Disease relevance of LDOC1

• Leucine-zipper protein, LDOC1, inhibits NF-kappaB activation and sensitizes pancreatic cancer cells to apoptosis [1].
• LDOC1 was isolated as a gene encoding a leucine-zipper protein whose expression was decreased in pancreatic and gastric cancer cell lines in 1999 [2].
• Lifetime risks of death from LDOC and radiographic silicosis were estimated up to age 85 with an actuarial approach accounting for competing causes of death [3].

High impact information on LDOC1

• These observations suggest that LDOC1 is a novel regulator of NF-kappaB that can affect the PMA or TNF-alpha-mediated pathway to apoptosis through inhibition of NF-kappaB activation in BxPC3 pancreatic cancer cells [1].
• Viability studies demonstrated that TNF-alpha or PMA-induced antiproliferative effects were significantly enhanced by stable transfection of cells with LDOC1 [1].
• We have isolated a novel gene, LDOC1, which encodes for a leucine zipper protein that was downregulated in a series of human pancreatic cancer cell lines but was expressed in corresponding normal tissues [1].
• LDOC1, a novel MZF-1-interacting protein, induces apoptosis [2].
• The two transcription units mapping within this interval are the LDOC1 and SPANXC genes [4].

Biological context of LDOC1

• Here, we found that overexpression of LDOC1 caused externalization of the cell membrane phosphatidylserine, which was characteristic for early-phase apoptotic events, and reduced cell viability in some human cell lines [2].
• Although the function of LDOC1 is still unknown, our results suggest that this novel gene codes for a nuclear protein, and down-regulation of LDOC1 may have an important role in the development and/or progression of some cancers [5].
• OBJECTIVES: To estimate excess lifetime risk of (a) mortality from lung disease other than cancer (LDOC), and, (b) onset of radiographic silicosis, arising from occupational exposure to respirable crystalline silica dust [3].

Regulatory relationships of LDOC1

• The activation of NF-kappaB through ligand-induced stimulation by tumor necrosis factor-alpha (TNF-alpha) or phorbol 12-myristate 13-acetate (PMA) was also inhibited by transient expression of LDOC1 in a dose dependent manner [1].

References