Table 1 Opposite Roles of m6A regulators in Tumorigenesis

METTL3

Colorectal cancer

−

(1) Positive expression of METTL3 was significantly associated with longer survival time

(2) METTL3 suppresses colorectal cancer proliferation and migration through p38/ERK pathways

[62]

+

(1) METTL3 facilitates tumor progression via an m6A-IGF2BP2-dependent mechanism in colorectal carcinoma

(2) METTL3 promotes CRC cell stemness by increasing the expression of SOX2

[63]

+

METTL3 promotes metastasis of colorectal cancer via miR-1246/SPRED2/MAPK signaling pathway

[64]

Renal clear cell carcinoma

+

(1) METTL3 might be involved in the promotion proliferation through PI3K-AKT-mTOR pathway

(2) METTL3 increased cell cycle arrest in G1 phase by promoting a gain in P21 expression

[65]

−

METTL3 inhibites cellular migration and invasion through EMT pathway

[65]

Breast cancer

+

Hepatitis B X-interacting protein(HBXIP)-elevated METTL3 promotes the progression of breast cancer via inhibiting tumor suppressor let-7 g

[66]

+

METTL3 promotes the breast cancer progression via targeting Bcl-2

[67]

−

Reduced expression of METTL3 predicts poor prognosis in breast cancer

[68]

YTHDF2

Hepatocellular carcinoma

+

miR145 modulates m6A levels by targeting the 3’-UTR of YTHDF2 mRNA and is able to suppresses proliferation of hepatocellular carcinoma

[69]

+

YTHDF2 facilitates METTL3-mediated SOCS2 m6A modification and degradation thereby reducing the tumor suppressive effect of SOCS2

[70]

−

(1) Overexpression of YTHDF2 suppresses hepatocellular carcinoma cell proliferation and growth in vitro and in vivo

(2) YTHDF2 inhibits ERK/MAPK signaling cascades by destabilizing the EGFR mRNA in hepatocellular carcinoma cells

[71]

Pancreatic cancer

+

(1) YTHDF2 orchestrates EMT and proliferation in pancreatic cancer cells

(2) YTHDF2 promotes tumor proliferation by activating AKT/GSK3β/cyclin D1

[15]

−

YTHDF2 suppresses metastasis by destabilizing YAP mRNA

[15]