Disease relevance of LETMD1

• Transgenic mouse model for breast cancer: induction of breast cancer in novel oncogene HCCR-2 transgenic mice [1].
• Mice transgenic for HCCR-2 developed breast cancers and metastasis [1].
• Serum HCCR concentrations were measured using ELISA from 299 subjects, including 129 patients with breast cancer, 24 patients with benign breast disease, and 158 normal volunteers, and comparisons were made to CA15-3 [2].
• These 2 proteins colocalized in mitochondria but the expression of HCCR-1 showed negative correlation with that of DP1 in colorectal cancer (CRC) [3].
• Furthermore, HCCR expression was also detected in liver cirrhosis at an intermediate level between carcinoma and normal groups, which gave 88.1% sensitivity and 79.0% specificity using 8 microg/ml as a cutoff value [4].

High impact information on LETMD1

• BACKGROUND & AIMS: Human cervical cancer oncogene (HCCR-1) has appeared to act as a negative regulator of p53 and contributes to tumorigenesis of various organs including the colon [3].
• According to immunofluorescence study, HCCR was predominantly localized in the plasma membrane and cytoplasm of hepatocellular carcinoma [4].
• HCCR proteins were overexpressed in the tumorous compared with the nontumorous cirrhosis tissues [4].
• The level of p53 in HCCR-2 transgenic mice was elevated in most tissues including breast, brain, heart, lung, liver, stomach, kidney, spleen, and lymph node [1].
• Transgenic mice containing novel oncogene HCCR-2 were generated to analyse the phenotype and to characterize the role of HCCR-2 in cellular events [1].

Biological context of LETMD1

• Northern blot analysis revealed that the HCCR-1 gene expression was down-regulated by LY-294002 [5].
• The level of HCCR-1 expression was increased during the mouse embryogenesis [5].
• To determine the regulatory pathway involved in the HCCR-1 gene expression, we searched the 5' flanking region of HCCR-1 and identified HCCR-1 promoter including putative homeodomain protein binding sites [5].

Anatomical context of LETMD1

• Nude mice injected with NIH/3T3 cells stably transfected with HCCR-2 formed tumors in 4 weeks [6].
• Ectopic expression of HCCR-2 resulted in direct tumorigenic conversions of NIH/3T3 and Rat1 fibroblasts [6].

Physical interactions of LETMD1

• According to fluorescence-activated cell sorting and confocal microscopic analysis, BCS-1 was bound to HCCR antigen on the cell surface [2].

Other interactions of LETMD1

• The epitope regions of HCCR recognized by monoclonal antibody (BCS-1) were HFWTPK and QQTDFLDIYHAFR [2].

Analytical, diagnostic and therapeutic context of LETMD1

• EXPERIMENTAL DESIGN: HCCR expression in breast cancer cells was analyzed by quantitative PCR, ELISA, immunohistochemistry, Western blotting, fluorescence-activated cell sorting, and confocal microscopy [2].

References