Evidence map›Paper›PMID 42439618›Full record

ArticleCells2026

TDGF1 Mediates the Oncogenic Effects of the OLMALINC/miR-3614-5p ceRNA Axis in Colon Cancer Through Nodal/Smad2 and Glypican-1/MAPK-AKT Signaling.

Feng Gao, Xiaoli Li, Jiawei Li, Shuo Yang, Boyu Zhang, Ying Sun, Lihua Zheng, Guannan Wang, Lei Liu, Yongli Bao and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cells, 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

11 authors.

Feng GaoNational Engineering Laboratory for Druggable Gene and Protein Screening, Northeast Normal University, Changchun 130117, China.
Xiaoli LiNational Engineering Laboratory for Druggable Gene and Protein Screening, Northeast Normal University, Changchun 130117, China.
Jiawei LiNational Engineering Laboratory for Druggable Gene and Protein Screening, Northeast Normal University, Changchun 130117, China.ORCID 0000-0001-8229-1638
Shuo YangInternational Joint Research Center of Stem Cell Bank, Ministry of Science and Technology, Northeast Normal University, Changchun 130117, China.
Boyu ZhangInternational Joint Research Center of Stem Cell Bank, Ministry of Science and Technology, Northeast Normal University, Changchun 130117, China.
Ying SunNational Engineering Laboratory for Druggable Gene and Protein Screening, Northeast Normal University, Changchun 130117, China.
Lihua ZhengNational Engineering Laboratory for Druggable Gene and Protein Screening, Northeast Normal University, Changchun 130117, China.ORCID 0000-0001-5380-2021
Guannan WangNational Engineering Laboratory for Druggable Gene and Protein Screening, Northeast Normal University, Changchun 130117, China.
Lei LiuInternational Joint Research Center of Stem Cell Bank, Ministry of Science and Technology, Northeast Normal University, Changchun 130117, China.
Yongli BaoInternational Joint Research Center of Stem Cell Bank, Ministry of Science and Technology, Northeast Normal University, Changchun 130117, China.
Xiaoguang YangNational Engineering Laboratory for Druggable Gene and Protein Screening, Northeast Normal University, Changchun 130117, China.

Funding

Scientific Research Project of Jilin Provincial Education Department JJKH20250326KJ
6 · The paper itself

Abstract

The multifaceted oncogenic role of teratocarcinoma-derived growth factor 1 (TDGF1) in colon cancer remains incompletely understood. Through integrative bioinformatic and functional analyses, we identified a novel competing endogenous RNA (ceRNA) axis wherein the long non-coding RNA OLMALINC directly sponges hsa-miR-3614-5p, leading to the derepression of TDGF1. This OLMALINC/miR-3614-5p/TDGF1 axis promoted colon cancer cell proliferation, migration, invasion, and anti-apoptosis in vitro, whereas TDGF1 knockdown significantly suppressed tumor growth in vivo. Mechanistically, TDGF1 co-activated oncogenic signaling via the Thr88-dependent Nodal/Smad2 cascade and the Glypican-1-mediated MAPK/AKT pathway. Beyond cell-autonomous effects, transcriptomic and single-cell analyses revealed that elevated TDGF1 correlates with an immunosuppressive microenvironment, characterized by reduced immune infiltration and altered LGALS9-CD44 malignant-T cell communication. Clinically, high TDGF1 expression in a tissue microarray cohort was significantly associated with advanced T stage, reduced expression of specific mismatch repair proteins (MLH1/PMS2), and poor overall survival. Collectively, this study delineates the OLMALINC/miR-3614-5p/TDGF1 regulatory circuit and establishes TDGF1 as a multifaceted driver of tumor progression, highlighting its potential as a prognostic biomarker and therapeutic target in colon cancer.

Indexed as

CarcinogenesisColonic NeoplasmsGlypicansMicroRNAsRNA, Long NoncodingAnimalsCell Line, TumorCell MovementCell ProliferationGene Expression Regulation, NeoplasticGPI-Linked ProteinsHumansIntercellular Signaling Peptides and ProteinsMaleMiceNeoplasm ProteinsGlypicansGPI-Linked ProteinsIntercellular Signaling Peptides and ProteinsMicroRNAsNeoplasm ProteinsNodal ProteinProto-Oncogene Proteins c-aktRNA, Competitive EndogenousRNA, Long NoncodingTDGF1 protein, humancolon cancerimmune signaturencRNAsprognosissignaling pathwayTDGF1

Identifiers

PMID42439618
PMCPMC13360589

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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.