Evidence map›Paper›PMID 21949133›Full record

ArticleThe Journal of biological chemistry2011

In vitro and in vivo anticancer activity of a synthetic glycolipid as Toll-like receptor 4 (TLR4) activator.

Yong-Shiang Lin, Li-De Huang, Chao-Hsiung Lin, Po-Hsiung Huang, Yu-Jen Chen, Fen-Hwa Wong, Chun-Cheng Lin, Shu-Ling Fu

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.5field-weighted citation impact, top 19% of its field
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

11 citing papers in PubMed, 25 citations in OpenAlex.

  1. Review
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  4. Suppression of MD2 inhibits breast cancer in vitro and in vivo.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2021
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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

8 authors at 5 institutions in 1 country.

Yong-Shiang LinInstitute of Public Health, National Yang-Ming University, Taipei 11221, Taiwan; Program in Molecular Medicine, National Yang-Ming University and Academia Sinica, Taipei 11221, Taiwan.
Li-De HuangDepartment of Chemistry, National Tsing Hua University, Hsinchu 300, Taiwan.
Chao-Hsiung LinDepartment of Life Sciences and Institute of Genome Sciences, National Yang-Ming University, Taipei 11221, Taiwan.
Po-Hsiung HuangInstitute of Traditional Medicine, National Yang-Ming University, Taipei 11221, Taiwan.
Yu-Jen ChenDepartment of Radiation Oncology, Mackay Memorial Hospital, Taipei 10449, Taiwan.
Fen-Hwa WongDepartment of Life Sciences and Institute of Genome Sciences, National Yang-Ming University, Taipei 11221, Taiwan.
Chun-Cheng LinDepartment of Chemistry, National Tsing Hua University, Hsinchu 300, Taiwan. Electronic address: cclin66@mx.nthu.edu.tw.
Shu-Ling FuProgram in Molecular Medicine, National Yang-Ming University and Academia Sinica, Taipei 11221, Taiwan; Institute of Traditional Medicine, National Yang-Ming University, Taipei 11221, Taiwan. Electronic address: slfu@ym.edu.tw.
National Yang Ming Chiao Tung University · TWAcademia Sinica · TWMackay Memorial Hospital · TWNational Tsing Hua University · TWNational Yang Ming Chiao Tung University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Activation of Toll-like receptor 4 (TLR4) triggers the innate immune response and leads to the induction of adaptive immunity. TLR4 agonists are known to function as immunostimulants and exhibit promising therapeutic potential for cancer immunotherapy. We have previously developed a synthetic serine-based glycolipid (designated as CCL-34) that can activate TLR4-dependent signaling pathways. In this study, the anticancer immunity of CCL-34 was further demonstrated. CCL-34-activated macrophages induced cancer cell death via the apoptotic pathway, and this cytotoxicity was significantly inhibited by NG-monomethyl-L-arginine (an inducible NOS inhibitor). Notably, conditioned medium collected from CCL-34-treated splenocytes also induced cytotoxicity toward cancer cells. Furthermore, CCL-34 treatment suppressed tumor growth and increased the survival rate in TLR4-functional C3H/HeN mice but not in TLR4-defective C3H/HeJ mice. Increased apoptosis, the induction of cytokines (IFN-γ and IL-12) and chemokines (CXCL9 and CXCL10), and the elevation of leukocyte markers (CD11b, CD11c, CD4, and CD8) were detected at tumor sites in C3H/HeN mice but not in C3H/HeJ mice. Structure-and-activity relationship analysis of CCL-34 and its structural analogs revealed that a sugar moiety is essential for its activity. However, the substitution of the galactose in CCL-34 with glucose or fucose did not reduce its activity. Altogether, this study reveals the anticancer activity of a new synthetic TLR4 agonist and broadens the molecular basis of TLR4-activating glycolipids.

Indexed as

AnimalsAntineoplastic AgentsCarbohydratesCaspase 3Cell DeathCell LineDrug Delivery SystemsGlycolipidsHEK293 CellsHumansIn Vitro TechniquesMaleMiceMice, Inbred C3HNeoplasmsNitric Oxide Synthase Type IIAntineoplastic AgentsCarbohydratesCaspase 3CCL 34GlycolipidsNitric Oxide Synthase Type IISerineToll-Like Receptor 4

Identifiers

PMID21949133
PMCPMC3243550
OpenAlexW2082038304

What OpenQuestion 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 OpenQuestion graph.