Evidence map›Paper›PMID 38830348›Full record

ArticlePathobiology : journal of immunopathology, molecular and cellular biology2024

Identification of Early Events in Serrated Pathway Colorectal Tumorigenesis by Using Digital Spatial Profiling.

Min-Cheng Su, Ching-Hsiang Hsu, Ko-Chen Chen, Jun-Ru Lin, Huei-Ying Li, Yi-Ting Fang, Ruby Yun-Ju Huang, Yung-Ming Jeng

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Article in Pathobiology : journal of immunopathology, molecular and cellular biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

8 authors.

Min-Cheng SuDepartment of Pathology, Min-Sheng General Hospital, Taoyuan, Taiwan.
Ching-Hsiang HsuGraduate Institute of Pathology, National Taiwan University, Taipei, Taiwan.
Ko-Chen ChenSchool of Medicine, National Taiwan University, Taipei, Taiwan.
Jun-Ru LinGraduate Institute of Pathology, National Taiwan University, Taipei, Taiwan.
Huei-Ying LiMedical Microbiota Center of the First Core Laboratory, National Taiwan University College of Medicine, Taipei, Taiwan.
Yi-Ting FangDepartment of Pathology, National Taiwan University Hospital, Taipei, Taiwan.
Ruby Yun-Ju HuangSchool of Medicine, National Taiwan University, Taipei, Taiwan.
Yung-Ming JengGraduate Institute of Pathology, National Taiwan University, Taipei, Taiwan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionThe colorectal serrated pathway involves precursor lesions known as sessile serrated lesions (SSL) and traditional serrated adenomas (TSA). Mutations in BRAF or KRAS are crucial early events in this pathway. Additional genetic and epigenetic changes contribute to the progression of these lesions into high-grade lesions and, eventually, invasive carcinoma.

methodsWe employed digital spatial profiling to investigate the transcriptional changes associated with SSL and TSA. The genes identified are confirmed by immunohistochemical (IHC) staining. Colorectal cancer (CRC) cell lines with CEACAM6 overexpression and knockdown were established to study the roles of CEACAM6 on tumorigenesis of CRC.

resultsTen genes were upregulated in SSL and TSA, and seven were upregulated in both types of lesions. IHC staining confirmed overexpression of CEACAM6, LCN2, KRT19, and lysozyme in SSL and TSA. CEACAM6 expression is an early event in the serrated pathway but a late event in the conventional pathway. Using cell line models, we confirmed that CEACAM6 promotes CRC cells' proliferation, migration, and invasion abilities.

conclusionThese results highlight that the transcriptional changes in the early stages of tumorigenesis exhibit relative uniformity. Identifying these early events may hold significant promise in elucidating the mechanisms behind tumor initiation.

Indexed as

AdenomaAntigens, CDCarcinogenesisCell Adhesion MoleculesColorectal NeoplasmsAgedCell Line, TumorCell MovementCell ProliferationFemaleGene Expression Regulation, NeoplasticGPI-Linked ProteinsHumansMaleMiddle AgedAntigens, CDCEACAM6 protein, humanCell Adhesion MoleculesGPI-Linked ProteinsCEACAM6Colon cancerDigital spatial profilingSerrated pathwayTraditional serrated adenoma

Identifiers

PMID38830348
PMCPMC11614314

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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.