Long noncoding RNA UCA1 promotes osteosarcoma metastasis through CREB1-mediated epithelial-mesenchymal transition and activating PI3K/AKT/mTOR pathway

Ma, Hangzhan; Su, Rui‐Bin; Feng, Hongwei; Guo, Youming; Su, Gengxun

doi:10.1016/j.jbo.2019.100228

Cited by 45 publications

(38 citation statements)

References 16 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…A similar study documented that SOX2OT can attenuate the binding of miR‐194‐5p to SOX3 3′UTR by competitively binding to miR‐194‐5p, thus accelerating the development of glioma . Another study reported that UCA1 can attenuate the inhibitory effect of miR‐582 on CREB1 by competitively binding to miR‐582 to promote the occurrence and development of osteosarcoma . HMMR‐AS1 is able to attenuate its inhibitory effect on SIRT6 by competitively binding to miR‐138, accelerating the development and progression of lung adenocarcinoma …”

Section: Discussionmentioning

confidence: 87%

“…48 Another study reported that UCA1 can attenuate the inhibitory effect of miR-582 on CREB1 by competitively binding to miR-582 to promote the occurrence and development of osteosarcoma. 49 HMMR-AS1 is able to attenuate its inhibitory effect on SIRT6 by competitively binding to miR-138, accelerating the development and progression of lung adenocarcinoma. 50 We also observed the upregulation of the mRNA and protein expression levels of LASP1 by TFAP4 overexpression.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Transcription factor AP‐4 (TFAP4)‐upstream ORF coding 66 aa inhibits the malignant behaviors of glioma cells by suppressing the TFAP4/long noncoding RNA 00520/microRNA‐520f‐3p feedback loop

et al. 2020

View full text Add to dashboard Cite

Upstream ORF (uORF) is a translational initiation element located in the 5′UTR of eukaryotic mRNAs. Studies have found that uORFs play an important regulatory role in many diseases. Based on The Cancer Genome Atlas database, the results of our experiments and previous research evidence, we investigated transcription factor AP‐4 (TFAP4) and its uORF, LIM and SH3 protein 1 (LASP1), long noncoding RNA 00520 (LINC00520), and microRNA (miR)‐520f‐3p as candidates involved in glioma malignancy, which is a poorly understood process. Both TFAP4‐66aa‐uORF and miR‐520f‐3p were downregulated, and TFAP4, LASP1, and LINC00520 were highly expressed in glioma tissues and cells. TFAP4‐66aa‐uORF or miR‐520f‐3p overexpression or TFAP4, LASP1, or LINC00520 knockdown inhibited glioma cell proliferation, migration, and invasion, but promoted apoptosis. TFAP4‐66aa‐uORF inhibited the translation of TFAP4 by binding to the TFAP4 mRNA. MicroRNA‐520f‐3p inhibited TFAP4 expression by binding to its 3′UTR. However, LINC00520 could promote the expression of TFAP4 by competitively binding to miR‐520f‐3p. In addition, TFAP4 transcriptionally activated LASP1 and LINC00520 expression by binding to their promoter regions, forming a positive feedback loop of TFAP4/LINC00520/miR‐520f‐3p. Our findings together indicated that TFAP4‐66aa‐uORF inhibited the TFAP4/LINC00520/miR‐520f‐3p feedback loop by directly inhibiting TFAP4 expression, subsequently leading to inhibition of glioma malignancy. This provides a basis for developing new therapeutic approaches for glioma treatment.

show abstract

Section: Discussionmentioning

confidence: 87%

Section: Discussionmentioning

confidence: 99%

Transcription factor AP‐4 (TFAP4)‐upstream ORF coding 66 aa inhibits the malignant behaviors of glioma cells by suppressing the TFAP4/long noncoding RNA 00520/microRNA‐520f‐3p feedback loop

et al. 2020

View full text Add to dashboard Cite

show abstract

“…19 It is urgent to investigate new and effective molecular targets for the treatment of RB. In this study, 16 ovarian cancer 22 and lung cancer. 23 Furthermore, Sun et al 24 have reported that lncRNA-UCA1 is highly expressed in laryngeal squamous cell carcinoma.…”

Section: Rbmentioning

confidence: 97%

“…30 A study of Li et al 17 has indicated that lncRNA-UCA1 significantly promotes cell proliferation and suppresses apoptosis by activating PI3K-Akt-mTOR signaling pathway in gastric cancer. Ma et al 16 have suggested that lncRNA-UCA1 could promote osteosarcoma metastasis through the activation of PI3K/AKT signaling pathway. In the present study, silencing lncRNA-UCA1 significantly decreased the phosphorylation of PI3K and Akt, as well as the expression of S6k in HXO-RB44 cells, while lncRNA-…”

Section: Rbmentioning

confidence: 99%

Long noncoding RNA UCA1 facilitates cell proliferation and inhibits apoptosis via activating PI3K/Akt pathway in retinoblastoma

