Long noncoding RNA kcna3 inhibits the progression of colorectal carcinoma through down-regulating YAP1 expression

Zhong, Xiaolin; Lü, Muhan; Jiang, Wan; Zhou, Tiejun; Qin, Bo

doi:10.1016/j.biopha.2018.07.118

Cited by 21 publications

(21 citation statements)

References 27 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…As we know, Hippo pathway, especially the dysfunction of YAP1 plays tumor-promoting actions in several human cancers [20][21][22][23][24]. Our previous findings demonstrated that YAP1 expression was upregulated in OSC cells [8], which were confirmed in this study.…”

Section: Discussionsupporting

confidence: 87%

LncRNA FLVCR1-AS1 mediates miR-513/YAP1 signaling to promote cell progression, migration, invasion and EMT process in ovarian cancer

Yan

Silva

et al. 2019

J Exp Clin Cancer Res

View full text Add to dashboard Cite

Background Long noncoding RNAs (lncRNAs) have been reported to be associated with the proliferation of several cancer cells. The aim of this study was to investigate the role of FLVCR1-AS1 in ovarian serous cancer (OSC). Methods FLVCR1-AS1 expression was determined in human OSC tissues, serums and cell lines. The role of FLVCR1-AS1 knockdown or overexpression on OSC cell growth, migration, invasion, apoptosis and epithelial to mesenchymal transition (EMT) were evaluated in vitro using CCK8, colony formation assay, wound healing assay, transwell assay and western blot assay. Besides, luciferase reporter assays were performed to identify interactions among FLVCR1-AS1 and its target genes. Moreover, the in vivo effects were investigated using immunocompromised NSG female mice. Results In this study, FLVCR1-AS1 expression was upregulated in OSC tissues, serums, and cells. Knockdown FLVCR1-AS1 decreased cell growth, migration, invasion, and EMT, as well as increased apoptosis in OSC cells, whereas, overexpression of FLVCR1-AS1 increased cell proliferation, migration, invasion, and EMT, and decreased apoptosis of OSC cells. Besides, FLVCR1-AS1 directly bound to miR-513 and downregulated its expression. Moreover, FLVCR1-AS1 reversed the effect of miR-513 on the OSC cell growth, which might be associated with the role of YAP1. Furthermore, in terms of mechanism, FLVCR1-AS1 promoted EMT in OSC cells. Finally, mice models further confirmed that knockdown FLVCR1-AS1 distinctly suppressed cell growth and EMT in vivo. Conclusion Taken together, FLVCR1-AS1 mediated miR-513/YAP1 signaling to promote cell progression, migration, invasion and EMT process in OSC cells.

show abstract

Section: Discussionsupporting

confidence: 87%

LncRNA FLVCR1-AS1 mediates miR-513/YAP1 signaling to promote cell progression, migration, invasion and EMT process in ovarian cancer

Yan

Silva

et al. 2019

J Exp Clin Cancer Res

View full text Add to dashboard Cite

show abstract

“…Increasing evidences have revealed the vital role of lncRNAs in cancer progression, including initiation and differentiation [24][25][26]. Recently, the role of lncRNAs in gastric cancer has been studied [27,28].…”

Section: Discussionmentioning

confidence: 99%

LncRNA TTN-AS1 contributes to gastric cancer progression by acting as a competing endogenous RNA of miR-376b-3p

