Disease relevance of TMPRSS11A

• We previously cloned and identified the esophageal cancer related gene 1 (ECRG1), a novel candidate tumor suppressor gene, from human esophageal cells [1].
• A single nucleotide polymorphism (Arg290Gln) was identified in the coding region of ECRG1 and might play a role in susceptibility to esophageal squamous cell carcinoma (ESCC) [1].

High impact information on TMPRSS11A

• Identification of a novel polymorphism Arg290Gln of esophageal cancer related gene 1 (ECRG1) and its related risk to esophageal squamous cell carcinoma [1].
• We observed a statistically significantly increased risk of ESCC associated with the ECRG1 290Arg/Gln and 290Gln/Gln genotypes compared with the 290Arg/Arg [odds ratio (OR)=1.23, 95% confidence interval (CI)=1.03-1.46; P<0.05] [1].
• Taken together, our results indicate that the ECRG1 290Gln variant allele might be a genetic susceptibility factor for developing ESCC, especially in the smoking population [1].
• Induction of G1 cell cycle arrest and P15INK4b expression by ECRG1 through interaction with Miz-1 [2].
• Transfection of ECRG1 gene into the esophageal cancer (EC) cells inhibited cell proliferation and induced G1 phase arrest of cell cycle [2].

Biological context of TMPRSS11A

• It suggests that ECRG1 may inhibit tumor cell growth by affecting cell cycle, and that expression of P15(INK4b) may be likely to enhance G1 cell cycle arrest during the interaction of ECRG1 and Miz-1 [2].
• To study the biological role of ECRG1 gene, we performed a GAL4-based yeast two-hybrid screen of a human fetal liver cDNA library [2].
• Moreover, NIH3T3 cells transfected with ECRG1 stained positive for SA-beta-gal staining (pH 6.0), which is a specific marker of cellular senescence [3].

Anatomical context of TMPRSS11A

• ECRG1 is a novel candidate of tumor suppressor gene identified from human esophagus [2].
• When antisense ECRG1 interdicted expression of endogenous ECRG1 in Balb/c-3T3 cells, Transfection of Miz-1 couldn't induce P15(INK4b) expression [2].

Physical interactions of TMPRSS11A

• Previous studies showed that ECRG1 overexpression could inhibit cell growth and induce G1 cell cycle arrest and p15(INK4b) expression by interacting with Miz-1 (Myc-interacting zinc finger protein) [3].

Other interactions of TMPRSS11A

• Expression of ECRG1 in these cells caused senescence-like changes characterized in terms of altered cell morphology, cell cycle arrest at the G1/S phase, and significantly impaired cell proliferation (P < 0.01) [3].

Analytical, diagnostic and therapeutic context of TMPRSS11A

• ECRG1 was co-localized with Miz-1 in nucleus, as shown by confocal microscopy [2].
• The interaction of ECRG1 and Miz-1 was confirmed by glutathione-S-transferase (GST)-pull-down assays in vitro and co-immunoprecipitation experiments in vivo [2].

References