Table 1.

Roles of ALKBH1 in human cancer.

Cancer type	Expression	Modification types	Modification expression in cancer	Biological functions	Molecular mechanisms	Targets	Reference
Lung cancer	up	m6A	No study	facilitated cell migration and invasion	No study	No study	23
RCC	up	m6A	No study	promotes RCC cell malignancy	ALKBH1 reduces m6A levels of GPR137 mRNA, which upregulates GPR137 mRNA levels, resulting in the increased GPR137 protein expression and the enhanced RCC cell biological actions consequently	GPR137	73
CRC	up	m1A in mRNA	No study	Promote CRC metastasis	ALKBH1-mediated m1A demethylation of METTL3 mRNA promotes the metastasis of colorectal cancer by downregulating SMAD7 expression	METTL3	40
HNSCC	up	DNA 6mA	down	Depletion of ALKBH1 inhibits HNSCC cells proliferation and colony formation of HNSCC patients-derived organoids	ALKBH1 enhances DDX18 expression by erasing DNA 6mA level and regulating its promoter activity	DDX18	75, 76
GC	up	DNA 6mA	down	Not only enhances viability and migratory cell number, but also promotes the growth and metastasis of GC cells	ALKBH1-mediated 6mA demethylation in NRF1 transcriptional activity, leading to repressed AMPK signaling activation and a “Warburg” phenotype in GC cells	NRF1	81, 82
GC	down	No study	No study	No study	No study	No study	80
GBM	up	DNA 6mA	up	Knockdown of ALKBH1 decreased proliferation, self-renewal, and tumor formation capacity. Upregulation of ALKBH1 did not elicit any significant changes in cell viability, self-renewal or in vivo tumor formation.	Depletion of ALKBH1 led to an increased N6-mA level in genomic DNA, which coordinated with H3K9me3, caused to transcriptional silencing of oncogenic pathways through decreasing chromatin accessibility.	No study	59
TSCC	up	DNA 6mA	up	Knockdown of ALKBH1 promotes colony formation and cell migration	Knockdown of ALKBH1 results in increased 6mA levels	NF-κB pathway	83
HCC	down	DNA 6mA	up	ALKBH1 overexpression suppressed HCC cell viability, migration and invasion, enhanced apoptosis	When ALKBH1 was overexpressed, PARTICL was upregulated while PARTICL DNA 6mA modification was reduced	PARTICL	88
PAAD	down	m1A	No study	No study	ALKBH1 may participate in the occurrence and development of pancreatic cancer through mTOR and ErbB signaling pathway	mTOR and ErbB signaling pathway	89
PDAC	down	mtDNA 6mA	up	Knockdown of ALKBH1 blocks the transcription of mitochondrial DNA-coded genes, leads to mitochondrial dysfunction and inhibits pancreatic cancer cells	ALKBH1 can be downregulated by HRD1-SEL1L complex through ubiquitination when a tumor inhibitor, Sirtuin4 (SIRT4) overexpressed	mitochondrial DNA-coded genes	90, 91
OV	down	No study	No study	No study	No study	No study	93
TNBC	No change	DNA 6mA	down	No study	No study	No study	94