LncRNA FAL1 promotes cell proliferation and migration by acting as a CeRNA of miR-1236 in hepatocellular carcinoma cells

Li, Baoguo; Mao, Rui; Liu, Changfu; Zhang, Weihao; Tang, Yong; Guo, Zhi

doi:10.1016/j.lfs.2018.02.006

Cited by 184 publications

(130 citation statements)

References 33 publications

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“…LncRNAs can function through epigenetic, transcriptional, and post‐transcriptional regulation (X. Li, Wu, Fu, & Han, ; Wilusz et al, ). For instance, lncRNA FAL1 can promote cell proliferation and migration by sponging miR‐1236 in HCC (B. Li, Mao, et al, ; Q. Li, Zhou, et al, ). LncRNA CASC2 modulates HCC oncogenesis through miR‐362‐5p and Nf‐κB (Zhao, Zhang, & Zhang, ).…”

Section: Discussionmentioning

confidence: 99%

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Retracted: LINC00707 contributes to hepatocellular carcinoma progression via sponging miR‐206 to increase CDK14

Zhao

et al. 2018

Journal Cellular Physiology

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Recently, increasing numbers of long noncoding RNAs (lncRNAs) have been found to be aberrantly expressed in various cancers. However, the roles of lncRNAs in hepatocellular carcinoma (HCC) progression is largely unknown. In our current study, we identified that long intergenic nonprotein‐coding RNA 707 (LINC00707) was remarkably elevated in HCC cells, indicating that LINC00707 was involved in HCC development. Subsequently, LINC00707 was significantly decreased in HepG2 and Huh7 cells. The in vitro functional assays demonstrated that knockdown of LINC00707 significantly reduced HCC cell proliferation, induced cell apoptosis, and blocked the cell cycle progression. In addition, HCC cell migration and invasion was also greatly inhibited by downregulation of LINC00707. Increasing evidence has indicated that lncRNAs can act as molecular sponges of microRNAs. Currently, we observed that microRNA‐206 (miR‐206) was dramatically inhibited in HCC cells and LINC00707 can modulate HCC development through sponging miR‐206. The binding correlation between LINC00707 and miR‐206 was confirmed by dual‐luciferase reporter assay, RNA pull down and RNA immunoprecipitation assay in our study. Moreover, cyclin‐dependent kinase 14 (CDK14) was predicted as a target of miR‐206 and we found that miR‐206 suppressed CDK14 levels in HCC cells. Finally, in vivo assays were used and it was proved that silence of LINC00707 can restrain HCC development through modulating miR‐206 to upregulate CDK14. In conclusion, it was implied that LINC00707 can lead to HCC progression through sponging miR‐206 and modulating CDK14.

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Section: Discussionmentioning

confidence: 99%

“…Dysregulation of CDK14 is involved in various cancers (H. J. Yang, Wang, et al, ; L. Yang, Zhu, et al, ; T. Sun, Co, & Wong, ). MiR‐613 can impede glioma cells progression through targeting CDK14 (B. Li, Mao, et al, ; Q. Li, Zhou, et al, ). MiR‐216a can repress osteosarcoma cell progression by targeting CDK14 (Ji et al, ).…”

Section: Discussionmentioning

confidence: 99%

Retracted: LINC00707 contributes to hepatocellular carcinoma progression via sponging miR‐206 to increase CDK14

Zhao

et al. 2018

Journal Cellular Physiology

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“…FAL1 is a recently identified lncRNA. In this study, we found that the inhibition of FAL1 could significantly promote cell apoptosis in both of the esophageal cancer cell lines KYSE450 and EC9706 cells, which is consistent with a previous study demonstrating that FAL1 has the capacity to promote cell growth, proliferation, migration, and invasion in hepatocellular carcinoma (23). Notably, our results show that the inhibition of FAL1 induced mitochondrial dysfunction by reducing mitochondrial respiration and ATP production.…”

