Evidence map›Paper›PMID 41039015›Full record

ArticleCancer gene therapy2025

Demethoxycurcumin suppresses HK2-mediated glycolysis by targeting PTEN/Akt signaling.

Jinzhuang Liao, Shiming Tan, Shuangze Han, Ruirui Wang, Pengfei Guo, Wei Zheng, Xinfang Yu, Wei Li

Abstract read
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In one paragraph

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 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

8 authors.

Jinzhuang Liao *Department of Radiology, The Third Xiangya Hospital of Central South University, Changsha, Hunan, China.ORCID http://orcid.org/0000-0002-8377-8269
Shiming Tan *Department of Radiology, The Third Xiangya Hospital of Central South University, Changsha, Hunan, China.
Shuangze HanDepartment of Radiology, The Third Xiangya Hospital of Central South University, Changsha, Hunan, China.
Ruirui WangDepartment of Radiology, The Third Xiangya Hospital of Central South University, Changsha, Hunan, China.
Pengfei GuoDepartment of Radiology, The Third Xiangya Hospital of Central South University, Changsha, Hunan, China.
Wei ZhengDepartment of Radiology, The Third Xiangya Hospital of Central South University, Changsha, Hunan, China.
Xinfang YuKey Laboratory of Carcinogenesis and Cancer Invasion of Chinese Ministry of Education, Xiangya Hospital, Central South University, Changsha, China.
Wei LiDepartment of Radiology, The Third Xiangya Hospital of Central South University, Changsha, Hunan, China. weililx@csu.edu.cn.ORCID http://orcid.org/0000-0002-7267-6494

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aerobic glycolysis is a hallmark of tumor cells, with the expression of glycolytic enzymes often being upregulated in many cancers, leading to enhanced metabolic activity. Among the key rate-limiting enzymes in this process, Hexokinase 2 (HK2) plays a crucial role in sustaining the biological activities of human cancers. Therefore, HK2 is considered a potential therapeutic target, although effective targeted drugs for oral squamous cell carcinoma (OSCC) treatment are currently lacking. To confirm potent anti-tumor agents that inhibit HK2 expression, we screened a library of 639 natural products and discovered that Demethoxycurcumin (Deme) was the most effective anti-tumor agent via inhibiting HK2-mediated glycolysis in OSCC cells, inducing intrinsic apoptosis. Mechanistically, Deme enhanced the interaction between USP13 and PTEN, leading to the stabilization of PTEN and consequent downregulation of HK2 via the PTEN/Akt/HK2 pathway. Notably, HK2 overexpression reversed the inhibitory effect of Deme on OSCC cells. Furthermore, at the tumor-inhibitory dose, Deme showed no effect on non-tumor HaCat cells. In vivo, Deme significantly suppressed tumor growth without apparent toxicity to vital organs. Together, these data suggest that Deme is a promising and safe anti-tumor compound that downregulates HK2 expression, providing a potential therapeutic strategy for OSCC treatment.

Indexed as

DiarylheptanoidsGlycolysisHexokinaseMouth NeoplasmsProto-Oncogene Proteins c-aktPTEN PhosphohydrolaseAnimalsApoptosisCell Line, TumorHumansMiceMice, NudeSignal TransductionXenograft Model Antitumor AssaysdemethoxycurcuminDiarylheptanoidsHexokinaseHK2 protein, humanProto-Oncogene Proteins c-aktPTEN PhosphohydrolasePTEN protein, human

Identifiers

PMID41039015

What Socratic holds

Textmetadata
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.