Table 2 The role of glycolysis in the genesis and development of tumors

Tumor proliferation

TRIM47 can ubiquitinate FBP1 and accelerate the degradation of FBP1

Promote pancreatic cancer glycolysis and proliferation

[72]

Aurora-A phosphorylates LDHB to reduce the inhibition of substrate in the reaction

Promote tumor glycolysis and proliferation

[73]

Increase the expression of LDHA through STAT3/LINC00671/LDHA axis

Promote thyroid cancer glycolysis and proliferation

[74]

LINC00930 recruit the RBBP5-GCN5 complex to the PFKFB3 promoter and increase H3K4 trimethylation and H3K9 acetylation levels in the PFKFB3 promoter region

Promote nasopharyngeal carcinoma glycolysis and proliferation

[75]

The activity of PGK1 modified by O-GlcNAcylation is improved

Promote colon cancer glycolysis and proliferation

[76]

CD47 prevents ENO1 from ubiquitin-mediated degradation by inhibiting FBXW7

Promote colorectal cancer glycolysis and proliferation

[77]

Increase the expression of ENO1 through circ-ENO1/miR-22-3p/ENO1 axis

Promote lung adenocarcinoma glycolysis and proliferation

[78]

Tumor angiogenesis and lymphangiogenesis

DKK2 and LRP6 cooperate to activate downstream AKT/mTOR signal pathway to accelerate aerobic glycolysis of colorectal cancer cells

Accelerate colorectal cancer angiogenesis

[80]

S100A4 affects the position and movement of the tip cells in the new lymphatic vessels by regulating glycolysis

Accelerate melanoma lymphangiogenesis

[81]

Tumor metastasis

Oxidized ATM can phosphorylate GLUT1 and increase PKM2 expression to promote glycolysis and lactate production. Lactate can activate TGFβ1/p38 MAPK/MMP2/9 signal axis, stimulate the mitochondrial activity of cancer cells

Promote the invasion and metastasis ability of breast cancer

[84]

CircRPN2 inhibits aerobic glycolysis of HCC by accelerating ENO1 degradation and regulating the miR-183-5p/FOXO1 axis

Inhibit the metastasis of HCC

[85]

Through ZEB1/PFKM/glycolysis axis

Promote the tumorigenesis and intrahepatic metastasis of HCC

[86]

Tumor immune escape

Enhanced glycolysis of cancer cells inhibits T cell and NK cell activity by intensifying the accumulation of lactate

Promote lung cancer immune escape

[90]

Glycolysis can induce the expression of PD-L1 and CTLA4

Promote breast cancer immune escape

[91]

Glycolysis can promote the expression of G-CSF and GM-CSF in TNBC cells, and induce the generation of MDSCs

Promote TNBC immune escape

[92]

HK2 acts as a protein kinase to phosphorylate IκBα and induce PD-L1 expression

Promote glioblastoma immune escape

[93]

Tumor-associated macrophages secrete TNF to promote tumor glycolysis, and inhibit the expression of PD-L1 in tumor cells

Promote NSCLC immune escape

[94]

Tumor prognosis evaluation

Tumor cells are characterized by increased glucose metabolism

Evaluate the prognosis of multiple tumors

[95,96,97,98,99,100]

Tumor treatment

DHNQ reduces the expression of glycolytic enzyme genes such as PFK1 and PKM2

Inhibit the genesis and development of colorectal cancer

[102]

Inhibition of GLUT1 can significantly reduce the glycolysis of CRPC cells

CRPC is more sensitive to the treatment of enzalutamide and reduces drug resistance

[103]

Met can activate AMP-AMPK pathway and p53 pathway and destroy glycolysis of tumor cells. Besides, glucose oxidase reduces glucose content in tumor tissue

Inhibit the development of tumor

[104]

Chrysin slows down the glycolysis rate of liver cancer cells

Accelerate apoptosis of tumor cells

[105]

Piperlongumine can reduce the expression of HK2, inhibit the glycolysis of cancer cells

Induce apoptosis of NSCLC cells

[106]