Dong¹,

Peng²,

Yuan³

et al. 2019

neo

View full text Add to dashboard Cite

Long noncoding RNAs (lncRNAs) were reported to participate in the progression of gastric cancer (GC). However, little is known about the biological functions of TTN antisense RNA 1 (TTN-AS1) in GC. Using qRT-PCR examination, we found that TTN-AS1 was expressed at a higher level in GC tissues and cell lines compared to the normal controls. Kaplan-Meier analysis of GC patients revealed the negative correlation between TTN-AS1 expression and the overall survival. To detect the biological function of TTN-AS1 in GC, we silenced TTN-AS1 to perform loss-of-function assays. The experimental results revealed that knockdown of TTN-AS1 obviously inhibited GC cell proliferation, induced cell apoptosis and impaired cell migration and invasion. In mechanism, TTN-AS1 was located in the cytoplasm of GC cells, indicating the post-transcriptional regulation of TTN-AS1 on gene expression. Bioinformatics analysis revealed the potential binding relation between TTN-AS1 and miR-376b-3p as well as between miR-376b-3p and KLF12. Mechanism experiments such as luciferase reporter assay and RNA pull-down assay demonstrated the interaction between TTN-AS1 and miR-376b-3p as well as between miR-376b-3p and KLF12 in GC cells. At last, rescue assays certified that miR-376b-3p and KLF12 involved in TTN-AS1-mediated GC progression. Similarly, the role of TTN-AS1-miR-376b-3p-KLF12 axis in GC progression was analyzed and validated. Taken together, we concluded that TTN-AS1 might function as a novel potential therapeutic target in the treatment of gastric cancer.

show abstract

“…Long non-coding RNA (lncRNA), containing more than 200 bp of nucleotides, has been demonstrated to be an essential participant during the development of malignancies [5][6][7][8][9]. The host gene of TRPM2-AS, transient receptor potential cation channel subfamily M member 2 antisense RNA, consists of 3 exons and locates at chromosome 21q22.3.…”

Section: Introductionmentioning

confidence: 99%

TRPM2-AS promotes bladder cancer-genesis by targeting miR-22-3p thus releasing GINS2 mRNA

Tian¹,

Guan²,

Su³

et al. 2020

Preprint

View full text Add to dashboard Cite

Background: We aimed to study the effects of lncRNA TRPM2-AS in bladder cancer (BLCA) by interacting with its downstream effectors miR-22-3p and GINS2 mRNA.Methods: Online bioinformatic tools were used to identify the key lncRNA, miRNA and mRNA of interest in BLCA. TRPM2-AS, miR-22-3p and GINS2 mRNA expression was measured by qRT-PCR in bladder tissues and selected cell lines. Subcellular localization of TRPM2-AS in T24 and 5637 cell lines was identified using a cellular fractionation method. Luciferase reporter assay, RIP assay and RNA pull-down assay were employed to validate the direct binding relationship between TRPM2-AS, miR-22-3p and GINS2 mRNA. Cell viability, proliferation and apoptosis were measured by a series of cell functional experiments in T24 and 5637 cells.Results: TRPM2-AS was primarily located in cell cytoplasm and significantly up-regulated in BLCA tissues and cell lines. TRPM2-AS knockdown significantly inhibited cell viability and proliferation, but promoted cell apoptosis. miR-22-3p, a significant downstream target of TRPM2-AS, showed a lower expression level in BLCA tissues and cell lines. miR-22-3p inhibition resulted in a significant enhancement of BLCA cancer cell phenotypes. Lastly, GINS2 mRNA was a downstream target of miR-22-3p, and was significantly up-regulated in BLCA. The knockdown of GINS2 led to a significant suppression of BLCA cancer cell phenotypes.Conclusions: TRPM2-AS was a tumor promoter and fulfilling its role through binding to miR-22-3p to increase GINS2 expression. This novel interactome in BLCA might become a new therapy in BLCA.

show abstract

Long noncoding RNA kcna3 inhibits the progression of colorectal carcinoma through down-regulating YAP1 expression

Cited by 21 publications

References 27 publications

LncRNA FLVCR1-AS1 mediates miR-513/YAP1 signaling to promote cell progression, migration, invasion and EMT process in ovarian cancer

LncRNA FLVCR1-AS1 mediates miR-513/YAP1 signaling to promote cell progression, migration, invasion and EMT process in ovarian cancer

LncRNA TTN-AS1 contributes to gastric cancer progression by acting as a competing endogenous RNA of miR-376b-3p

TRPM2-AS promotes bladder cancer-genesis by targeting miR-22-3p thus releasing GINS2 mRNA

Contact Info

Product

Resources

About