Evidence map›Paper›PMID 40603870›Full record

ArticleCell death discovery2025

DNMBP-AS1/hsa-miR-30a-5p/PGC1α axis suppresses tumor progression of colorectal cancer by inhibiting PKM2-mediated Warburg effect and enhance anti-PD-1 therapy efficacy.

Tianxiao Wang, Wenxin Zhang, Jiafeng Liu, Xiang Mao, Xinhai Wang, Jiyifan Li, Yuxin Huang, Zimei Wu, Haifei Chen, Huanying Shi and 3 more

Abstract read
In one paragraph

Article in Cell death discovery, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Article
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  4. Review
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.

Tianxiao Wang *Department of Pharmacy, Huashan Hospital, Fudan University, Shanghai, China.
Wenxin Zhang *Department of Pharmacy, Huashan Hospital, Fudan University, Shanghai, China.
Jiafeng LiuDepartment of Pharmacy, Huashan Hospital, Fudan University, Shanghai, China.
Xiang MaoDepartment of Surgery, Huashan Hospital, Fudan University, Shanghai, China.
Xinhai WangDepartment of Surgery, Huashan Hospital, Fudan University, Shanghai, China.
Jiyifan LiDepartment of Pharmacy, Huashan Hospital, Fudan University, Shanghai, China.
Yuxin HuangDepartment of Pharmacy, Huashan Hospital, Fudan University, Shanghai, China.
Zimei WuDepartment of Pharmacy, Huashan Hospital, Fudan University, Shanghai, China.
Haifei ChenDepartment of Pharmacy, Huashan Hospital, Fudan University, Shanghai, China.ORCID http://orcid.org/0009-0005-6633-5107
Huanying ShiDepartment of Pharmacy, Huashan Hospital, Fudan University, Shanghai, China.ORCID http://orcid.org/0009-0001-5646-0140
Huijie QiDepartment of Pharmacy, Huashan Hospital, Fudan University, Shanghai, China.
Lu ChenDepartment of Pharmacy, Huashan Hospital, Fudan University, Shanghai, China. chenlu7091@126.com.
Qunyi LiDepartment of Pharmacy, Huashan Hospital, Fudan University, Shanghai, China. qyli1234@163.com.ORCID http://orcid.org/0000-0001-5522-1562

Funding

National Natural Science Foundation of China (National Science Foundation of China) 72402058National Natural Science Foundation of China (National Science Foundation of China) 81901399Natural Science Foundation of Shanghai (Natural Science Foundation of Shanghai Municipality) 24ZR1408100
6 · The paper itself

Abstract

The Warburg effect, which is aerobic glycolysis, constitutes a major driver of various cancer progression. Therefore, we aimed to examine the role of peroxisome proliferator-activated receptor-gamma coactivator-1α (PGC1α) and its competing endogenous RNA (ceRNA) network in colorectal cancer (CRC) metabolic reprogramming. We used bioinformatics analysis and dual-luciferase reporter gene experiments and identified the DNMBP-AS1/hsa-miR-30a-5p/PGC1α ceRNA network. Additionally, we investigate the impact of PGC1α expression alterations on CRC proliferation and metabolic reprogramming. Moreover, we studied the influence of PGC1α on pyruvate kinase M2 (PKM2), and CRC malignant behavior manifestation. Our study has uncovered a significant association between the DNMBP-AS1/hsa-miR-30a-5p/PGC1α ceRNA network and CRC patient prognosis. Additionally, PGC1α overexpression impeded CRC growth, reduced glycolytic capacity, and enhanced anti-PD-1 therapy efficacy. PGC1α inhibited tumor cell glycolysis by downregulating the WNT/β-catenin pathway depending on peroxisome proliferator-activated receptor gamma (PPARγ), thereby suppressing PKM2. The PPARγ agonist rosiglitazone could hinder CRC proliferation and glycolytic activity. Combined with the PGC1α agonist ZLN005, it exhibits synergistic effects for treating CRC. Moreover, we verified that ZLN005 significantly potentiated PD-1 induced tumor suppression in xenograft mice. Finally, we demonstrated that PGC1α and PKM2 expression patterns in tumor tissues were closely related to patient prognosis. Moreover, we constructed a predictive model to predict the 5-year survival events in CRC patients using random forest model. Our results offer novel perspectives on the role of DNMBP-AS1/hsa-miR-30a-5p/PGC1α network in controlling CRC proliferation, metabolism and immune responses. Furthermore, our investigation reveals that using rosiglitazone combined with PGC1α agonist presents a promising therapeutic approach for managing CRC.

Identifiers

PMID40603870
PMCPMC12222716

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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.