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Table 3 m6A-targeted anti-tumor treatment

From: Functions of N6-methyladenosine in cancer metabolism: from mechanism to targeted therapy

Cancer Type

m6A

Treatment

Reference

Colorectal cancer

METTL3

METTL3 knockout via lentiviral-based CRISPR gene editing system decreases HK2 and GLUT1 level and the reduces hexokinase activity to inhibit tumorigenesis.

[79]

Liver cancer

METTL3

The knockdown of METTL3 via shRNA attenuates PDK4 mRNA stability, inhibits glycolysis and exhibits anti-tumor effect.

[92]

Cervical cancer

METTL3

The knockdown of METTL3 via shRNA induces reduced lactate production and ATP level and suppresses tumorigenesis.

[75]

Hepatocellular carcinoma

METTL5

METTL5 depletion and siACSL4 reduce the levels of free fatty acids, triglycerides and intracellular lipid droplets and blocks tumor initiation.

[121]

Colorectal cancer

KIAA1429

KIAA1429 knockdown via shRNA represses tumor growth, which leads to reduced glucose uptake and lack of ATP production.

[80]

Acute myeloid leukemia

IGF2BP2

IGF2BP2 knockdown via shRNA and IGF2BP2 inhibition by CWI1-2 delay leukemogenesis and development.

[128]

 

METTL16

METTL16 knockdown via shRNA suppresses the expression of BCAT1 and BCAT2 in amino acid metabolism to inhibit tumorigenesis and development.

[129]

Papillary thyroid cancer

FTO

FTO overexpression via lentiviruses containing complete FTO coding sequence reduces GLUT1, HK2 and LDHA levels, attenuates glycolysis and suppresses tumor growth.

[134]

Clear cell renal cell carcinoma

FTO

FTO knockdown via shRNA reduces the levels of SLC1A5 and glutamine uptake to inhibit tumor growth.

[126]

Gastric cancer

YTHDF1

YTHDF1 depletion via siRNA encapsulated by sEV modulates immune responses and suppresses tumor development and metastasis.

[135]