Alpha-enolase promotes gastric cancer cell proliferation and metastasis via regulating AKT signaling pathway

Sun, Liang; Lü, Ting; Tian, Kangjun; Zhou, Diyuan; Yuan, Jingfeng; Wang, Xuchao; Zhu, Zheng; Wan, Daiwei; Yao, Yizhou; Zhu, Xinguo; He, Songbing

doi:10.1016/j.ejphar.2018.12.035

Cited by 45 publications

(53 citation statements)

References 31 publications

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“…17,[19][20][21][22]25,26 The present research described above also confirmed that ENO1 is highly expressed in chemoresistant SCLC cells. 17,[19][20][21][22]25,26 The present research described above also confirmed that ENO1 is highly expressed in chemoresistant SCLC cells.…”

Section: Fgfrl1 Promotes Chemoresistance Of Sclc Through Eno1supporting

confidence: 86%

“…Increasing evidence has shown that ENO1 can function as an oncogenic protein by promoting cell proliferation, invasion and metastasis in many cancers. 17,[19][20][21][22]25,26 The present research described above also confirmed that ENO1 is highly expressed in chemoresistant SCLC cells. To examine whether ENO1 promotes chemoresistance of SCLC, we knocked down its expression in chemoresistant SCLC cells and then analysed drug resistance.…”

Section: Fgfrl1 Promotes Chemoresistance Of Sclc Through Eno1supporting

confidence: 86%

“…These results suggest that FGFRL1 potentially mediates chemoresistance of SCLC via ENO1. 19,21,25 According to the sequencing data, SCLC patients were equally separated into high, medium and low FGFRL1 expression groups. It has been confirmed that ENO1 can regulate the PI3K/AKT pathway positively.…”

Section: Fgfrl1 Promotes Chemoresistance Of Sclc Through Eno1mentioning

confidence: 99%

“…It has been confirmed that ENO1 can regulate the PI3K/AKT pathway positively. 19,21,25 According to the sequencing data, SCLC patients were equally separated into high, medium and low FGFRL1 expression groups. 27 Differential analysis and enrichment analysis were performed in patients with high and low expression of FGFRL1.…”

Section: Fgfrl1 Regulates Eno1 Expression and The Pi3k/akt Pathwaymentioning

confidence: 99%

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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: Fgfrl1 Promotes Chemoresistance Of Sclc Through Eno1supporting

confidence: 86%

Section: Fgfrl1 Promotes Chemoresistance Of Sclc Through Eno1supporting

confidence: 86%

Section: Fgfrl1 Promotes Chemoresistance Of Sclc Through Eno1mentioning

confidence: 99%

Section: Fgfrl1 Regulates Eno1 Expression and The Pi3k/akt Pathwaymentioning

confidence: 99%

See 2 more Smart Citations

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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“…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%

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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Energy metabolism: a new target for gastric cancer treatment

et al. 2023

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Alpha-enolase promotes gastric cancer cell proliferation and metastasis via regulating AKT signaling pathway

Cited by 45 publications

References 31 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

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

Energy metabolism: a new target for gastric cancer treatment

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