Targetting an LncRNA P5848-ENO1 axis inhibits tumor growth in hepatocellular carcinoma

Zhu, Xiao Feng; Yu, Hui; Li, Baolin; Quan, Jing; Zeng, Zhangrui; Li, Chang-Jiu; Wang, Zhibin

doi:10.1042/bsr20180896

Cited by 9 publications

(9 citation statements)

References 11 publications

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“…Therefore, further studies should be performed to identify other glycolytic enzymes in cancer progression. Recently, the glycolytic enzyme ENO1 has attracted the attention of oncologists because it is dys-regulated in various cancer types, including gastric cancer, HCC, glioma and pancreatic cancer [14,30–32]. However, it remains unknown whether ENO1 serves as a tumor suppressor, oncogene or neither in BC.…”

Section: Discussionmentioning

confidence: 99%

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Up-regulated ENO1 promotes the bladder cancer cell growth and proliferation via regulating β-catenin

Wang

Chen

et al. 2019

Bioscience Reports

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Bladder cancer (BC) is the ninth most common malignancy throughout the world. The molecular mechanisms of this disease remain largely unclear. The glycolytic enzyme enolase 1 (ENO1) has been shown to regulate the development of various cancers. However, the significance of ENO1 in BC is underdetermined. In this study, we found that ENO1 was highly expressed in BC tissues and cells. High expression of ENO1 was associated with the poor survival of BC patients. Using lentivirus-mediated knockdown and over-expression, we revealed that ENO1 was critical for the growth and proliferation of BC cells. ENO1 over-expression also promoted the proliferation of SV-HUC-1 cells. At the molecular level, the cell cycle and apoptosis related genes were regulated by ENO1. β-catenin expression was positively regulated by ENO1. Furthermore, ectopic expression of β-catenin reversed the effect of ENO1 knockdown on T24 cell proliferation and growth. Opposite results were observed in β-catenin knockdown T24 cells. Our findings suggested that ENO1 functioned as an oncogene in BC through regulating cell cycle, apoptosis and β-catenin. Targeting ENO1/β-catenin cascade may benefit for BC patients.

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Section: Discussionmentioning

confidence: 99%

“…For example, ENO1 is a potential biomarker for hepatocellular carcinoma (HCC) [13]. It serves as a target for LncRNA P5848 and promotes tumor growth and survival in HCC [14]. Targeting ENO1 suppresses the proliferation and growth of gastric cancer cells [15].…”

Section: Introductionmentioning

confidence: 99%

Up-regulated ENO1 promotes the bladder cancer cell growth and proliferation via regulating β-catenin

Wang

Chen

et al. 2019

Bioscience Reports

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“…22 It was also noticed that ENO1 promoted cancer progression in hepatocellular carcinoma, breast cancer, and gastric cancer. 10,[23][24][25] Generally, most studies support the idea that ENO1 expression is elevated and promotes the Warburg effect and cancer proliferation and invasion; ENO1 overexpression and modifications have diagnostic and prognostic value. 26 However, it may play distinctive roles in different cancer types.…”

Section: Discussionmentioning

confidence: 96%

<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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“…Indeed, upregulated a-enolase expression has been shown to regulate cell proliferation in various solid tumours in vitro [11,13,[57][58][59][60][61] , and to increase tumour growth in a HCT116 colorectal cancer xenograft model in vivo [11] [ Table 2]. Conversely, silencing of a-enolase in glioma, pancreatic, lung, endometrial, colorectal and breast cancer cells was found to induce cell cycle arrest and senescence, and also to reduce tumour volume in CFPAC-1 pancreatic, MDA-MB-231 breast and U-87MG glioma xenograft models in vivo [6,11,12,62,63] .…”

Section: Increased Alpha-enolase Expression Enhances Cell Proliferatimentioning

confidence: 99%

“…Overexpression of a-enolase has been shown to increase the migration and invasion of hepatocellular carcinoma, colorectal and gastric cancer cells in vitro [11,58,60,61,67] and to enhance colorectal cancer metastasis in vivo [11] , demonstrating that it is an important driver of metastasis in multiple cancer types [ Table 3]. Conversely, knockdown or pharmacological inhibition of a-enolase decreased the migration and invasion of glioma, colorectal, pancreatic and endometrial carcinoma in vitro [6,12,63,68,69] , and decreased tumourigenesis and metastasis of endometrial carcinoma in vivo [12] .…”

Section: Role In Invasion and Migrationmentioning

confidence: 99%

Unlikely role of glycolytic enzyme ��-enolase in cancer metastasis and its potential as a prognostic biomarker

Schofield¹,

Lincz²,

Skelding³

2020

JCMT

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Reliance on glycolysis for energy production is considered a hallmark of cancer and the glycolytic enzyme a-enolase is overexpressed in a range of cancer types. However, recent studies have revealed that a-enolase is involved in a variety of unrelated physiological processes and can be found in multiple unexpected cellular locations. This review focuses on the unlikely role of a-enolase as an extracellular plasminogen-binding receptor localised to the plasma membrane. Conversion of plasminogen to plasmin on the surface of cancer cells enhances their ability to invade through stroma by activating collagenases and degrading fibrin as well as extracellular matrix proteins. Increased expression of a-enolase is associated with increased migration and invasion of cancer cells, and decreased metastasis-free survival in patients with several cancer types, including non-small cell lung, pancreatic, breast and colorectal cancers. Due to its overexpression in a range of cancer types and multi-functional roles in key areas of tumour metabolism and metastasis, a-enolase may be useful as a universal cancer prognostic biomarker or therapeutic target.

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Targetting an LncRNA P5848-ENO1 axis inhibits tumor growth in hepatocellular carcinoma

Cited by 9 publications

References 11 publications

Up-regulated ENO1 promotes the bladder cancer cell growth and proliferation via regulating β-catenin

Up-regulated ENO1 promotes the bladder cancer cell growth and proliferation via regulating β-catenin

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

Unlikely role of glycolytic enzyme ��-enolase in cancer metastasis and its potential as a prognostic biomarker

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