Evidence map›Paper›PMID 40520181›Full record

ArticleFrontiers in pharmacology2025

HGF/c-MET axis contributes to CLL cell survival by regulating multiple mechanisms making it a potential therapeutic target for CLL treatment.

Shihao Liang, Xiaoya Shao, Xueqiong Meng, Ying Cui, Chuanyue Sun, Jie Sun, Binghui Zhang, Guomin Shen, Ling Qin, Haiping Yang and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in pharmacology, 2025. 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. 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

11 authors.

Shihao Liang *Henan International Joint Laboratory of Thrombosis and Hemostasis, School of Basic Medical Sciences, Henan University of Science and Technology, Luoyang, China.
Xiaoya Shao *The Second Affiliated Hospital, Henan University of Science and Technology, Luoyang, China.
Xueqiong MengLuoyang Key Laboratory of POCT Diagnostic Technology, Luoyang Polytechnic, Luoyang, China.
Ying CuiHenan International Joint Laboratory of Thrombosis and Hemostasis, School of Basic Medical Sciences, Henan University of Science and Technology, Luoyang, China.
Chuanyue SunHenan International Joint Laboratory of Thrombosis and Hemostasis, School of Basic Medical Sciences, Henan University of Science and Technology, Luoyang, China.
Jie SunHenan International Joint Laboratory of Thrombosis and Hemostasis, School of Basic Medical Sciences, Henan University of Science and Technology, Luoyang, China.
Binghui ZhangHenan International Joint Laboratory of Thrombosis and Hemostasis, School of Basic Medical Sciences, Henan University of Science and Technology, Luoyang, China.
Guomin ShenHenan International Joint Laboratory of Thrombosis and Hemostasis, School of Basic Medical Sciences, Henan University of Science and Technology, Luoyang, China.
Ling QinThe First Affiliated Hospital, Henan University of Science and Technology, Luoyang, China.
Haiping YangThe First Affiliated Hospital, Henan University of Science and Technology, Luoyang, China.
Yixiang ChenHenan International Joint Laboratory of Thrombosis and Hemostasis, School of Basic Medical Sciences, Henan University of Science and Technology, Luoyang, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Despite significant advances in understanding the occurrence, progression and treatment of chronic lymphocytic leukemia (CLL), there remains a need to explore novel mechanisms and therapeutic strategies. In this study, we discovered that hepatocyte growth factor (HGF), a cytokine highly expressed by bone marrow mesenchymal stem cells within the microenvironment, activates the AKT, ERK and STAT3 signaling pathways, promotes the expression of anti-apoptotic proteins BCL-2, MCL-1, and BCL-xL, thereby enhancing CLL cell survival and resistance to both natural and ABT-199-induced apoptosis. Knockdown of c-MET, the unique receptor for HGF, using lentivirus-mediated shRNA, significantly attenuated the activation of these pro-survival signaling pathways and downregulated the expression of anti-apoptotic proteins in the BCL-2 family. Consequently, this inhibited CLL cell proliferation and promoted apoptosis. Similarly, pharmacological targeting of the HGF/c-MET pathway with the inhibitor capmatinib markedly suppressed the activation of pro-survival signaling pathways, reduced the expression of anti-apoptotic proteins, inhibited cell proliferation, arrested cell cycle at G0/G1 stage, induced apoptosis, and enhanced the pro-apoptotic effect of ABT-199. In summary, this study highlights the critical role of HGF/c-MET axis in CLL cell survival and demonstrates that targeting this pathway holds therapeutic potential for the treatment of CLL.

Indexed as

anti-apoptotic proteinscapmatinibchronic lymphocytic leukemiaHGF/c-Metsignaling pathway

Identifiers

PMID40520181
PMCPMC12162569

What Socratic holds

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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 Socratic graph.