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Page 6 of 12 Schofield et al. J Cancer Metastasis Treat 2020;6:10 I http://dx.doi.org/10.20517/2394-4722.2019.43

Table 2. Alpha-enolase controls cancer cell proliferation and survival
Cancer Experimental model Effect of modulation of ENO1 expression Ref.
Bladder cancer Overexpression and knockdown in Knockdown decreased cell proliferation and colony formation. [59]
T253 and 5637 cells Overexpression increased cell proliferation and colony
formation
Breast cancer Downregulation in MDA-MB-231 Downregulation decreased cell proliferation and survival in [62]
cells vitro and reduced tumour growth in vivo
Colorectal cancer Overexpression and knockdown in Overexpression promoted cell proliferation and tumour growth [11]
HCT116 cells in vivo; Decreased expression decreased cell proliferation and
tumour growth in vivo
Endometrial carcinoma Knockdown in HEC-1B and Ishikawa Decreased expression reduced cell proliferation in vitro and [12]
tumourigenesis in vivo
Gastric cancer Knockdown in MGC-803 and MKN45 Knockdown led to cell cycle arrest at the G 1 phase and [13]
cells promoted apoptosis, and repressed the rate of cell
proliferation and colony formation
Knockdown in MKN45 cells Knockdown decreased cell proliferation, induced apoptosis [64]
and increased sensitivity to chemotherapeutics
Knockdown in AGS cells and Knockdown decreased proliferation and colony formation, [60]
overexpression in SGC7901 cells whereas overexpression increased cell proliferation and colony
formation
Overexpression in AGS cells Overexpression increased cell proliferation and colony [61]
formation
Glioma Knockdown in U-87MG cells Knockdown suppressed cell proliferation and colony formation [6]
in vitro and tumour growth in vivo
HCC Knockdown in HCC cells Knockdown inhibited cell growth [58]
Lung cancer Knockdown in NCI-H441 cells Knockdown decreased cell proliferation and survival [62]
Pancreatic cancer Knockdown in CFPAC-1 cells Downregulation decreased cell proliferation and survival in [62]
vitro and reduced tumour growth in vivo
Retinoblastoma Knockdown in Y79 cells and Knockdown led to cell cycle arrest at the G 1 phase, decreased [57]
overexpression in Meri-RB1 cells cell proliferation and increased apoptosis. Overexpression
increased cell proliferation.

HCC: hepatocellular carcinoma

Figure 3. Alpha-enolase acts as a surface plasminogen-binding receptor to mediate cancer cell invasion and metastasis formation. PLG
binds to its receptors and is subsequently converted to PLIN by plasminogen activators (e.g., uPA). Cell surface-associated plasmin
facilitates degradation of the ECM, allowing tumour cells to invade and metastasise into other tissues. PLG: plasminogen; PLIN: plasmin;
ECM: extracellular matrix; uPA: urokinase-type plasminogen activator