Yuan

2019

Preprint

View full text Add to dashboard Cite

Background This study aimed to explored the effect of lncRNA-UCA1 on retinoblastoma (RB) and its potential molecular mechanisms.Methods In our study, the expression of lncRNA-UCA1 was measured by qRT-RCR in both RB tissues and RB HXO-RB44 and Y79 cells. The relationship between lncRNA-UCA1 expression and clinical parameters in RB patients were evaluated. Cell proliferation, cell clones, apoptosis and cell cycle of HXO-RB44 and Y79 cells were measured by cell counting kit-8 (CCK-8) assay, colony formation assay and flow cytometry, respectively. In addition, the expressions of PCNA, Caspase-3, survivin, p16, p21, CDK2, PI3K, p-PI3K, Akt, p-Akt and S6k in HXO-RB44 and Y79 cells were measured by western blot.Results lncRNA-UCA1 was highly expressed in both RB tissues and RB HXO-RB44 and Y79 cells. Moreover, the expression of lncRNA-UCA1 in RB patients was remarkedly correlated with tumor size, optic nerve invasion and pathologic grade. lncRNA-UCA1 markedly facilitated cell proliferation and cell cycle procession, as well as inhibited cell apoptosis in HXO-RB44 and Y79 cells. lncRNA-UCA1 dramatically increased the expression of S6k and the phosphorylation of PI3K and Akt in RB cells. LY294002 (PI3K inhibitor) reversed the effects of lncRNA-UCA1 on RB cell proliferation, apoptosis and cell cycle procession.Conclusions Our study indicated that lncRNA-UCA1 could promote cell proliferation and cell cycle procession, as well as inhibit cell apoptosis in RB via activating PI3K/Akt pathway.

show abstract

“…PI3K/Akt pathway has been considered to exert a crucial impact in tumor. 11−13 In OS, Ma H et al 14 have revealed that LncRNA UCA1 promotes OS metastasis through EMT by activating PI3K/AKT/mTOR pathway. MDA19 has been reported to inhibit OS cell metastasis by PI3K/Akt/mTOR pathway.…”

Section: Introductionmentioning

confidence: 99%

LncRNA NCRNA00173 is down-regulated in pediatric osteosarcoma and suppresses cell metastasis of osteosarcoma cells through regulating PI3k/Akt pathway

Zhao¹,

Chen²,

Xia³

2019

Preprint

View full text Add to dashboard Cite

Background: Osteosarcoma (OS) is a primary malignant tumor with high mortality and disability rate in childhood and adolescent, whereas the influence of LncRNA00173 (NCRNA00173) on pediatric OS progression is not obvious yet. Therefore, this study aimed to investigate the expression of NCRNA00173 in pediatric OS and its effect on OS progression. Methods: In our study, qRT-PCR was adopted to test the NCRNA00173 expression in 40 pairs of pediatric OS tissues and OS cell lines. Kaplan-Meier method and Cox proportional hazard model were performed to analyze the prognosis of pediatric OS patients. The cell proliferation, apoptosis, migration and invasion of U2OS and HOS cells were test by MTT assay, flow cytometry, wound-healing, and transwell assay, respectively. The protein expression levels of PI3K/Akt pathway were measured by western blot. In addition, tumor growth in nude mice was also detected. Results: The expression of NCRNA00173 was down-regulated and relevant with poor prognosis in pediatric OS. Overexpression of NCRNA00713 inhibited cell proliferation, migration and invasion, as well as accelerated cell apoptosis in U2OS and HOS cells. Overexpression of NCRNA00713 suppressed tumor growth in nude mice. The protein expression of p-PI3K and p-Akt were remarkedly decreased in U2OS and HOS cells after transfection with NCRNA00173. In addition, 740 Y-P (PI3K/Akt pathway activator) eliminated the impact of NCRNA00173 in HOS. Conclusions: NCRNA00173 was down-regulated in pediatric OS and suppressed metastasis of OS cells by regulating PI3k/Akt pathway.

show abstract

Long noncoding RNA UCA1 promotes osteosarcoma metastasis through CREB1-mediated epithelial-mesenchymal transition and activating PI3K/AKT/mTOR pathway

Cited by 45 publications

References 16 publications

Transcription factor AP‐4 (TFAP4)‐upstream ORF coding 66 aa inhibits the malignant behaviors of glioma cells by suppressing the TFAP4/long noncoding RNA 00520/microRNA‐520f‐3p feedback loop

Transcription factor AP‐4 (TFAP4)‐upstream ORF coding 66 aa inhibits the malignant behaviors of glioma cells by suppressing the TFAP4/long noncoding RNA 00520/microRNA‐520f‐3p feedback loop

Long noncoding RNA UCA1 facilitates cell proliferation and inhibits apoptosis via activating PI3K/Akt pathway in retinoblastoma

LncRNA NCRNA00173 is down-regulated in pediatric osteosarcoma and suppresses cell metastasis of osteosarcoma cells through regulating PI3k/Akt pathway

Contact Info

Product

Resources

About