Evidence map›Paper›PMID 39690180›Full record

ArticleCancer gene therapy2025

ITGA3 promotes pancreatic cancer progression through HIF1α- and c-Myc-driven glycolysis in a collagen I-dependent autocrine manner.

Rongkun Li, Qian Ji, Shengqiao Fu, Jichun Gu, Dejun Liu, Lu Wang, Xiao Yuan, Yi Wen, Chunhua Dai, Hengchao Li

Abstract read
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Article in Cancer gene therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing 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

19 citing papers in PubMed.

  1. Article
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  6. S3RL: Enhancing Spatial Single-Cell Transcriptomics With Separable Representation Learning.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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  16. CDK4/6 inhibitors for metastatic breast cancer in routine clinical practice in Spain: survey of patterns of use and oncologists' perceptions.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025
    Article
  17. Article
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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

10 authors.

Rongkun Li *Chest Oncology Department, Cancer Institute of Jiangsu University, Affiliated Hospital of Jiangsu University, Zhenjiang, 212001, China. 1000012753@ujs.edu.cn.ORCID http://orcid.org/0000-0002-0056-2025
Qian Ji *Department of Pulmonary Oncology, Zhongnan Hospital, Wuhan University, Wuhan, 430071, China.
Shengqiao Fu *Chest Oncology Department, Cancer Institute of Jiangsu University, Affiliated Hospital of Jiangsu University, Zhenjiang, 212001, China.
Jichun Gu *Department of Pancreatic surgery, Huashan Hospital, Fudan University, Shanghai, 200040, China.
Dejun LiuDepartment of Biliary-Pancreatic Surgery, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200127, China.ORCID http://orcid.org/0000-0002-8091-0375
Lu WangAbdominal Oncology Department, Cancer Institute of Jiangsu University, Affiliated Hospital of Jiangsu University, Zhenjiang, 212001, China.
Xiao YuanChest Oncology Department, Cancer Institute of Jiangsu University, Affiliated Hospital of Jiangsu University, Zhenjiang, 212001, China.
Yi WenChest Oncology Department, Cancer Institute of Jiangsu University, Affiliated Hospital of Jiangsu University, Zhenjiang, 212001, China.ORCID http://orcid.org/0009-0009-9572-1049
Chunhua DaiChest Oncology Department, Cancer Institute of Jiangsu University, Affiliated Hospital of Jiangsu University, Zhenjiang, 212001, China. daichunhua8@163.com.ORCID http://orcid.org/0000-0002-6423-5445
Hengchao LiDepartment of Pancreatic surgery, Huashan Hospital, Fudan University, Shanghai, 200040, China. lihengchao@huashan.org.cn.ORCID http://orcid.org/0000-0002-4681-3854

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82103105Natural Science Foundation of Jiangsu Province (Jiangsu Provincial Natural Science Foundation) BK20210143
6 · The paper itself

Abstract

Pancreatic cancer is characterized by severe metabolic stress due to its prominent desmoplasia and poor vascularization. Integrin subunit alpha 3 (ITGA3) is a cell surface adhesion protein involved in tumor progression. However, the role of ITGA3 in pancreatic cancer progression, especially in metabolic reprogramming, remains largely unknown. In this study, we found that ITGA3 expression is elevated in pancreatic cancer tissues and predicts poor prognosis for patients with pancreatic cancer. Functional assays revealed that ITGA3 promotes the growth and liver metastasis of pancreatic cancer via boosting glycolysis. Mechanistically, Collagen I (Col1) derived from cancer cells acts as a ligand for ITGA3 to activate the FAK/PI3K/AKT/mTOR signaling pathway in an autocrine manner, thereby increasing the expression of HIF1α and c-Myc, two critical regulators of glycolysis. Blockade of Col1 by siRNA or of ITGA3 by a blocking antibody leads to specific inactivation of the FAK/PI3K/AKT/mTOR pathway and impairs malignant tumor behaviors induced by ITGA3. Thus, our data indicate that ITGA3 enhances glycolysis to promote pancreatic cancer growth and metastasis via increasing HIF1α and c-Myc expression in a Col1-dependent autocrine manner, making ITGA3 as a candidate diagnostic biomarker and a potential therapeutic target for pancreatic cancer.

Indexed as

Collagen Type IHypoxia-Inducible Factor 1, alpha SubunitIntegrin alpha3Pancreatic NeoplasmsProto-Oncogene Proteins c-mycAnimalsAutocrine CommunicationCell Line, TumorCell ProliferationDisease ProgressionFemaleGene Expression Regulation, NeoplasticGlycolysisHumansMaleMiceCollagen Type IHIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitIntegrin alpha3MYC protein, humanProto-Oncogene Proteins c-myc

Identifiers

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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.