A novel lncRNA, TCONS_00006195, represses hepatocellular carcinoma progression by inhibiting enzymatic activity of ENO1

Yu, Songman; Li, Ning; Huang, Zebing; Chen, Ruochan; Yi, Panpan; Kang, Rui; Tang, Daolin; Hu, Xingwang; Xue, Fan

doi:10.1038/s41419-018-1231-4

Cited by 46 publications

(40 citation statements)

References 38 publications

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“…18 Previous studies have indicated that ENO1 promotes malignant biological behaviour of tumour cells by activating glycolysis and the PI3K/Akt pathway in non-small-cell lung cancer and glioma cells. 19,23,24 This study is the first to show that FGFRL1 is involved in SCLC. 22 More importantly, some lncRNAs and proteins have been reported to interact with ENO1 to regulate its expression or activity in tumours.…”

Section: Introductionmentioning

confidence: 72%

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FGFRL1 affects chemoresistance of small‐cell lung cancer by modulating the PI3K/Akt pathway via ENO1

Chen

Zheng

et al. 2020

J Cellular Molecular Medi

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Fibroblast growth factor receptor-like 1 (FGFRL1), a member of the FGFR family, has been demonstrated to play important roles in various cancers. However, the role of FGFRL1 in small-cell lung cancer (SCLC) remains unclear. Our study aimed to investigate the role of FGFRL1 in chemoresistance of SCLC and elucidate the possible molecular mechanism. We found that FGFRL1 levels are significantly up-regulated in multidrug-resistant SCLC cells (H69AR and H446DDP) compared with the sensitive parental cells (H69 and H446). In addition, clinical samples showed that FGFRL1 was overexpressed in SCLC tissues, and high FGFRL1 expression was associated with the clinical stage, chemotherapy response and survival time of SCLC patients. Knockdown of FGFRL1 in chemoresistant SCLC cells increased chemosensitivity byincreasing cell apoptosis and cell cycle arrest, whereas overexpression of FGFRL1 in chemosensitive SCLC cells produced the opposite results. Mechanistic investigations showed that FGFRL1 interacts with ENO1, and FGFRL1 was found to regulate the expression of ENO1 and its downstream signalling pathway (the PI3K/Akt pathway) in SCLC cells. In brief, our study demonstrated that FGFRL1 modulates chemoresistance of SCLC by regulating the ENO1-PI3K/Akt pathway. FGFRL1 may be a predictor and a potential therapeutic target for chemoresistance in SCLC. K E Y W O R D Schemoresistance, ENO1, FGFRL1, PI3K/Akt pathway, small-cell lung cancer

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Section: Introductionmentioning

confidence: 72%

“…22 More importantly, some lncRNAs and proteins have been reported to interact with ENO1 to regulate its expression or activity in tumours. 19,23,24 This study is the first to show that FGFRL1 is involved in SCLC. We demonstrated that FGFRL1 was up-regulated in multidrug-resistant SCLC cells compared with the parental sensitive cells.…”

Section: Introductionmentioning

confidence: 72%

FGFRL1 affects chemoresistance of small‐cell lung cancer by modulating the PI3K/Akt pathway via ENO1

Chen

Zheng

et al. 2020

J Cellular Molecular Medi

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“…8 Several studies on cancer cells showed that raised ENO1 can result in the promotion of cell proliferation. 9,10 However, the mechanism of ENO1 regulation has not been well studied yet.…”

Section: Introductionmentioning

confidence: 99%

<p>The circ-AMOTL1/ENO1 Axis Implicated in the Tumorigenesis of OLP-Associated Oral Squamous Cell Carcinoma</p>

