TABLE 1.
Level and effect of BACH in digestive system diseases.
Name | Organs | Disease | Alteration | Function | References |
---|---|---|---|---|---|
BACH1 | Esophagus | ESCC | Upregulated | Promotes the proliferation, invasion and metastasis by inducing EMT and angiogenesis | Jiang et al. (2015); Xie et al. (2023) |
Inhibits biosynthesis of MUFAs by transcriptionally inhibiting SCD1 gene to induce ferroptosis, thereby promoting lymphatic metastasis and inhibiting hematogenous metastasis | |||||
BACH1 | stomach | GC | Upregulated | Promotes macrophage-dependent GC progression via polarization into M2 macrophages | Fang and Lu. (2020); Yang et al. (2022) |
BACH2 | Stomach | GC | Upregulated | Associated with poor prognosis in patients with GC of MSI-H | Tian et al. (2020); Haam et al. (2014) |
BACH2 deficiency promotes GC cell proliferation in vitro | |||||
BACH1 | Bowel | CRC | Dynamically altered | Enhances CRC cell migration, invasion by increasing the expression of STARD8, TIAM2, MMP-1, MMP-9, MMP-13, SNAIL1, CXCR4, and HMGA2 | Chang et al. (2020); El-Deek et al. (2019); Zhu et al. (2018); Chen et al. (2022) |
Promotes or have no effect on proliferation | |||||
BACH1 | Bowel | IBD | BACH1-deficiency macrophages inhibit TNBS-induced colitis by promoting M2 phenotype | Harusato et al. (2013); Takagi et al. (2018); Pradhan et al. (2022) | |
BACH1 deficiency promotes NLRP3 inflammasome activation and affects mitochondrial function | |||||
Reduced BACH1 expression protects the intestinal mucosa in DSS-induced colitis mouse model | |||||
Indometha-cin induced intestinal injury | Attenuates injury via suppressing inflammation and apoptosis | Harusato et al. (2011) | |||
BACH2 | Bowel | CRC | Promotes immune homeostasis, durable tumor immunosuppression and metastasis by regulating Treg and NK cells | Grant et al. (2020); Li et al. (2022) | |
UC(IBD) | Upregulated | Significantly associated with UC | Ding et al. (2021) | ||
CD (IBD) | CD susceptibility gene | Romani et al. (2021); Laffin et al. (2018) | |||
Closely related to the postoperative recurrence in patients with CD | |||||
IBD | Regulates CD161+ Treg cells to enhance wound healing of epithelium | Povoleri et al. (2018) | |||
CeD | Downregulated | Associated with CeD pathogenesis | Medrano et al. (2019); Quinn et al. (2015) | ||
BACH1 | Liver | HCC | Upregulated | Promotes growth, metastasis, or cellular inflammation through transcriptional activation of IGF1R, PKT and HK2 or influencing P53 pathway | Xie et al. (2022); Sun et al. (2021); Du et al. (2022); Sun et al. (2020a); Xu et al. (2016); Zhao et al. (2022) |
Suppresses autophagy, proliferation, metastasis by influencing P53 pathway or targeting TKT gene | |||||
Regulates glucose and glutathione metabolism | |||||
BACH1 | Liver | HCV | Deficient BACH1 inhibits HCV replication | Ghaziani et al. (2006); Chen et al. (2019) | |
Influences cytotoxic effects of HCV proteins | |||||
NASH | Inhibition of BACH1 reduces steatohepatitis and fibrosis | Inoue et al. (2011) | |||
ATDH | SNPs importantly associated with ATDH | Zhang et al. (2018a) | |||
BACH1 | Liver | APAP-induced liver injury | Upregulated | Involved in oxidative stress promoting liver damage | Abo El-Magd and Eraky (2020) |
Sepsis-induced liver injury | Dynamically altered | Knockdown of BACH1 attenuates liver injury via increasing hepatic blood flow and decreasing oxidative stress and inflammation | Tanioka et al. (2021); Cai et al. (2022) | ||
BACH1 | Liver | Ethinylestr-adiol induced cholestasis | Influences bile flow and urinary bile acid clearance | Muchova et al. (2015) | |
Bile duct | |||||
BACH1 | Bile duct | CCA | Downregulated | Inhibits the transcription of genes encoding proteasome subunits | Jiang et al. (2020b); Liu et al. (2022b) |
BACH2 | Bile duct | PSC | Associated with the susceptibility | Liu et al. (2013b) | |
BACH1 | Pancreas | Pancreatic cancer | Upregulated or Downregulated | Promotes EMT by increasing iron and the expression of vimentin and SNAI2 and decreasing E-cadherin, FOXA1, CLDN3, and CLDN4 expression | Kim et al. (2021); Sato et al. (2020); Liu et al. (2022); Huang et al. (2018); Liu et al. (2022) |
Inhibits EMT by increasing E-cadherin and ZO-1 expression and decreasing ZEB1, vimentin and Slug expression | |||||
Suppresses cell growth and angiogenesis | |||||
SNPs is related with worse overall survival and resistant to gemcitabine | |||||
BACH2 | Chronic pancreatitis | Downregulated | BACH2 inhibition promotes polarization toward Th17 cells and a higher inflammatory response | Sasikala et al. (2018) | |
Associated with advanced clinical features |
Abbreviations: ESCC, Esophageal squamous cell carcinoma; GC, Gastric cancer; CRC, Colorectal cancer; HCC, Hepatocellular carcinoma; CCA, Cholangiocarcinoma; NASH, Nonalcoholic steatohepatitis ; ATDH, Anti-tuberculosis drug-induced hepatotoxicity; APAP, Acetaminophen; UC, Ulcerative colitis; CD, Crohn’s disease; IBDs, Inflammatory bowel diseases; CeD, Coeliac disease; PSC, Primary sclerosing cholangiti; MSI-H, microsatellite instability-high status microsatellite instability-high status; MUFAs, monounsaturated fatty acids.