Evidence map›Paper›PMID 41683622›Full record

ArticleInternational journal of molecular sciences2026

Splicing Factor 3a Subunit 1 Promotes Colorectal Cancer Growth via Anti-Apoptotic Effects of Syntaxin12.

Takahiro Sasaki, Hiroaki Konishi, Tatsuya Dokoshi, Aki Sakatani, Hiroki Tanaka, Koji Yamamoto, Keitaro Takahashi, Katsuyoshi Ando, Nobuhiro Ueno, Shin Kashima and 4 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of molecular sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

14 authors.

Takahiro SasakiDivision of Gastroenterology, Department of Internal Medicine, Asahikawa Medical University, Midorigaoka-Higashi 2-1-1-1, Asahikawa 078-8510, Hokkaido, Japan.ORCID 0000-0002-0412-8760
Hiroaki KonishiDepartment of Gastroenterology and Advanced Medical Sciences, Asahikawa Medical University, Midorigaoka-Higashi 2-1-1-1, Asahikawa 078-8510, Hokkaido, Japan.ORCID 0000-0002-6477-721X
Tatsuya DokoshiDepartment of Gastroenterological Sciences, Asahikawa Medical University, Midorigaoka-Higashi 2-1-1-1, Asahikawa 078-8510, Hokkaido, Japan.ORCID 0000-0003-3678-6781
Aki SakataniDepartment of Gastroenterological Sciences, Asahikawa Medical University, Midorigaoka-Higashi 2-1-1-1, Asahikawa 078-8510, Hokkaido, Japan.
Hiroki TanakaDivision of Tumor Pathology, Department of Pathology, Asahikawa Medical University, Midorigaoka-Higashi 2-1-1-1, Asahikawa 078-8510, Hokkaido, Japan.
Koji YamamotoDepartment of Gastroenterology and Advanced Medical Sciences, Asahikawa Medical University, Midorigaoka-Higashi 2-1-1-1, Asahikawa 078-8510, Hokkaido, Japan.
Keitaro TakahashiDivision of Gastroenterology, Department of Internal Medicine, Asahikawa Medical University, Midorigaoka-Higashi 2-1-1-1, Asahikawa 078-8510, Hokkaido, Japan.
Katsuyoshi AndoDivision of Gastroenterology, Department of Internal Medicine, Asahikawa Medical University, Midorigaoka-Higashi 2-1-1-1, Asahikawa 078-8510, Hokkaido, Japan.ORCID 0000-0003-3500-5488
Nobuhiro UenoDivision of Gastroenterology, Department of Internal Medicine, Asahikawa Medical University, Midorigaoka-Higashi 2-1-1-1, Asahikawa 078-8510, Hokkaido, Japan.
Shin KashimaDivision of Gastroenterology, Department of Internal Medicine, Asahikawa Medical University, Midorigaoka-Higashi 2-1-1-1, Asahikawa 078-8510, Hokkaido, Japan.
Kentaro MoriichiDivision of Gastroenterology, Department of Internal Medicine, Asahikawa Medical University, Midorigaoka-Higashi 2-1-1-1, Asahikawa 078-8510, Hokkaido, Japan.
Hiroki TanabeDivision of Gastroenterology, Department of Internal Medicine, Asahikawa Medical University, Midorigaoka-Higashi 2-1-1-1, Asahikawa 078-8510, Hokkaido, Japan.ORCID 0000-0001-9029-5081
Toshikatsu OkumuraDivision of Gastroenterology, Department of Internal Medicine, Asahikawa Medical University, Midorigaoka-Higashi 2-1-1-1, Asahikawa 078-8510, Hokkaido, Japan.
Mikihiro FujiyaDivision of Gastroenterology, Department of Internal Medicine, Asahikawa Medical University, Midorigaoka-Higashi 2-1-1-1, Asahikawa 078-8510, Hokkaido, Japan.

Funding

Grants-in-Aid for Scientific Research 21K07929Grants-in-Aid for Scientific Research 21KK0291Grants-in-Aid for Scientific Research 22K08047Grants-in-Aid for Scientific Research 22K15363Intractable Disease Health and Labour Sciences Research Grants from the Ministry of Health, Labour and Welfare noneTHE SUHARA MEMORIAL FOUNDATION none
6 · The paper itself

Abstract

RNA dysregulation mediated by aberrant RNA-binding proteins (RBPs) is closely associated with tumorigenesis. However, the tumorigenic mechanisms of each RBP remained unclear. In this study, we demonstrate that downregulation of Splicing factor 3A1 (SF3A1) markedly suppressed the proliferation of colorectal cancer (CRC) cells, with minimal cytotoxicity observed in non-cancerous epithelial cells. The tumor-promoting function of SF3A1 was further validated in an HCT116 xenograft mouse model. Multiple apoptosis assays-including TdT-mediated dUTP nick end labeling (TUNEL) staining, poly-ADP-ribose polymerase (PARP) immunoblotting, and caspase-3/7 activity measurements-showed that SF3A1 inhibited apoptotic signaling in CRC cells. Transcriptome analysis, combined with RNA-immunoprecipitation (RIP), identified Syntaxin 12 (STX12) as a downstream effector of SF3A1. Knockdown of STX12 induced apoptosis in CRC cells but had no effect on the viability of non-cancerous HCEC-1CT epithelial cells. Furthermore, STX12 mRNA levels were significantly reduced following SF3A1 knockdown, indicating that SF3A1-mediated stabilization of STX12 contributes to apoptosis resistance in CRC cells. Collectively, our findings establish that SF3A1 promotes CRC progression by stabilizing STX12 mRNA and selectively inhibiting apoptosis in malignant cells, thereby identifying the SF3A1-STX12 regulatory axis as a novel and selective therapeutic target for CRC.

Indexed as

ApoptosisColorectal NeoplasmsQa-SNARE ProteinsRNA Splicing FactorsAnimalsCell Line, TumorCell ProliferationGene Expression Regulation, NeoplasticHCT116 CellsHumansMiceMice, NudeQa-SNARE ProteinsRNA Splicing Factorsapoptosiscolorectal cancerRNA binding proteinsplicing factor 3A1Syntaxin 12

Identifiers

PMID41683622
PMCPMC12897669

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Registered trials

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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.