Evidence map›Paper›PMID 41321626›Full record

ArticleiScience2025

Depletion of LINC01133 from cancer-associated fibroblasts exacerbates the progression of gastric adenocarcinoma.

Xiao Liang, Shengnan Jiang, Qian Zhang, Jiaqi Li, Kexian Dong, He Zhang, Liqiang Wang, Xue Guan, Yimin Wang, Tianyi Fang and 14 more

Abstract read
In one paragraph

Article in iScience, 2025. 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

24 authors.

Xiao LiangKey Laboratory of Preservation of Genetic Resources and Disease Control in China (Harbin Medical University), Ministry of Education, Harbin, China.
Shengnan JiangKey Laboratory of Preservation of Genetic Resources and Disease Control in China (Harbin Medical University), Ministry of Education, Harbin, China.
Qian ZhangKey Laboratory of Preservation of Genetic Resources and Disease Control in China (Harbin Medical University), Ministry of Education, Harbin, China.
Jiaqi LiKey Laboratory of Preservation of Genetic Resources and Disease Control in China (Harbin Medical University), Ministry of Education, Harbin, China.
Kexian DongKey Laboratory of Preservation of Genetic Resources and Disease Control in China (Harbin Medical University), Ministry of Education, Harbin, China.
He ZhangKey Laboratory of Preservation of Genetic Resources and Disease Control in China (Harbin Medical University), Ministry of Education, Harbin, China.
Liqiang WangKey Laboratory of Preservation of Genetic Resources and Disease Control in China (Harbin Medical University), Ministry of Education, Harbin, China.
Xue GuanKey Laboratory of Preservation of Genetic Resources and Disease Control in China (Harbin Medical University), Ministry of Education, Harbin, China.
Yimin WangDepartment of Gastroenterological Surgery, Harbin Medical University Cancer Hospital, Harbin, China.
Tianyi FangDepartment of Gastroenterological Surgery, Harbin Medical University Cancer Hospital, Harbin, China.
Yingwei XueDepartment of Gastroenterological Surgery, Harbin Medical University Cancer Hospital, Harbin, China.
Yunlong LiDepartment of General Surgery, the Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Weixin QinDepartment of Pathology, Harbin Medical University Cancer Hospital, Harbin, China.
Jingcui YuKey Laboratory of Preservation of Genetic Resources and Disease Control in China (Harbin Medical University), Ministry of Education, Harbin, China.
Jie WuKey Laboratory of Preservation of Genetic Resources and Disease Control in China (Harbin Medical University), Ministry of Education, Harbin, China.
Xiangning MengKey Laboratory of Preservation of Genetic Resources and Disease Control in China (Harbin Medical University), Ministry of Education, Harbin, China.
Wenjing SunKey Laboratory of Preservation of Genetic Resources and Disease Control in China (Harbin Medical University), Ministry of Education, Harbin, China.
Yuting WengKey Laboratory of Preservation of Genetic Resources and Disease Control in China (Harbin Medical University), Ministry of Education, Harbin, China.
Mengya LiKey Laboratory of Preservation of Genetic Resources and Disease Control in China (Harbin Medical University), Ministry of Education, Harbin, China.
Genping FuKey Laboratory of Preservation of Genetic Resources and Disease Control in China (Harbin Medical University), Ministry of Education, Harbin, China.
Shuaihang PangKey Laboratory of Preservation of Genetic Resources and Disease Control in China (Harbin Medical University), Ministry of Education, Harbin, China.
Linlin LiKey Laboratory of Preservation of Genetic Resources and Disease Control in China (Harbin Medical University), Ministry of Education, Harbin, China.
Songbin FuKey Laboratory of Preservation of Genetic Resources and Disease Control in China (Harbin Medical University), Ministry of Education, Harbin, China.
Mengdi CaiKey Laboratory of Preservation of Genetic Resources and Disease Control in China (Harbin Medical University), Ministry of Education, Harbin, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

During tumorigenesis, fibroblasts transition from homeostatic cells to cancer-promoting entities, a process potentially mediated by long non-coding RNAs (lncRNAs). While some oncogenic lncRNAs facilitate carcinogenesis, the role of downregulated homeostatic lncRNAs remains unclear. This study reveals that LINC01133, primarily expressed in fibroblasts, is significantly reduced in cancer-associated fibroblasts. The decreased expression of LINC01133 in gastric adenocarcinoma-associated fibroblasts diminishes its extracellular-vesicle-mediated uptake by tumor cells, leading to the acceleration of gastric cancer progression. KLF4 regulates the transcription of LINC01133 in fibroblasts. Mechanistically, binding of LINC01133 to the 173-191 residue region of CDC42 suppresses the activity of its downstream kinases PAK3 and MLK3, and LINC01133 was also the sponge of miR-199a-5p, thereby competing with PHLPP1.

Indexed as

Biological sciencesCancerOncology

Identifiers

PMID41321626
PMCPMC12664395

What Socratic holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

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 Socratic graph.