Evidence map›Paper›PMID 42410499›Full record

ArticleMolecular medicine (Cambridge, Mass.)2026

MIR133B-SEPT9 axis suppresses colorectal cancer progression by inhibiting β-catenin-mediated EMT signaling and is associated with poor prognosis.

Ji-Su Mo, Sang Jae Noh, Kyoung Min Kim, Jun Sang Bae

Abstract read
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Article in Molecular medicine (Cambridge, Mass.), 2026. 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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4 · The record

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5 · Who and what money

Authors and funding

4 authors.

Ji-Su Mo *Digestive Disease Research Institute, Wonkwang University, Iksan, Jeonbuk, 54538, Republic of Korea.
Sang Jae Noh *Department of Forensic Medicine, Jeonbuk National University Medical School, Jeonju, Jeonbuk, 54907, Republic of Korea.
Kyoung Min KimDepartment of Pathology, Jeonbuk National University Medical School, Jeonju, Jeonbuk, 54907, Republic of Korea. kmkim@jbnu.ac.kr.
Jun Sang BaeDepartment of Pathology, College of Korean Medicine, Wonkwang University, Iksan, Jeonbuk, 54538, Republic of Korea. jsbae78@wku.ac.kr.

Funding

National Research Foundation of Korea RS-2021-NR061789
6 · The paper itself

Abstract

backgroundMIR133B is a colorectal cancer (CRC)-associated gene, and its mature product, miR-133b, is significantly downregulated in CRC tissues.

methodsWe aimed to elucidate the tumor-suppressive role of miR-133b in CRC. To identify its downstream target genes, we compared the transcriptome of miR-133b-overexpressing cells with bioinformatic predictions and identified 23 potential target genes. We focused on SEPT9, a gene involved in tumor progression. We confirmed that SEPT9 is a direct target of miR-133b and investigated its role in cell proliferation, invasion, and epithelial-mesenchymal transition (EMT). In addition, we evaluated the expression and prognostic relevance of SEPT9 and active β-catenin in 219 patients with CRC.

resultsWe confirmed the direct interaction between miR-133b and SEPT9 using luciferase reporter assay, qRT-PCR, and western blot. SEPT9 expression was significantly upregulated in CRC tissues compared with that in adjacent normal controls. In HCT116 and SW48 CRC cell lines, overexpression of miR-133b or knockdown of SEPT9 significantly reduced SEPT9 protein levels; suppressed proliferation, colony formation, and invasiveness; inhibited KRAS, BRAF, PI3K, pAKT, and pERK expression; and regulated EMT by downregulating N-cadherin, Vimentin, Snail, Twist, and active β-catenin while upregulating E-cadherin. Nuclear SEPT9 expression positively correlated with active β-catenin in human CRC tissues. In multivariate analysis, SEPT9 positivity independently predicted poor OS and RFS, and the combined SEPT9/active β-catenin expression pattern was an independent predictor of OS for both subgroups and of RFS specifically for the co-positive (SEPT9+/active β-catenin+) subgroup.

conclusionThis study suggests that miR-133b suppresses CRC progression by directly targeting SEPT9 and inhibiting β-catenin-mediated EMT, as well as identifies the miR-133b-SEPT9-β-catenin axis as a potential prognostic indicator in patients with CRC.

Indexed as

beta CateninColorectal NeoplasmsEpithelial-Mesenchymal TransitionMicroRNAsSeptinsSignal TransductionCell Line, TumorCell MovementCell ProliferationDisease ProgressionFemaleGene Expression Regulation, NeoplasticHumansMaleMiddle AgedPrognosisbeta CateninMicroRNAsMIRN133 microRNA, humanSEPTIN9 protein, humanSeptinsColorectal cancerEpithelial–mesenchymal transitionMIR133BSEPT9β-catenin

Identifiers

PMID42410499
PMCPMC13621550

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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.