Evidence map›Paper›PMID 42368569›Full record

ArticleActa pharmaceutica Sinica. B2026

Syringin disrupts the DLAT/MYC axis to dampen TAM polarization and suppress hepatocellular carcinoma progression.

Lingyun Xiao, Jiawei Lv, Yuan Lu, Zun Li, Liang-Mei Yang, Zheng Li, Shu Liang, Ke-Bin Huang, Xiongjun Wang

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Acta pharmaceutica Sinica. B, 2026. 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

9 authors.

Lingyun XiaoPrecise Genome Engineering Center, School of Life Sciences, Guangzhou University, Guangzhou 510006, China.
Jiawei LvPrecise Genome Engineering Center, School of Life Sciences, Guangzhou University, Guangzhou 510006, China.
Yuan LuKey Laboratory for Chemistry and Molecular Engineering of Medicinal Resources (Ministry of Education of China), Guangxi Key Laboratory of Chemistry and Molecular Engineering of Medicinal Resources, School of Chemistry and Pharmaceutical Sciences, Guangxi Normal University, Guilin 541004, China.
Zun LiPrecise Genome Engineering Center, School of Life Sciences, Guangzhou University, Guangzhou 510006, China.
Liang-Mei YangKey Laboratory for Chemistry and Molecular Engineering of Medicinal Resources (Ministry of Education of China), Guangxi Key Laboratory of Chemistry and Molecular Engineering of Medicinal Resources, School of Chemistry and Pharmaceutical Sciences, Guangxi Normal University, Guilin 541004, China.
Zheng LiPrecise Genome Engineering Center, School of Life Sciences, Guangzhou University, Guangzhou 510006, China.
Shu LiangPrecise Genome Engineering Center, School of Life Sciences, Guangzhou University, Guangzhou 510006, China.
Ke-Bin HuangKey Laboratory for Chemistry and Molecular Engineering of Medicinal Resources (Ministry of Education of China), Guangxi Key Laboratory of Chemistry and Molecular Engineering of Medicinal Resources, School of Chemistry and Pharmaceutical Sciences, Guangxi Normal University, Guilin 541004, China.
Xiongjun WangPrecise Genome Engineering Center, School of Life Sciences, Guangzhou University, Guangzhou 510006, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumor-associated macrophages (TAMs) are pivotal drivers of hepatocellular carcinoma (HCC) progression, and blocking TAM M2 polarization has the potential to dampen tumor microenvironment remodeling. In this study, we screened a series of phenylethanoid and phenylpropanoid glycosides and identified syringin as a natural compound capable of inhibiting M2 polarization while promoting M1 polarization in macrophages. Single-cell RNA sequencing confirmed that syringin reduced TAM M2 polarization and significantly impaired tumor microenvironment remodeling. In detail, syringin indirectly reduced the stability of MYC proto-oncogene protein (MYC), which is required for driving a broad set of targets, including

Indexed as

Dihydrolipoamide S-acetyltransferase (DLAT)Hepatocellular carcinoma (HCC)Macrophage polarizationMYC degradationSingle-cell RNA sequencing (scRNA-seq)SyringinTumor-associated macrophages (TAMs)Tumor microenvironment (TME)

Identifiers

PMID42368569
PMCPMC13304691

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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.