m6A-centered Crosstalk Information

Mechanism of Crosstalk between m6A Modification and Epigenetic Regulation

m6A Modification:
Crosstalk ID	M6ACROT00484				[1], [2], [3]
m⁶A modification SNAI1 SNAI1 ZC3H13 Methylation : m⁶A sites Indirect Enhancement RNA modification MIR22 MIR22 FTO Demethylation : modification sites
m6A Regulator	Zinc finger CCCH domain-containing protein 13 (ZC3H13)			WRITER	Regulator Info
m6A Target	Zinc finger protein SNAI1 (SNAI1)				Targert Gene
Epigenetic Regulation that have Cross-talk with This m6A Modification:
Epigenetic Regulation Type	RNA modification (RNAMod) >> N6,2'-O-dimethyladenosine (m6Am)
Epigenetic Regulator	Fat mass and obesity-associated protein (FTO)			ERASER	View Details
Regulated Target	hsa-mir-22				View Details
Crosstalk Relationship	m6Am → m6A			Enhancement
Crosstalk Mechanism	RNA modification indirectly impacts m6A modification through downstream signaling pathways
Crosstalk Summary	FTO interacts with hsa-mir-22, decreasing it's m6Am level and promoting its physical interaction with Zinc finger protein SNAI1 (SNAI1), which was regulated by ZC3H13-mediated m6A modification.
In-vitro Model	HCT 116	Colon carcinoma	Homo sapiens		CVCL_0291
	SW480	Colon adenocarcinoma	Homo sapiens		CVCL_0546
	HEK293	Normal	Homo sapiens		CVCL_0045

References

Ref 1	ZC3H13 suppresses colorectal cancer proliferation and invasion via inactivating Ras-ERK signaling. J Cell Physiol. 2019 Jun;234(6):8899-8907. doi: 10.1002/jcp.27551. Epub 2018 Oct 12.
Ref 2	N6-adenosine methylation in MiRNAs. PLoS One. 2015 Feb 27;10(2):e0118438. doi: 10.1371/journal.pone.0118438. eCollection 2015.
Ref 3	Long non?coding RNA H19 regulates cell growth and metastasis via the miR?22?3p/Snail1 axis in gastric cancer. Int J Oncol. 2019 Jun;54(6):2157-2168. doi: 10.3892/ijo.2019.4773. Epub 2019 Apr 4.