Evidence map›Paper›PMID 41107665›Full record

ArticleDigestive diseases and sciences2026

Impaired Bicarbonate Transport via SLC26A3 and CFTR Downregulation Promotes Mucous Cap Formation in Sessile Serrated Lesions.

Hiroyoshi Ota, Miharu Suzuki, Heiwa Tanabe, Yukiko Kusama, Ayako Seki, Etsuo Hara, Takeshi Uehara

Abstract read
In one paragraph

Article in Digestive diseases and sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

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1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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2 · The registry

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3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Review
4 · The record

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5 · Who and what money

Authors and funding

7 authors.

Hiroyoshi OtaDepartment of Clinical Laboratory Sciences, Shinshu University School of Medicine, 3-1-1 Asahi, Matsumoto, Nagano, 390-8621, Japan. hohta@shinshu-u.ac.jp.
Miharu SuzukiDepartment of Health and Medical Sciences, Shinshu University Graduate School of Medicine, 3-1-1 Asahi, Matsumoto, Nagano, 390-8621, Japan.
Heiwa TanabeDepartment of Health and Medical Sciences, Shinshu University Graduate School of Medicine, 3-1-1 Asahi, Matsumoto, Nagano, 390-8621, Japan.
Yukiko KusamaDepartment of Pathology, Nagano Municipal Hospital, 1333-1 Tomitake, Nagano, 381-8551, Japan.
Ayako SekiDepartment of Gastroenterology, Nagano Municipal Hospital, 1333-1 Tomitake, Nagano, 381-8551, Japan.
Etsuo HaraDepartment of Gastroenterology, Nagano Municipal Hospital, 1333-1 Tomitake, Nagano, 381-8551, Japan.
Takeshi UeharaDepartment of Laboratory Medicine, Shinshu University School of Medicine, 3-1-1 Asahi, Matsumoto, Nagano, 390-8621, Japan.

Funding

Grants-in-Aid for Scientific Research (KAKENHI) 23590664
6 · The paper itself

Abstract

backgroundSessile serrated lesions (SSLs) are recognized as precursors in the serrated neoplastic pathway leading to microsatellite instability-high colorectal cancer. A hallmark feature of SSLs on endoscopic examination is the mucous cap.

aimsWe aimed to investigate the expression of the bicarbonate transporters SLC26A3 and CFTR in SSLs, using immunohistochemistry to elucidate their potential involvement in the pathogenesis of mucous cap formation.

methodsWe analysed 14 SSLs from 12 patients using formalin-fixed, paraffin-embedded tissue sections. Histochemical staining with high-iron diamine-Alcian blue (HID-AB) and immunohistochemistry for MUC2, MUC5AC, SLC26A3, and CFTR were conducted.

resultsIn normal colonic mucosa, MUC2 was strongly expressed in goblet cells, whereas MUC5AC was absent. SLC26A3 was expressed on the apical membrane and in the cytoplasm of surface epithelial and upper crypt cells, while CFTR was localized to the apical membrane of epithelial cells along the crypt axis. In SSLs, crypts showed architectural distortion with mucin retention in the dilated lumina and an overlying mucous cap. HID-AB staining revealed the presence of sulfomucins and sialomucins. Goblet cells coexpressed MUC2 and MUC5AC, with MUC2 showing broader and stronger expression. These mucins showed a partially distinct and mutually exclusive distribution. Notably, SLC26A3 and CFTR expression levels were markedly reduced or absent in SSLs.

conclusionSSLs showed a mixed acidic mucin phenotype and downregulated epithelial bicarbonate transporters. This may impair mucin expansion and hydration, leading to the formation of adhesive mucous caps, showing the potential link between defective bicarbonate transport and mucin physiology in SSLs.

Indexed as

AntiportersBicarbonatesColorectal NeoplasmsCystic Fibrosis Transmembrane Conductance RegulatorIntestinal MucosaAgedChloride-Bicarbonate AntiportersDown-RegulationFemaleHumansMaleMiddle AgedMucin-2Mucin 5ACSulfate TransportersAntiportersBicarbonatesCFTR protein, humanChloride-Bicarbonate AntiportersCystic Fibrosis Transmembrane Conductance RegulatorMUC2 protein, humanMUC5AC protein, humanMucin-2Mucin 5ACSLC26A3 protein, humanSulfate TransportersBicarbonate transportCFTRMucous capSessile serrated lesionSLC26A3

Identifiers

PMID41107665
PMCPMC12982260

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.