Section: Discussionsupporting

confidence: 92%

Focally amplified lncRNA on chromosome 1 regulates apoptosis of esophageal cancer cells via DRP1 and mitochondrial dynamics

et al. 2018

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Long noncoding RNAs (lncRNAs), a family of noncoding RNA transcripts with a length of <200 nucleotides (nts), have been associated with the pathological development of various types of carcinogenesis. Focally amplified lncRNA on chromosome 1 (FAL1) is a recently identified lncRNA. In the current study, we aimed to investigate the physiological function of FAL1 in esophageal squamous cell carcinoma (ESCC). Our findings demonstrate that FAL1 was associated with esophageal cancer cell survival by regulating mitochondrial fission. First, we found that the expression of the mitochondrial fission protein dynamin‐related protein 1 (DRP1) was significantly reduced, but the expression of the mitochondrial fusion protein mitofusin 1 (Mfn1) was increased in ESCC tissues and esophageal cancer cell lines as compared with adjacent normal tissues and a normal esophagus epithelial cell line. In addition, we found that reduced expression of DRP1 in the esophageal cancer cell lines KYSE450 and EC9706 cells was associated with increased expression of FAL1. Inhibition of FAL1 promoted mitochondrial fission and mitochondrial dysfunction in KYSE450 and EC9706 cells mediated by DRP1. Silencing of DRP1 abolished FAL1‐induced apoptosis through a mitochondrial‐dependent pathway. Our findings suggest that FAL1/DRP1 could be a therapeutic target for the treatment of ESCC. © 2018 IUBMB Life, 71(1):254–260, 2019

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“…8,9 For example, lncRNA F11-AS1 is reported to bind to miR-3146 to affect the HCC progression. 8,9 For example, lncRNA F11-AS1 is reported to bind to miR-3146 to affect the HCC progression.…”

Section: Introductionmentioning

confidence: 99%

Long non‐coding RNA F11‐AS1 inhibits HBV‐related hepatocellular carcinoma progression by regulating NR1I3 via binding to microRNA‐211‐5p

Deng

Wei

Huang

et al. 2019

J Cellular Molecular Medi

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Long non-coding RNAs (lncRNAs) could regulate growth and metastasis of hepatocellular carcinoma (HCC). In this study, we aimed to investigate the mechanism of lncRNA F11-AS1 in hepatitis B virus (HBV)-related HCC. The relation of lncRNA F11-AS1 expression in HBV-related HCC tissues to prognosis was analysed in silico. Stably HBVexpressing HepG2.2.15 cells were established to explore the regulation of lncRNA F11-AS1 by HBx protein, as well as to study the effects of overexpressed lncRNA F11-AS1 on proliferation, migration, invasion and apoptosis in vitro. Subsequently, the underlying interactions and roles of lncRNA F11-AS1/miR-211-5p/NR1I3 axis in HBV-related HCC were investigated. Additionally, the influence of lncRNA F11-AS1 and miR-211-5p on tumour growth and metastasis capacity of HepG2.2.15 cells were studied on tumour-bearing nude mice. Poor expression of lncRNA F11-AS1 was correlated with poor prognosis in patients with HBV-related HCC, and its down-regulation was caused by the HBx protein. lncRNA F11-AS1 was proved to up-regulate the NR1I3 expression by binding to miR-211-5p. Overexpression of lncRNA F11-AS1 reduced the proliferation, migration and invasion, yet induced apoptosis of HepG2.2.15 cells in vitro, which could be abolished by overexpression of miR-211-5p. Additionally, either lncRNA F11-AS1 overexpression or miR-211-5p inhibition attenuated the tumour growth and metastasis capacity of HepG2.2.15 cells in vivo. Collectively, lncRNA F11-AS1 acted as a modulator of miR-211-5p to positively regulate the expression of NR1I3, and the lncRNA F11-AS1/miR-211-5p/NR1I3 axis participated in HBV-related HCC progression via interference with the cellular physiology of HCC. K E Y W O R D S hepatitis B virus, hepatocellular carcinoma, long non-coding RNA F11-antisense 1, microRNA-211-5p, nuclear receptor constitutive androstane receptor | 1849 DENG Et al.

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LncRNA FAL1 promotes cell proliferation and migration by acting as a CeRNA of miR-1236 in hepatocellular carcinoma cells

Cited by 184 publications

References 33 publications

Retracted: LINC00707 contributes to hepatocellular carcinoma progression via sponging miR‐206 to increase CDK14

Retracted: LINC00707 contributes to hepatocellular carcinoma progression via sponging miR‐206 to increase CDK14

Focally amplified lncRNA on chromosome 1 regulates apoptosis of esophageal cancer cells via DRP1 and mitochondrial dynamics

Long non‐coding RNA F11‐AS1 inhibits HBV‐related hepatocellular carcinoma progression by regulating NR1I3 via binding to microRNA‐211‐5p

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