PITPNA-AS1 abrogates the inhibition of miR-876-5p on WNT5A to facilitate hepatocellular carcinoma progression

Sun, Juan; Zhang, Yubao; Li, Bing; Dong, Yuandi; Sun, Chengming; Zhang, Fang; Jin, Li; Chen, Dongqin; Wang, Wansheng

doi:10.1038/s41419-019-2067-2

Cited by 27 publications

(26 citation statements)

References 39 publications

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“…PiTPna-aS1 is a newly reported lncrna, which is located on chromosome 17p13.3 (11). a previous study revealed that PiTPna-aS1 could facilitate the progression of hepatocellular carcinoma via the regulation of the mir-876-5p/WnT5a signaling pathway (11). analyzing data from TcGa database, the present results demonstrated that the expression of PITPNA-AS1 in NSCLC tissues was significantly increased compared with that in the adjacent non-tumor tissues.…”

Section: Discussionsupporting

confidence: 54%

Section: Discussionmentioning

confidence: 99%

“…In addition, the expression profiles of lncRNA have been associated with a number of diseases, including cancer, suggesting that they may serve as potential mediators in carcinogenesis (10). PiTPna antisense rna 1 (PiTPna-aS1) is a newly reported lncrna, which is located on chromosome 17p13.3 (11). it has been reported that PiTPna-aS1 facilitates hepatocellular carcinoma progression via regulation of the microrna(mirna/mir)-876-5p/WnT5a signaling pathway (11).…”

Section: Introductionmentioning

confidence: 99%

“…PiTPna antisense rna 1 (PiTPna-aS1) is a newly reported lncrna, which is located on chromosome 17p13.3 (11). it has been reported that PiTPna-aS1 facilitates hepatocellular carcinoma progression via regulation of the microrna(mirna/mir)-876-5p/WnT5a signaling pathway (11). Moreover, emerging evidence supports the hypothesis that PiTPna-aS1 accelerates cervical cancer progression via regulating cellular proliferation and apoptosis by targeting the mir-876-5p/c-MeT axis (12).…”

Section: Introductionmentioning

confidence: 99%

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Long non‑coding RNA PITPNA‑AS1 silencing suppresses proliferation, metastasis and epithelial‑mesenchymal transition in non‑small cell lung cancer cells by targeting microRNA‑32‑5p

Chen

Zheng²,

et al. 2021

Mol Med Rep

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lung cancer is one of the most common types of cancer and has a high mortality rate, worldwide. The major histopathological subtype is non-small cell lung cancer (nSclc). The aim of the present study was to investigate the role of long non-coding (lnc) rna PiTPna antisense rna 1 (PiTPna-aS1) in nSclc and elucidate its potential mechanisms. The expression of PiTPna-aS1 was determined in several nSclc cell lines. Following PiTPna-aS1-silencing, cell proliferation, invasion and migration were evaluated using cell counting Kit-8, colony formation, Transwell assay and wound healing assays, respectively. The expression levels of proliferation-, migration-and epithelial-mesenchymal transition (eMT)-associated proteins were examined using immunofluorescence assay or western blot analysis. a luciferase reporter assay was conducted to verify the potential interaction between PiTPna-aS1 and microrna(mir)-32-5p. Subsequently, rescue assays were performed to investigate the effects of PiTPna-aS1 and mir-32-5p on nSclc progression. The results demonstrated that PiTPna-aS1 was highly expressed in nSclc tissues and cell lines. it was found that PiTPna-aS1 silencing inhibited the proliferation, invasion and migration of nSclc cells. Furthermore, the protein expression of e-cadherin was upregulated, while the expression levels n-cadherin and vimentin were downregulated. The luciferase reporter assay confirmed that miR-32-5p was a direct target of PITPNA-AS1. The rescue experiments suggested that a mir-32-5p inhibitor significantly reversed the inhibitory effects of PITPNA-AS1 silencing on proliferation, invasion, migration and eMT in nSclc cells. collectively, the present results demonstrated that PiTPna-aS1 silencing could suppress the progression of nSclc by targeting mir-32-5p, suggesting a promising biomarker in nSclc diagnosis and treatment.

