Identification of a colon mucosa gene that is down-regulated in colon adenomas and adenocarcinomas.

Schweinfest, Clifford W.; Henderson, Kelly W.; Suster, Saul; Kondoh, Nobuo; Papas, Takis S.

doi:10.1073/pnas.90.9.4166

Cited by 181 publications

(125 citation statements)

References 34 publications

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“…1) (14), soybean nodule-specific GmAK170 (10), Stylosanthes shstl, shst2 and shst3, rat liver sat-i (12), mouse sulfate transporter (accession no. D42049), human diastrophic dysplasia (DTD) (13), and human colon mucosa (DRA) (9). In addition, there are two fragments in the sequence data bases that belong to this family, rice expressed sequence tag fragment (accession No.…”

Section: Resultsmentioning

confidence: 99%

“…These data provide preliminary evidence that shstl and shst2 may represent homoeologous genes from the two different progenitor genomes, shstl originating from St (26) and ileal tissue (27) (14); a soybean nodule-specific gene product, GrnAK170 (10); a rat liver H+/sulfate transporter, sat-1 (12); a mouse sulfate transporter (accession no. D42049); the human diastrophic dysplasia gene product, DTD (13); and the human colon mucosa DRA gene product, whose expression is down-regulated in adenomas and adenocarcinomas (9). The sequence data bases also contain an Arabidopsis expressed sequence tag fragment (accession no.…”

Section: Resultsmentioning

confidence: 99%

“…Sequence homologies between the Neurospora crassa sulfate transporter (8) and a number of genes not previously associated with sulfate transport, including a human mucosa protein (9) and a nodulespecific protein (10), have been recognized recently (11). More recent additions to this group are a rat liver sulfate transporter (12), a human gene, DTD, a mutation in which results in diastrophic dysplasia (13), and the yeast high-affinity sulfate transporter (14).…”

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confidence: 99%

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Plant members of a family of sulfate transporters reveal functional subtypes.

Smith¹,

Ealing²,

Hawkesford³

et al. 1995

Proc. Natl. Acad. Sci. U.S.A.

332

277

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Three plant sulfate transporter cDNAs have been isolated by complementation of a yeast mutant with a cDNA library derived from the tropical forage legume Stylosanthes hamata. Two of these cDNAs, shstl and shst2, encode high-affinity H+/sulfate cotransporters that mediate the uptake of sulfate by plant roots from low concentrations of sulfate in the soil solution. The third, shst3, represents a different subtype encoding a lower affinity H+/sulfate cotransporter, which may be involved in the internal transport of sulfate between cellular or subcellular compartments within the plant. The steady-state level of mRNA corresponding to both subtypes is subject to regulation by signals that ultimately respond to the external sulfate supply. These cDNAs represent the identification of plant members of a family of related sulfate transporter proteins whose sequences exhibit significant amino acid conservation in filamentous fungi, yeast, plants, and mammals.All plants need to absorb essential nutrient anions against large gradients of electrochemical potential; this is true for plants in both natural and agricultural environments. Evidently, transport mechanisms of high affinity have evolved, but their precise nature remains obscure, although they have been a major research topic for decades. Despite a wealth of physiological information, the molecular nature of the transporters and the way in which they are regulated are unknown.Sulfate transport in plant roots or cultured cells has highand low-affinity components (1); the former clearly respond to the sulfur-status of the organism, being strongly derepressed by sulfur-starvation and rapidly repressed by the restoration of a sufficient sulfur supply (2-4). High rates of sulfate uptake by previously sulfur-starved cells or roots appear to depend on protein synthesis; treatment with cycloheximide decreases sulfate influx with kinetics very similar to repression by sulfate (4, 5). Such results raised the question as to whether the control of transport activity was translational, or by posttranslational modification of the transporter, rather than by transcription of the genes that encode it. Here we present results demonstrating that changes in the level of the mRNA encoding the transporter are remarkably rapid and are quite compatible with changes in transport activity.Membrane transport proteins from a wide variety of sources may be placed into distinct groups based upon primary sequence similarity or structural features (6, 7). Sequence homologies between the Neurospora crassa sulfate transporter (8) and a number of genes not previously associated with sulfate transport, including a human mucosa protein (9) and a nodulespecific protein (10), have been recognized recently (11). More recent additions to this group are a rat liver sulfate transporter (12), a human gene, DTD, a mutation in which results in diastrophic dysplasia (13), and the yeast high-affinity sulfate transporter (14). In this paper we report the cloning and analysis of plant members of this family,...

