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. 2021 May 14;23(6):551–560. doi: 10.1016/j.neo.2021.04.002

Table 1.

List of reported functions of m6A regulatory proteins in breast cancer.

Gene name Role in RNA modification Role in cancer Mechanism m6A regulation References DepMapa
METTL3 writer Oncogene Promoting the expression of Bcl-2 through m6A modification m6A dependent [26] Essential
Oncogene Promoting the expression of HBXIP through enhancing m6A modification and be suppressed by let-7g m6A dependent [27]
Oncogene Promoting the expression of LINC00958 through enhancing m6A m6A dependent [49]
Tumor suppressor Inhibiting the expression of COL3A1 by m6A modification m6A dependent [48]
Oncogene Promoting the expression of miR-221-3p by increasing pri-miR-221-3p m6A mRNA modification m6A dependent [65]
METTL14 writer Oncogene Promoting the expression of hsa-miR-146a-5p Unkown [28] Essentialb
Oncogene Promoting the expression of CXCR4 and CYP1B1 through m6A modification which are the targets of LNC942 m6A dependent [29]
VIRMA cofactor Oncogene Increasing the stability of CDK1 mRNA m6A independent [32] Very essentialb
CBLL1 cofactor Tumor suppressor Interfering with the recruitment of coactivators of ERα: SRC-1 and SRC-2 m6A independent [50] Essential
FTO eraser Oncogene Inducing BNIP3 mRNA degradation through modulating m6A m6A dependent [33] Partial-essentialc
Oncogene Promoting glycolysis and lactic acid production through PI3K/AKT signaling pathway Unkown [52]
Oncogene Promoting miR-181b-3p/ARL5B signaling pathway Unkown [58]
ALKBH5 eraser Oncogene Inducing by hypoxia and promoting the mRNA stability and the expression of NANOG m6A dependent [34] Partial-essential
YTHDF3 reader Oncogene Promoting the translation of ST6GALNAC5, GJA1 and EGFR through m6A modification m6A dependent [62] No data
IGF2BP1 reader Tumor suppressor Promoting the degradation of UCA1 through recruiting the CCR4-NOT1 deadenylase complex Unkown [63] Partial-essentialc
Oncogene Interacting with lncRNA KB-1980E6.3 and promoting c-Myc mRNA stability through modulating m6A m6A dependent [66]
IGF2BP2 reader Oncogene Interacting with pseudogene-transcribed RPSAP52 Unkown [53] Partial-essential
Oncogene Suppressing the transcription of miR-200a by destabilizing the mRNA of the progesterone receptor (PR) Unkown [38]
IGF2BP3 reader Oncogene Promoting the expression of CD44 via binding the mRNA of CD44 Unkown [54] Partial-essentialc
Oncogene Inhibiting TRIM25 mRNA degradation mediated by miR-3614 through blocking the maturation of miR-3614 Unkown [55]
Oncogene Promoting the mRNA stability of CERS6 as an RNA sponge for long non-coding RNA CERS6-AS1 Unkown [56]
Oncogene Suppressing the transcription of miR-200a by destabilizing the mRNA of the progesterone receptor (PR) Unkown [38]
Oncogene Promoting the expression of SOX2 by binding to the mRNA of SLUG Unkown [64]
Oncogene Promoting the expression of BCRP via binding to BCRP mRNA Unkown [70]
eIF3d reader Oncogene Promoting Wnt/β-catenin signaling Unkown [40] Very essentialc
eIF3h reader Oncogene Catalyzing the deubiquitylation of YAP and resulting in the stabilization of YAP m6A independent [44] Essentialc
HNRNPC reader Oncogene Regulating Alu-enriched dsRNA and the down-stream interferon response Unkown [46] Very essential
HNRNPA2B1 reader Oncogene Promoting ERK1/2 and STAT3 pathway Unkown [58] Partial-essentialc
Tumor suppressor Regulating ERK-MAPK/Twist, GR-β/TCF4, STAT3 and WNT/TCF4 signaling pathways Unkown [47]
a

Data were retrieved from breast cancer cell lines dataset from DepMap portal (https://depmap.org/portal/). Very essential, dependency score ≤ -1.0; Essential, -0.1 < dependency score ≤ -0.5; Partial essential, -0.5 < dependency score ≤ 0; Non-essential, dependency score > 0. For RNAi data, Combined RNAi (Broad, Novartis, Marcotte) dataset was queried. For CRISPR data, CRISPR (Avana) Public 21Q1 dataset was queried. Lower dependency score from either CRISPR or RNAi data was chosen for default.

b

Conflict with RNAi data.

c

Supported by both RNAi data and CRISPR data.