Disease relevance of ARL11

• Transfection of wild-type ARLTS1 into A549 lung-cancer cells suppressed tumor formation in immunodeficient mice and induced apoptosis, whereas transfection of truncated ARLTS1 had a limited effect on apoptosis and tumor suppression [1].
• Association of the ARLTS1 Cys148Arg variant with familial breast cancer risk [2].
• ARLTS1 variants and melanoma risk [3].
• This study presents analysis of the germ-line G446A polymorphism in the ARLTS1 gene among 1686 consecutively collected patients with breast cancer, prostate cancer, malignant melanoma, thyroid papillary cancer or laryngeal cancer in Poland [4].
• ARLTS1 variants and risk of colorectal cancer [5].
• We performed a large case-control association study within the EPICOLON project aimed at evaluating the sporadic and familial colorectal cancer (CRC) risk associated with ARLTS1 genetic variants [6].

High impact information on ARL11

• Recently, ARLTS1 (ADP-ribosylation factor-like tumor suppressor gene 1) has been identified as a tumor suppressor gene, playing a major role in apoptotic signaling [2].
• ARLTS1 - a member of ADP-ribosylation factor family, is a newly described candidate tumour suppressor gene [4].
• Previously, the truncating single nucleotide polymorphism (SNP) of ARLTS, G446A (W149X) has been reported to act as a multi-site tumor susceptibility allele [7].
• Relationship between ARLTS1 polymorphisms and risk of chronic lymphocytic leukemia [7].
• ARLTS1, a member of the Ras superfamily and putative tumor-suppressor gene resides at chromosome 13q14, a region commonly deleted in hematopoietic and solid tumors [7].

Associations of ARL11 with chemical compounds

• After its restoration by adenoviral transduction, ARLTS1-negative A549 and H1299 cells underwent apoptosis and inhibition of cell growth [8].

Biological context of ARL11

• RESULTS: We found a gene at 13q14, ARLTS1, a member of the ADP-ribosylation factor family, with properties of a tumor-suppressor gene [1].
• ARLTS1 was down-regulated by promoter methylation in 25 percent of the primary tumors we analyzed [1].

Anatomical context of ARL11

• We performed functional studies of cell lines lacking ARLTS1 expression with the use of both the full-length ARLTS1 gene and a truncated variant [1].
• The results of this study suggest that the G446A in ARLTS1 gene is probably not associated with an increased risk of sporadic breast cancer, prostate cancer, melanoma, thyroid papillary cancer or laryngeal cancer [4].

References