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

mentioning

confidence: 99%

See 1 more Smart Citation

Plant members of a family of sulfate transporters reveal functional subtypes.

Smith¹,

Ealing²,

Hawkesford³

et al. 1995

Proc. Natl. Acad. Sci. U.S.A.

332

277

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“…Trisomy 7 as a sole anomaly occurs in a wide variety of tumour types and has also been reported in non-neoplastic diseases, such as Dupytren's contracture and atherosclerotic plaques; its tumorigenic importance remains undetermined 178 . Interestingly, a candidate colorectal tumour suppressor gene,`downregulated in adenoma' (DRA), which is expressed exclusively in colonic mucosa, has been localized to chromosome 7 179,180 , and downregulation of this gene correlates with tumour progression 181 . As in colorectal cancer, chromosomes 13 and 20 are often gained in adenomas (30 and 17 per cent respectively) and chromosome 18 is frequently lost (13 per cent) 174 .…”

Section: Cytogenetic Evidencementioning

confidence: 99%

The colorectal adenoma–carcinoma sequence

Leslie

Carey

Pratt

et al. 2002

British Journal of Surgery

589

448

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Background: It is widely accepted that the adenoma±carcinoma sequence represents the process by which most, if not all, colorectal cancers arise. The evidence supporting this hypothesis has increased rapidly in recent years and the purpose of this article is to review this evidence critically and highlight its clinical signi®cance.Methods: Medline searches were used to identify recent key articles relating to the adenoma±carcinoma sequence. Further pertinent articles were obtained by manual scanning of the reference lists of identi®ed papers.Results: The evidence supporting the adenoma±carcinoma sequence can be classi®ed as epidemiological, clinicopathological and genetic. The most recent and largest body of data relates to molecular genetic events and their cellular effects; however, many other approaches, such as cytogenetics, molecular cytogenetics and cytometry, have also yielded valuable information.Conclusion: Recent work continues to support the adenoma±carcinoma sequence, but there is a paucity of data on the interrelationship between different genetic mutations and on the relationship between molecular and other types of genetic abnormalities. The clinical utility of the observations described has yet to be fully realized and global genetic analysis of colorectal tumours may prove to be central in rational adenoma management. IntroductionColorectal cancer is the second leading cause of cancerrelated death in the Western world; in the UK there are currently around 30 000 new cases per annum and 17 000 related deaths 1 . In recent years our understanding of the cellular and molecular events underlying the development of colorectal cancer has improved immeasurably but, despite this and advances in surgery, radiotherapy and chemotherapy, the average 5-year survival rate remains around 40 per cent 1 . One of the most important fundamental concepts in colorectal cancer to emerge in recent years has been the adenoma±carcinoma sequence, a term that describes the stepwise progression from normal to dysplastic epithelium to carcinoma associated with the accumulation of multiple clonally selected genetic alterations. This concept not only provides an excellent model to study the genesis of invasive cancer, but also affords a means of preventing colorectal cancer by endoscopic removal of precursor lesions.The appropriate management of individuals with precursor adenomatous polyps (adenomas) is of the utmost importance. It is known that after removal of such polyps 30±35 per cent of patients will have further adenomas detected at 3±4 years 2±4 and this has led to a policy of endoscopic surveillance for all adenoma-bearers 5 . However, given that approximately 40 per cent of the Western population will develop adenomas 6±8 and only 3 per cent will go on to suffer from colorectal cancer, it is clear that only a small proportion of adenomas progress to malignancy. Unfortunately, there are no reliable criteria available that can predict adenoma progression or recurrence, and the important questions of which individuals...

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“…Although ClC-2 was suggested as a likely candidate (10,11), recent reports have questioned the apical localization and role of ClC-2 in gastric acid secretion (12,13). SLC26 (human)/Slc26 (mouse) homologs are members of a conserved family of anion exchangers that display selective and limited tissue expression in epithelial cells (14)(15)(16)(17)(18)(19)(20)(21)(22). Several SLC26 members can function as chloride/bicarbonate exchangers.…”

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confidence: 99%