b

Technology in Cancer Research & Treatment ◽

10.1177/1533033820967462 ◽

2020 ◽

Vol 19 ◽

pp. 153303382096746

Author(s):

Da Liu ◽

Min Qiu ◽

Lili Jiang ◽

Kuiran Liu

Keyword(s):

Endometrial Carcinoma ◽

Long Noncoding Rna ◽

Noncoding Rna ◽

Competing Endogenous Rna ◽

Tissue Samples ◽

Invasion And Migration ◽

Underlying Mechanisms ◽

And Migration ◽

Oncogenic Function

The functions of Long noncoding RNA (lncRNA) HOXB-AS1 have been investigated in glioblastoma and multiple myeloma. However, the role of lncRNA HOXB-AS1 in endometrial carcinoma (EC) remains largely unknown. This study investigated the underlying mechanisms of the lncRNA HOXB-AS1 on the progression of EC. In this study, We found that HOXB-AS1 expression was significantly upregulated in EC tissue samples and was associated with shorter survival time. Furthermore, upregulation of HOXB-AS1 promoted proliferation, invasion, and migration of EC cell. HOXB-AS1 and Wnt10b directly bound to miR-149-3p. HOXB-AS1 increased the expression of Wnt10b by binding to miR-149-3p. We further verified the upregulation of β-catenin, cyclin D1, and c-myc induced by HOXB-AS1. In conclusion, our results indicated that HOXB-AS1 exerted oncogenic function as competing endogenous RNA (ceRNA) of miR-149-3p to release Wnt10b and activated Wnt/β-catenin pathway.

Download Full-text

Lentivirus-Mediated RNA Interference Targeting the Long Noncoding RNA HOTAIR Inhibits Proliferation and Invasion of Endometrial Carcinoma Cells In Vitro and In Vivo

International Journal of Gynecological Cancer ◽

10.1097/igc.0000000000000121 ◽

2014 ◽

Vol 24 (4) ◽

pp. 635-642 ◽

Cited By ~ 41

Author(s):

Jiaming Huang ◽

Peiqi Ke ◽

Luyan Guo ◽

Wei Wang ◽

Hao Tan ◽

...

Keyword(s):

Cell Cycle ◽

Cell Proliferation ◽

Endometrial Cancer ◽

Endometrial Carcinoma ◽

Cancer Cells ◽

Long Noncoding Rna ◽

Noncoding Rna ◽

Proliferation And Invasion

ObjectiveThe overexpression of long noncoding RNA HOTAIR is associated with various aggressive solid carcinomas. However, its relationship with endometrial carcinoma has not been reported. The present study aimed to investigate the expression of the long noncoding RNA HOTAIR in endometrial carcinoma, its relationship with the carcinoma’s clinicopathologic features, and the biological function of HOTAIR in regulating endometrial cancer cell proliferation and invasion in vitro and in vivo.MethodsThe expression of HOTAIR was detected in different tissues and cell lines by real-time PCR. Lentivirus-mediated HOTAIR-specific shRNAvectors were transfected into endometrial cancer HEC-1A cells. Cell proliferation and colony formation were examined by CCK-8 assays and colony formation assays, respectively. Invasion and migration were examined by Transwell assays. Flow cytometry assay was used to examine the cell cycle. In addition, xenograft model assays were performed to analyze the growth of endometrial cancer cells in vivo.ResultsOur data showed that HOTAIR expression was higher in endometrial cancer cells and tissues than in normal endometrial tissues. HOTAIR expression was closely related to the tumor stage (P= 0.045), myometrial invasion (P= 0.014), and lymph node metastasis (P= 0.033). The down-regulation of HOTAIR resulted in a significant inhibition of cell proliferation, migration, and invasion and in cell cycle arrest at the G0/G1 phase. Furthermore, HOTAIR depletion significantly suppressed the endometrial cancer tumorigenesis in vivo.ConclusionsThis study is the first to suggest that HOTAIR plays an important role in the carcinogenesis of endometrial cancer. Targeting HOTAIR may be a novel therapeutic strategy for endometrial cancer.

Download Full-text

Long noncoding RNA LSINCT5 promotes endometrial carcinoma cell proliferation, cycle, and invasion by promoting the Wnt/β-catenin signaling pathway via HMGA2

Therapeutic Advances in Medical Oncology ◽

10.1177/1758835919874649 ◽

2019 ◽

Vol 11 ◽

pp. 175883591987464 ◽

Cited By ~ 5

Author(s):

Hongye Jiang ◽

Yong Li ◽

Jie Li ◽

Xuyu Zhang ◽

Gang Niu ◽

...

Keyword(s):

Cell Cycle ◽

Cell Proliferation ◽

Cell Migration ◽

Endometrial Carcinoma ◽

Signaling Pathway ◽

Long Noncoding Rna ◽

Noncoding Rna ◽

Critical Role ◽

Migration And Invasion ◽

Migration Assay

Background: A review of the evidence has indicated the critical role of long noncoding RNA (lncRNA) LSINCT5 in a large number of human cancers. However, the mechanistic involvement of LSINCT5 in endometrial carcinoma (EC) is still unknown. Here the authors aim to characterize the expression status of LSINCT5 and elucidate its mechanistic relevance to EC. Methods: Relative expression of LSINCT5 and HMGA2 were quantified by a real-time polymerase chain reaction. SiRNAs were employed to specifically knockdown endogenous LSINCT5 in EC cells. Cell proliferation was measured with Cell Count Kit-8 kit (CCK-8, Dojindo, Kumamoto, Japan) and cell growth was assessed by a colony formation assay. The cell cycle was analyzed with propidium iodide (PI) staining. Apoptotic cells were determined by flow cytometry after Annexin V/PI double-staining. Cell migration was evaluated by a wound-healing assay, and cell invasion was assessed using a transwell migration assay. The protein levels of HMGA2, Wnt3a, p-β-catenin, c-myc, β-actin, and GAPDH were determined by western blot. Results: The authors observed positively correlated and aberrantly up-regulated LSINCT5 and HMGA2 in EC. LSINCT5 deficiency significantly inhibited cell proliferation, cell cycle progression, and induced apoptosis. Meanwhile, cell migration and invasion were greatly compromised by the LSINCT5 knockdown. LSINCT5 stabilized HMGA2, which subsequently stimulated activation of Wnt/β-catenin signaling and consequently contributed to the oncogenic properties of LSINCT5 in EC. Conclusions: Our data uncovered the oncogenic activities and highlighted the mechanistic contributions of the LSINCT5-HMGA2-Wnt/β-catenin signaling pathway in EC.

Download Full-text