scholarly journals Comprehensive analysis of aberrantly expressed long non‑coding RNAs, microRNAs, and mRNAs associated with the competitive endogenous RNA network in cervical cancer

2020 ◽  
Vol 22 (1) ◽  
pp. 405-415 ◽  
Author(s):  
Peng Chen ◽  
Weiyuan Zhang ◽  
Yu Chen ◽  
Xiaoli Zheng ◽  
Dong Yang
Keyword(s):  
Cervical Cancer ◽  
Comprehensive Analysis ◽  
Non Coding Rnas ◽  
Competitive Endogenous Rna

scholarly journals lncRNA DLG1-AS1 Promotes Cell Proliferation by Competitively Binding with miR-107 and Up-Regulating ZHX1 Expression in Cervical Cancer

2018 ◽  
Vol 49 (5) ◽  
pp. 1792-1803 ◽  
Author(s):  
Xiaohui Rui ◽  
Yun Xu ◽  
Yaqing Huang ◽  
Linjuan Ji ◽  
Xiping Jiang
Keyword(s):  
Cervical Cancer ◽  
Cancer Cells ◽  
Target Genes ◽  
Cell Counting ◽  
Cervical Cancer Cells ◽  
A Cell ◽  
Non Coding Rnas ◽  
Biological Methods ◽  
Cancer Tissues ◽  
Competitive Endogenous Rna

Background/Aims: Recent studies have revealed that long non-coding RNAs (lncRNAs) are involved in the occurrence and development of various tumors, thereby attracting increasing attention from researchers. The important biological functions of lncRNAs have been recognized gradually, but their mechanism in cervical cancer remains unclear. Methods: Differentially expressed lncRNAs in cervical cancer and para-carcinoma tissues were identified by screening using an lncRNA array, and candidate lncRNAs were verified by quantitative real-time PCR. A series of bioinformatics and molecular biological methods were adopted to investigate the interactions among lncRNAs, microRNAs (miRNAs), and miRNA target genes in cervical cancer. Cell viability was measured using a Cell Counting Kit-8 assay. Results: DLG1-AS1 was the most significantly up-regulated lncRNA in cervical cancer tissues, and it was confirmed that cervical cancer patients with high DLG1-AS1 expression had a poor prognosis. Down-regulation of DLG1-AS1 expression suppressed the proliferation of cervical cancer cells. Further investigation revealed that DLG1-AS1 eliminated the inhibition of miR-107 on the expression of its target gene ZHX1 by competitively binding to miR-107. Moreover, rescue assays proved that the effect of DLG1-AS1 on the proliferation of cervical cancer cells was dependent on miR-107. Conclusion: DLG1-AS1/miR-107/ZHX1 can form a competitive endogenous RNA network that regulates the proliferation of cervical cancer cells, resulting in tumor progression.

MALAT1 as a Versatile Regulator of Cancer: Overview of the updates from Predatory role as Competitive Endogenous RNA to Mechanistic In-sights

2020 ◽  
Vol 20 ◽  
Author(s):  
Ammad Ahmad Farooqi ◽  
Evangelia Legaki ◽  
Maria Gazouli ◽  
Silvia Rinaldi ◽  
Rossana Berardi
Keyword(s):  
Molecular Biology ◽  
Detailed Analysis ◽  
Signaling Pathways ◽  
Individualized Medicine ◽  
Signaling Cascades ◽  
Oncogenic Signaling ◽  
Non Coding Rnas ◽  
Oncogenic Signaling Pathways ◽  
Competitive Endogenous Rna

: Central dogma of molecular biology has remained cornerstone of classical molecular biology but serendipitous discovery of microRNAs (miRNAs) in nematodes paradigmatically shifted our current understanding of the intricate mech-anisms which occur during transitions from transcription to translation. Discovery of miRNA captured tremendous attention and appreciation and we had witnessed an explosion in the field of non-coding RNAs. Ground-breaking discoveries in the field of non-coding RNAs have helped in better characterization of microRNAs and long non-coding RNAs (LncRNAs). There is an ever-increasing list of miRNA targets which are regulated by MALAT1 to stimulate or repress expression of tar-get genes. However, in this review our main focus is to summarize mechanistic insights related to MALAT1-mediated regu-lation of oncogenic signaling pathways. We have discussed how MALAT1 modulated TGF/SMAD and Hippo pathways in various cancers. We have also comprehensively summarized how JAK/STAT and Wnt/β-catenin pathways stimulated MALAT1 expression and consequentially how MALAT1 potentiated these signaling cascades to promote cancer. MALAT1 research has undergone substantial broadening however, there is still a need to identify additional mechanisms. MALAT1 is involved in multi-layered regulation of multiple transduction cascades and detailed analysis of different pathways will be helpful in getting a step closer to individualized medicine.

scholarly journals Construction and comprehensive analysis of a competitive endogenous RNA network to reveal potential biomarkers for the malignant differentiation of glioma

