lncRNA FLVCR1‐AS1 silencing inhibits lung cancer cell proliferation, migration, and invasion by inhibiting the activity of the Wnt/β‐catenin signaling pathway

Lin, Heping; Shangguan, Zongxiao; Zhu, Mengchu; Bao, Lianmin; Zhang, Qing; Pan, Shenghua

doi:10.1002/jcb.28352

Cited by 21 publications

(24 citation statements)

References 47 publications

(88 reference statements)

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“…FLVCR1-AS1 expression has been reported to be upregulated in lung gastric and hepatocellular cancers [11][12][13][14]. Similarly, elevated FLVCR1-AS1 expressions were found in OSC tissues, serums, and cell lines in the current study.…”

Section: Discussionsupporting

confidence: 72%

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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: 72%

“…FLVCR1-AS1 is recently discovered upregulated in hepatocellular cancer, gastric cancer and lung cancer [11][12][13][14]. However, few studies have studied FLVCR1-AS1 in OSC.…”

mentioning

confidence: 99%

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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“…For example, Kumar et al (39) reported that mir-30b-3p acts as a direct regulator of androgen receptor signaling in prostate cancer. it was also reported that FlVcr1-aS1 may interact with mir-513, mir-573 and the Wnt/β-catenin signaling pathway in hepatocellular carcinoma, lung cancer and ovarian cancer (14)(15)(16)(17). Furthermore, liu et al (40) demonstrated that FlVcr1-aS1 can act as a sponge for mir-155, promoting therefore gastric cancer tumorigenesis by targeting c-Myc.…”

Section: Discussionmentioning

confidence: 96%

“…The lncrna Feline leukemia Virus Subgroup c cellular receptor 1 antisense rna 1 (FlVcr1-aS1) is a novel tumor suppressor located on chromosome 1q32.3 (13). Previous studies have identified impaired expression of FlVcr1-aS1 in hepatocellular carcinoma, lung cancer and ovarian cancer (14)(15)(16)(17); however, the underlying mechanism of FlVcr1-aS1 in glioma remains unknown.…”

Section: Introductionmentioning

confidence: 99%

Long non‑coding RNA FLVCR1‑AS1 promotes glioma cell proliferation and invasion by negatively regulating miR‑30b‑3p

Gao

Liu

et al. 2020

Mol Med Rep

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Glioblastoma (GBM) is the most common and malignant primary brain tumor in adults that originates from glial cells. The prognosis of patients with high-grade glioma is poor. it is therefore crucial to develop effective therapeutic strategies. long non-coding rnas (lncrnas) have been reported as potential inducers or suppressors of tumor progression. Previous studies have indicated that the lncrna Feline leukemia Virus Subgroup c cellular receptor 1 antisense rna 1 (FlVcr1-aS1) is involved in the development and progression of gastric and lung cancer, as well as hepatocellular carcinoma and cholangiocarcinoma; however, the biological effect of FlVcr1-aS1 in glioma is not completely understood. The aim of the present study was to investigate how FlVcr1-aS1 modulates cell proliferation and invasion in glioma. FLVCR1-AS1 expression was significantly upregulated in GBM tissues compared with adjacent normal brain samples, and was higher in GBM cell lines compared with normal human astrocyte cells. Furthermore, the microrna (mir)-30b-3p was revealed to be a putative target of FlVcr1-aS1, and the suppressive effects of mir-30b-3p on cellular proliferation and invasion were reversed following FlVcr1-aS1-knockdown. The results from cell counting Kit-8 and Transwell assays confirmed that FLVCR1-AS1-knockdown inhibited GBM cell proliferation and invasion ability. in addition, FlVcr1-aS1 was found to directly interact with mir-30b-3p, and a rescue experiment further established that FlVcr1-aS1 contributed to glioma progression by inhibiting mir-30b-3p. The results from the present study demonstrated that FlVcr1-aS1 may serve an oncogenic role in GBM and promote disease progression by interacting with miR-30b-3p. These findings suggested that FlVcr1-aS1 may be considered as a novel therapeutic target and diagnostic biomarker for GBM.

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“…41 The silence of FLVCR1-AS1 inhibits proliferation and migration of SPCA1 and A549 cells, resulting in Wnt/β-catenin signaling abrogation by notably downregulating target genes, such as CTNNB1, SOX4, cyclin D1, cyclin D2 (CCND2), and c-myc in SPCA1 and A549 cells. 42 GSK3β, which is regulated by the lncRNA MIR31HG, 43 the long intergenic non-protein coding RNA 968 (LINC00968; also known as LOC554202) 44 and lncRNA JPX, 45 is an important component of the Wnt/βcatenin signaling pathway. Studies have shown that the knockdown of MIR31HG represses Wnt/β-catenin signaling through down-regulating the expression of GSK3β and βcatenin, but increasing the phosphorylation of GSK3β in NSCLC cells.…”

Section: Cell Metastasis and Invasionmentioning

confidence: 99%

<p>Roles of Wnt/β-Catenin Signaling Pathway Regulatory Long Non-Coding RNAs in the Pathogenesis of Non-Small Cell Lung Cancer</p>

Lin¹,

Yu²,

Guan³

et al. 2020

CMAR

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Lung cancer is one of the leading causes of cancer-related mortality worldwide. Non-small cell lung cancer (NSCLC) is the most common pathological type of lung cancer. Long non-coding RNAs (lncRNAs) are promising novel diagnostic and prognostic biomarkers, as well as potential therapeutic targets for lung cancer. Long non-coding RNAs (lncRNAs) have been demonstrated to modulate tumor cells proliferation, cell cycle progression, invasion, and metastasis by regulating gene expression at transcriptional, post-transcriptional, and epigenetic levels. The oncogenic aberrant Wnt/β-catenin signaling is prominent in lung cancer, playing a vital role in tumorigenesis, prognosis, and resistance to therapy. Interestingly, compelling studies have demonstrated that lncRNAs exert either oncogenic or tumor suppressor roles by regulating Wnt/β-catenin signaling. In this review, we aim to present the current accumulated knowledge regarding the roles of Wnt/β-catenin signaling-regulated lncRNAs in the pathogenesis of non-small cell lung cancer (NSCLC). Better understanding of the effects of lncRNAs on Wnt/β-catenin signaling might contribute to the improved understanding of the molecular tumor pathogenesis and to the uncovering of novel therapeutic targets in NSCLC.

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lncRNA FLVCR1‐AS1 silencing inhibits lung cancer cell proliferation, migration, and invasion by inhibiting the activity of the Wnt/β‐catenin signaling pathway

Cited by 21 publications

References 47 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

Long non‑coding RNA FLVCR1‑AS1 promotes glioma cell proliferation and invasion by negatively regulating miR‑30b‑3p

<p>Roles of Wnt/β-Catenin Signaling Pathway Regulatory Long Non-Coding RNAs in the Pathogenesis of Non-Small Cell Lung Cancer</p>

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