Liu¹,

Yang²,

Sun³

et al. 2020

CMAR

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Background: Oral squamous cell carcinoma (OSCC) may develop from a variety of oral potentially malignant disorders, but the mechanism of malignant transformation is still unknown. Among them, oral lichen planus (OLP) has a high prevalence. Previous studies have shown that α-enolase (ENO1) can promote cell proliferation and play an important role in tumorigenesis. In this study, we aim to explore the mechanism of ENO1 regulation in the process of OSCC tumorigenesis from OLP. Methods: ENO1 expression in tissues was determined by real-time quantitative PCR and immunohistochemistry. ENO1 was knocked down in cal-27 to observe the change in cell proliferation. Then, RNA-seq and bioinformatics analyses were conducted between OLP and OSCC samples. The expression of circ-AMOTL1, miRNA-22-3p, and miRNA-1294 was assessed using the real-time quantitative PCR. With knockdown and overexpression of circ-AMOTL1 in vitro, the change of ENO1 in the mRNA level was also assessed. Results: ENO1 was enhanced in the OSCC samples in comparison with OLP. Immunohistochemistry and real-time quantitative PCR results showed that ENO1 was significantly higher in OSCC tissue than in the OLP group, with a statistically significant difference (p<0.05). When ENO1 was knocked down in cal-27, cell proliferation was inhibited (p<0.05). The expression of miR-22-3p and miR-1294 was decreased in OSCC tissues, whereas ENO1 and circ-AMOTL1 increased. In an in vitro study, knockdown of circ-AMOTL1 resulted in a decrease of ENO1, while overexpression of circ-AMOTL1 led to an increase of ENO1 in the mRNA level. Conclusion: We confirmed that ENO1 expression was elevated in OSCC and increased cell proliferation. In an in vitro study, ENO1 expression was promoted by circ-AMOTL1. ENO1 may play a role as a tumor-promoting gene in OSCC through the circ-AMOTL1/miR-22-3p/ miR-1294 network. These novel findings may shed further light on the pathogenesis from OLP to OSCC and the potential precursor markers.

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“…Numerous studies have showed that lncRNAs widely participate in the cell proliferation, invasion and apoptosis [4][5][6] . The lncRNAs located in the nuclear and cytoplasm may exhibit different functions ADDIN EN.CITE 11 . As reported, lncRNAs located in the nucleus can function as scaffolds to bring proteins to form ribonucleoprotein complexes and as guides to recruit chromatinmodifying complexes to target genes [6][7][8] .…”

Section: Introductionmentioning

confidence: 99%

“…The lncRNAs located in the cytoplasm can function as competing endogenous RNAs (ceRNAs) to modulate the depression of miRNAs targets through competitively binding miRNAs 9,10 . For instance, the TCONS_00006195 located in the nucleus can represses the progression of liver cancer by repressing the activity of ENO1 11 . lncRNA MIR31HG located in cytoplasm can suppress the development of HCC by binding to miR-575 12 .…”

Section: Introductionmentioning

confidence: 99%

A Novel lncRNA loc339803 acts as CeRNA of miR-30a-5p to promote the migration and invasion of hepatocellular carcinoma cells

Xue

Zhang

Gao

et al. 2020

Preprint

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Background Hepatocellular carcinoma (HCC) is one of the most common malignant tumors, and has an unfavorable clinical outcome. Emerging evidences have demonstrated that long noncoding RNAs (lncRNAs) play an important role in the carcinogenesis and progression of HCC. However, the clinical significances, the biological roles of most lncRNAs in HCC remain poorly understood. Methods The expression levels of lncRNA loc339803 in HCC tissues and cell lines were determined by quantitative real-time polymerase chain reaction(qRT-PCR) assay. The cellular sublocalization of loc339803 were determined by fluorescence in situ hybridization and nuclear & cytoplasmic RNA isolation assay. Western blot, CCK-8, Edu, colony formation, migration and invasion assays were used to investigate the roles of loc339803 in progression of HCC in vitro. A mouse model for lung metastasis was constructed to evaluate the role of loc339803 in HCC development in vivo. The correlations among loc339803, miR-30a-5p and SNAIL1 were validated by qRT-PCR and a dual- luciferase reporter assay. Results The expression of loc339803 was upregulated in HCC tissues and cell lines, and positively correlated with tumor size, advanced tumor stage, higher serum AFP level and poor prognosis of HCC patients. loc339803 can promote the migration and invasion of HCC cells in vivo and in vitro. Further studies demonstrated the loc339803 functioned as a competing endogenous RNA (ceRNA) by directly binding to miR-30a-5p, thus up-regulating the expression of snai1, a target gene of miR-30a-5p. Moreover, miR-30a-5p upregulation blocked the enhancement of migration and invasion of HCC cells induced by loc339803 overexpression. Conclusions Loc339803 may be oncogenic in HCC and associated with poor clinical outcomes. LncRNA loc339803 might promote the invasion and migration of HCC cells through regulating miR-30a-5p/ SNAIL1 axis.

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A novel lncRNA, TCONS_00006195, represses hepatocellular carcinoma progression by inhibiting enzymatic activity of ENO1

Cited by 46 publications

References 38 publications

FGFRL1 affects chemoresistance of small‐cell lung cancer by modulating the PI3K/Akt pathway via ENO1

FGFRL1 affects chemoresistance of small‐cell lung cancer by modulating the PI3K/Akt pathway via ENO1

<p>The circ-AMOTL1/ENO1 Axis Implicated in the Tumorigenesis of OLP-Associated Oral Squamous Cell Carcinoma</p>

A Novel lncRNA loc339803 acts as CeRNA of miR-30a-5p to promote the migration and invasion of hepatocellular carcinoma cells

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