Medicine ◽  
2021 ◽  
Vol 100 (39) ◽  
pp. e27248
Author(s):  
Xin Li ◽  
Jingwen Zhang ◽  
Min Zhang ◽  
Xianghua Qi ◽  
Shiyuan Wang ◽  
...  
Keyword(s):  
Comprehensive Analysis ◽  
Competitive Endogenous Rna ◽  
Potential Biomarkers

scholarly journals LINC00885 promotes cervical cancer progression through sponging miR-3150b-3p and upregulating BAZ2A

2022 ◽  
Vol 17 (1) ◽  
Author(s):  
Yeling Liu ◽  
Jingrui Chen ◽  
Lizhong Zhou ◽  
Chunhua Yin
Keyword(s):  
Cervical Cancer ◽  
Cancer Progression ◽  
Animal Experiments ◽  
Cell Behaviors ◽  
Protein Levels ◽  
Non Coding Rna ◽  
Promising Therapeutic Target ◽  
Proliferation And Apoptosis ◽  
Non Coding Rnas ◽  
Oncogenic Function

Abstract Background Cervical cancer (CC) is one of the most common malignancies affecting female worldwide. Long non-coding RNAs (lncRNAs) are increasingly indicated as crucial participants and promising therapeutic targets in human cancers. The main objective of this study was to explore the functions and mechanism of LINC00885 in CC. Methods RT-qPCR and western blot were used to detect RNA and protein levels. Functional and mechanism assays were respectively done for the analysis of cell behaviors and molecular interplays. Results Long intergenic non-coding RNA 885 (LINC00885) was discovered to be upregulated in CC tissues and cell lines through bioinformatics analysis and RT-qPCR. Overexpression of LINC00885 promoted proliferation and inhibited apoptosis, whereas its silence exerted opposite effects. The cytoplasmic localization of LINC00885 was ascertained and furthermore, LINC00885 competitively bound with miR-3150b-3p to upregulate BAZ2A expression in CC cells. Rescue assays confirmed that LINC00885 regulated CC proliferation and apoptosis through miR-3150b-3p/BAZ2A axis. Finally, we confirmed that LINC00885 aggravated tumor growth through animal experiments. Conclusions LINC00885 exerted oncogenic function in CC via regulating miR-3150b-3p/BAZ2A axis. These findings suggested LINC00885 might serve as a potential promising therapeutic target for CC patients.

scholarly journals Inhibition of lncRNA-NEAT1 sensitizes 5-Fu resistant cervical cancer cells through de-repressing the microRNA-34a/LDHA axis

2021 ◽  
Author(s):  
Xuecheng Shao ◽  
Xuehui Zheng ◽  
Dan Ma ◽  
Yang Liu ◽  
Guoyan Liu
Keyword(s):  
Cervical Cancer ◽  
Cancer Cells ◽  
Cervical Cancer Patient ◽  
Cervical Cancer Cells ◽  
Key Enzyme ◽  
Direct Targeting ◽  
Cancer Tissues ◽  
Lncrna Neat1 ◽  
Competitive Endogenous Rna ◽  
Resistant Cells

Cervical cancer is one of the most diagnosed malignancies among females. The 5-fluorouracil (5-Fu) is a widely used chemotherapeutic agent against diverse cancers. Despite the initially encouraging progresses, a fraction of cervical cancer patients developed 5-Fu resistance. We detected that NEAT1 was significantly upregulated in cervical cancer tissues and cell lines. Moreover, NEAT1 was positively associated with 5-Fu resistance. Furthermore, expression of NEAT1 was significantly upregulated in 5-Fu resistant CaSki cervical cancer cells. Knocking down NEAT1 by shRNA dramatically promoted the sensitivity of 5-Fu resistant CaSki cells. We observed a negative correlation between lncRNA-NEAT1 and miR-34a in cervical cancer patient tissues. Overexpression of miR-34a significantly sensitized 5-Fu resistant cells. Bioinformatical analysis uncovered that NEAT1 functions as a competitive endogenous RNA (ceRNA) of miR-34a in cervical cancer cells via sponging it at multiple sites to suppress expression of miR-34a. This negative association between NEAT1 and miR-34a was further verified in cervical cancer tissues. We found the 5-Fu resistant cells displayed significantly increased glycolysis rate. Overexpression of miR-34a suppressed cellular glycolysis rate and sensitized 5-Fu resistant cells through direct targeting the 3’UTR of LDHA, a glycolysis key enzyme. Importantly, knocking down NEAT1 successfully downregulated LDHA expressions and glycolysis rate of cervical cancer cells by upregulating miR-34a, a process could be further rescued by miR-34a inhibition. Finally, we demonstrated inhibition of NEAT1 significantly sensitized cervical cancer cells to 5-Fu through the miR-34a/LDHA pathway. In summary, this study suggests a new molecular mechanism for the NEAT1-mediated 5-Fu resistance via the miR-34a/LDHA-glycolysis axis

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