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Section: Discussionsupporting

confidence: 54%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Long non‑coding RNA PITPNA‑AS1 silencing suppresses proliferation, metastasis and epithelial‑mesenchymal transition in non‑small cell lung cancer cells by targeting microRNA‑32‑5p

Chen

Zheng²,

et al. 2021

Mol Med Rep

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“…MiR-876-5p was reported to have different roles in different types of tumorigenesis. For example, PITPNA-AS1 abrogated the inhibition of miR-876-5p on WNT5A to facilitate HCC progression [ 34 , 35 ]. MicroRNA-876-5p inhibited cell proliferation, migration and invasion by targeting c-Met in osteosarcoma [ 36 ].…”

Section: Discussionmentioning

confidence: 99%

Long noncoding RNA SNHG14 promotes hepatocellular carcinoma progression by regulating miR-876-5p/SSR2 axis

Liao

Zhang

et al. 2021

J Exp Clin Cancer Res

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Background Aberrant expressions of long noncoding RNAs (lncRNAs) have been demonstrated to be related to the progress of HCC. The mechanisms that SNHG14 has participated in the development of HCC are obscure. Methods Quantitative real-time PCR (qRT-PCR) was used to measure the lncRNA, microRNA and mRNA expression level. Cell migration, invasion and proliferation ability were evaluated by transwell and CCK8 assays. The ceRNA regulatory mechanism of SNHG14 was evaluated by RNA immunoprecipitation (RIP) and dual luciferase reporter assay. Tumorigenesis mouse model was used to explore the roles of miR-876-5p in vivo. The protein levels of SSR2 were measured by western blot assay. Results In this study, we demonstrated that SNHG14 was highly expressed in HCC tissues, meanwhile, the elevated expression of SNHG14 predicted poor prognosis in patients with HCC. SNHG14 promoted proliferation and metastasis of HCC cells. We further revealed that SNHG14 functioned as a competing endogenous RNA (ceRNA) for miR-876-5p and that SSR2 was a downstream target of miR-876-5p in HCC. Transwell, CCK8 and animal experiments exhibited miR-876-5p inhibited HCC progression in vitro and in vivo. By conducting rescue experiments, we found the overexpression of SSR2 or knocking down the level of miR-876-5p could reverse the suppressive roles of SNHG14 depletion in HCC. Conclusion SNHG14 promotes HCC progress by acting as a sponge of miR-876-5p to regulate the expression of SSR2 in HCC.

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CircVAPA exerts oncogenic property in non‐small cell lung cancer by the miR‐876‐5p/WNT5A axis

Zhao

Dai

et al. 2021

The Journal of Gene Medicine

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Background: Non-small cell lung cancer (NSCLC) is one of the most fatal malignant tumors. Emerging studies have clarified the crucial roles of circular RNAs (circRNAs) in the tumorigenesis of cancers. CircVAPA was demonstrated to function in some human cancers. The present study aimed to investigate the role of circVAPA in NSCLC.Methods: A quantitative real-time polymerase chain reaction was used to measure the expression of genes. Actinomycin D and RNase R were employed to examine the stability of circVAPA. Cell-counting kit-8, 5-ethynyl-2 0 -deoxyuridine, Transwell and sphere formation assays, and well as western blot analysis, were conducted to examine the changes of NSCLC cells in response to circVAPA knockdown. A luciferase reporter assay was conducted for the molecular mechanism.Results: Our findings demonstrated high expression of circVAPA in tissues and cell lines of NSCLC. Knockdown of circVAPA had a suppressive effect on cell proliferation, migration, invasion and stemness, and also inhibited tumor growth in vivo.Mechanistically, circVAPA acted as a competing endogenous RNA to up-regulate WNT5A by sponging miR-876-5p. Moreover, circVAPA activated Wnt/β-catenin signaling by up-regulation of WNT5A. Rescue assays showed that silencing of miR-876-5p or overexpression of WNT5A reversed the circVAPA knockdownmediated inhibition on cellular processes in NSCLC.Conclusions: CircVAPA promotes aggressive phenotypes of NSCLC cells by the miR-876-5p/WNT5A axis activating Wnt/β-catenin signaling.

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PITPNA-AS1 abrogates the inhibition of miR-876-5p on WNT5A to facilitate hepatocellular carcinoma progression

Cited by 27 publications

References 39 publications

Long non‑coding RNA PITPNA‑AS1 silencing suppresses proliferation, metastasis and epithelial‑mesenchymal transition in non‑small cell lung cancer cells by targeting microRNA‑32‑5p

Long non‑coding RNA PITPNA‑AS1 silencing suppresses proliferation, metastasis and epithelial‑mesenchymal transition in non‑small cell lung cancer cells by targeting microRNA‑32‑5p

Long noncoding RNA SNHG14 promotes hepatocellular carcinoma progression by regulating miR-876-5p/SSR2 axis

CircVAPA exerts oncogenic property in non‐small cell lung cancer by the miR‐876‐5p/WNT5A axis

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