Evidence map›Paper›PMID 41888092›Full record

ArticleCell death & disease2026

HIF-1α suppresses SNPH expression to facilitate liver metastasis of colorectal cancer through regulating mitochondrial dynamics and filopodia formation.

Lei Zhan, Xiaoxi Li, Xiaoyan Li, Qian Fei, Yue Jin, Jiaxing Yu, Luyao Tian, Feifei Li, Chunning Li, Qian Dong and 3 more

Abstract read
In one paragraph

Article in Cell death & disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Article
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

13 authors.

Lei ZhanMedical Oncology Department of Gastrointestinal Cancer, Cancer Hospital of China Medical University, Liaoning Cancer Hospital & Institute, Cancer Hospital of Dalian University of Technology, Shenyang, Liaoning, China.ORCID http://orcid.org/0000-0002-7926-8573
Xiaoxi LiCentral Laboratory, Cancer Hospital of China Medical University, Liaoning Cancer Hospital & Institute, Cancer Hospital of Dalian University of Technology, Shenyang, China.ORCID http://orcid.org/0000-0002-2295-9533
Xiaoyan LiDepartment of Pathology, Cancer Hospital of China Medical University, Liaoning Cancer Hospital & Institute, Cancer Hospital of Dalian University of Technology, Shenyang, Liaoning, China.ORCID http://orcid.org/0000-0002-9806-1850
Qian FeiDepartment of Oncology, Shengjing Hospital of China Medical University, Shenyang, Liaoning, China.ORCID http://orcid.org/0000-0003-1638-8583
Yue JinMedical Oncology Department of Gastrointestinal Cancer, Cancer Hospital of China Medical University, Liaoning Cancer Hospital & Institute, Cancer Hospital of Dalian University of Technology, Shenyang, Liaoning, China.ORCID http://orcid.org/0009-0003-5233-9110
Jiaxing YuMedical Oncology Department of Gastrointestinal Cancer, Cancer Hospital of China Medical University, Liaoning Cancer Hospital & Institute, Cancer Hospital of Dalian University of Technology, Shenyang, Liaoning, China.ORCID http://orcid.org/0009-0009-0104-4682
Luyao TianMedical Oncology Department of Gastrointestinal Cancer, Cancer Hospital of China Medical University, Liaoning Cancer Hospital & Institute, Cancer Hospital of Dalian University of Technology, Shenyang, Liaoning, China.
Feifei LiMedical Oncology Department of Gastrointestinal Cancer, Cancer Hospital of China Medical University, Liaoning Cancer Hospital & Institute, Cancer Hospital of Dalian University of Technology, Shenyang, Liaoning, China.ORCID http://orcid.org/0000-0002-1321-3385
Chunning LiCentral Laboratory, Cancer Hospital of China Medical University, Liaoning Cancer Hospital & Institute, Cancer Hospital of Dalian University of Technology, Shenyang, China.
Qian DongMedical Oncology Department of Gastrointestinal Cancer, Cancer Hospital of China Medical University, Liaoning Cancer Hospital & Institute, Cancer Hospital of Dalian University of Technology, Shenyang, Liaoning, China.ORCID http://orcid.org/0000-0001-9810-1368
Yong ZhangDepartment of Pathology, Cancer Hospital of China Medical University, Liaoning Cancer Hospital & Institute, Cancer Hospital of Dalian University of Technology, Shenyang, Liaoning, China.ORCID http://orcid.org/0000-0001-9124-6281
Shulan SunCentral Laboratory, Cancer Hospital of China Medical University, Liaoning Cancer Hospital & Institute, Cancer Hospital of Dalian University of Technology, Shenyang, China.
Jingdong ZhangMedical Oncology Department of Gastrointestinal Cancer, Cancer Hospital of China Medical University, Liaoning Cancer Hospital & Institute, Cancer Hospital of Dalian University of Technology, Shenyang, Liaoning, China. jdzhang@cancerhosp-ln-cmu.com.ORCID http://orcid.org/0000-0002-0711-2764

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82002568
6 · The paper itself

Abstract

Colorectal cancer (CRC) is a leading cause of cancer-associated deaths, with liver metastases developing in about 50% of patients. Mitochondrial dynamics play critical roles in a diverse range of cellular functions, including cell migration and cancer metastasis. However, the influence of mitochondrial dynamics deregulation in CRC liver metastasis is incompletely understood. Through multiple transcriptomic data analysis and validation, we found that low expression of SNPH significantly correlated with poor prognosis of CRC patients. SNPH knockdown altered mitochondrial dynamics to increase cell migration and invasion by promoting filopodia formation. Moreover, the reduced levels of SNPH were linked to HIF-1α expression. Luciferase reporter assay revealed that HIF-1α transcriptionally activated miR-130a-3p expression, which targeted SNPH mRNA to inhibit its protein levels. Furthermore, miR-130a-3p inhibitor suppressed SNPH downregulation, filopodia formation, and CRC cells metastasis under hypoxic conditions. Mechanistically, SNPH downregulation promoted ROS production, resulting in the activation of the AKT/cdc42 pathway and downstream PAK1/Cofilin cascade. The overexpression of SNPH increased mitochondrial fusion and deterred the liver metastasis ability of CRC cells in vivo. Together, our results suggest that SNPH suppression imposed by the HIF-1α/miRNA-130a-3p axis under hypoxia conditions promotes the liver metastasis of CRC cells by activating the AKT/cdc42-PAK1/Cofilin cascade through mitochondrial dynamics-mediated ROS production.

Indexed as

Colorectal NeoplasmsGTP PhosphohydrolasesHypoxia-Inducible Factor 1, alpha SubunitLiver NeoplasmsMitochondrial DynamicsPseudopodiaAnimalsCell Line, TumorCell MovementGene Expression Regulation, NeoplasticHumansMaleMiceMice, NudeMicroRNAsp21-Activated KinasesGTP PhosphohydrolasesHIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitMicroRNAsMIRN130 microRNA, humanp21-Activated KinasesProto-Oncogene Proteins c-aktReactive Oxygen Species

Identifiers

PMID41888092
PMCPMC13039215

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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.