Long noncoding RNA APTR contributes to osteosarcoma progression through repression of miR‐132‐3p and upregulation of yes‐associated protein 1

Guan, Hongya; Shang, Guowei; Cui, Yuanbo; Liu, Jiu; Sun, Xiaoya; Cao, Wei; Wang, Yisheng; Li, Yuebai

doi:10.1002/jcp.27572

Cited by 46 publications

(46 citation statements)

References 29 publications

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“…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

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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.

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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

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“…Over the past few years, previous studies have reported that non-coding RNAs, including miRNAs and long non-coding RNAs, serve important roles in cancer (23)(24)(25). For example, miR-543 was observed to promote ESCC cell migration, invasion and EMT via targeting phospholipase A2 Group IVA (26).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‑590 inhibits migration, invasion and epithelial‑to‑mesenchymal transition of esophageal squamous cell carcinoma by targeting low‑density lipoprotein receptor‑related protein 6

Guan

Liu

et al. 2020

Oncol Rep

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MicroRNA-590 (miR-590) has been revealed as a tumor suppressor, while low-density lipoprotein receptor-related protein 6 (LRP6) is considered to act as a tumor promoter. However, their roles and underlying molecular regulatory mechanisms in esophageal squamous cell carcinoma (ESCC) have yet to be fully elucidated. Therefore, the present study aimed to investigate these mechanisms. The expression levels of miR-590 and LRP6 in human ESCC samples and cell lines were determined using reverse transcription-quantitative PCR. Bioinformatics analysis was used to predict the relationship between miR-590 and LRP6, and luciferase assay was performed to validate the relationship between these factors. Transwell assays were used to determine cell migration and invasion, while western blotting assays were used to detect the protein expression levels of LRP6, E-cadherin, N-cadherin and Vimentin. The present study demonstrated that miR-590 was downregulated and LRP6 was upregulated in ESCC tissues and cell lines. Furthermore, it was found that miR-590 overexpression and LRP6 knockdown inhibited cell migration, invasion and epithelial-to-mesenchymal transition (EMT) in ESCC cell lines. Additional mechanistic studies identified that LRP6 was a target of, and was inhibited by, miR-590. Collectively, the present findings suggested that miR-590 inhibited the invasion, migration and EMT of ESCC cells by mediating LRP6.

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“…In osteosarcoma (OS), ANRIL has been reported to be closely associated with the malignant behavior of OS cells (9). In addition, APTR has been reported to inhibit miR-132-3p and upregulate YAP1 to accelerate OS progression (34). In hepatocellular carcinoma, DLGAP1-AS1 has been confirmed to facilitate cell proliferation via the miR-486-5p/H3F3B axis (35).…”

Section: Discussionmentioning

confidence: 99%

Long non‑coding RNA NR2F1‑AS1 facilitates the osteosarcoma cell malignant phenotype via the miR‑485‑5p/miR‑218‑5p/BIRC5 axis

Jia

Wang

et al. 2020

Oncol Rep

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Long non-coding RNA (lncRNA) NR2F1 antisense RNA 1 (NR2F1-AS1) has been reported to be an oncogene in several cancer types, including osteosarcoma (OS). However, the underlying fundamental molecular mechanism of NR2F1-AS1 in OS remains largely unknown, which the present study aimed to elucidate. The present study demonstrated that NR2F1-AS1 expression is markedly increased in OS, and NR2F1-AS1 was shown to exert oncogenic functions in OS. Further molecular mechanistic studies revealed that microRNA (miR)-485-5p and miR-218-5p were direct targets of NR2F1-AS1. More importantly, miR-485-5p and miR-218-5p exhibited low expression levels and were negatively correlated with NR2F1-AS1 expression in OS tissues. It was then identified that baculoviral inhibitor of apoptosis repeat-containing 5 (BIRC5) was a direct target of miR-485-5p and miR-218-5p in OS cells. Furthermore, a series of experiments suggested that NR2F1-AS1 affects the proliferation, migration, invasion and apoptosis of OS cells by regulating BIRC5. Finally, it was revealed that silencing of NR2F1-AS1 repressed the OS cell malignant phenotype by binding with miR-485-5p and miR-218-5p, and then downregulating BIRC5 expression, which suggests that the NR2F1-AS1/miR-485-5p/miR-218-5p/BIRC5 axis could be a potential target for treating OS.

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Long noncoding RNA APTR contributes to osteosarcoma progression through repression of miR‐132‐3p and upregulation of yes‐associated protein 1

Cited by 46 publications

References 29 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

MicroRNA‑590 inhibits migration, invasion and epithelial‑to‑mesenchymal transition of esophageal squamous cell carcinoma by targeting low‑density lipoprotein receptor‑related protein 6

Long non‑coding RNA NR2F1‑AS1 facilitates the osteosarcoma cell malignant phenotype via the miR‑485‑5p/miR‑218‑5p/BIRC5 axis

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