Evidence map›Paper›PMID 33455075›Full record

ArticleFEBS open bio2021

Inhibition of galectin-3 augments the antitumor efficacy of PD-L1 blockade in non-small-cell lung cancer.

Hongxin Zhang, Pengfei Liu, Yan Zhang, Lujun Han, Zhihui Hu, Ziqi Cai, Jianhui Cai

Open access · goldAbstract read
In one paragraph

Article in FEBS open bio, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

22 citing papers in PubMed, 24 citations in OpenAlex.

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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

7 authors at 4 institutions in 1 country.

Hongxin ZhangDepartment of Surgery, Hebei Medical University, Shijiazhuang, China.
Pengfei LiuDepartment of Oncology, Tianjin Academy of Traditional Chinese Medicine Affiliated Hospital, China.
Yan ZhangDepartment of Oncology, Shijiazhuang First Hospital, China.
Lujun HanDepartment of Oncology, Shijiazhuang First Hospital, China.
Zhihui HuDepartment of Oncology, Shijiazhuang First Hospital, China.
Ziqi CaiHebei Engineering Technology Research Center for Cell Therapy, Hebei HOFOY Bio-Tech Co. Ltd, Shijiazhuang, China.
Jianhui CaiDepartment of Surgery, Hebei Medical University, Shijiazhuang, China.ORCID 0000-0001-5683-8855
First Hospital of Shijiazhuang · CNHebei Medical University · CNChina Academy of Traditional Chinese Medicine Hospital of Ophthalmology · CNHebei Science and Technology Department · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multiple clinical trials have shown that monoclonal antibodies (mAbs) against programmed death-ligand 1 (PD-1/PD-L1) can benefit patients with lung cancer by increasing their progression-free survival and overall survival. However, a significant proportion of patients do not respond to anti-PD-1/PD-L1 mAbs. In the present study, we investigated whether galectin (Gal)-3 inhibitors can enhance the antitumor effect of PD-L1 blockade. Using the NSCLC-derived cell line A549, we examined the expression of Gal-3 in lung cancer cells under hypoxic conditions and investigated the regulatory effect of Gal-3 on PD-L1 expression, which is mediated by the STAT3 pathway. We also explored whether Gal-3 inhibition can facilitate the cytotoxic effect of T cells induced by PD-L1 blockade. The effects of combined use of a Gal-3 inhibitor and PD-L1 blockade on tumor growth and T-cell function were also investigated, and we found that hypoxia increased the expression and secretion of Gal-3 by lung cancer cells. Gal-3 increased PD-L1 expression via the upregulation of STAT3 phosphorylation, and administration of a Gal-3 inhibitor enhanced the effect of PD-L1 blockade on the cytotoxic activity of T cells against cancer cells in vitro. In a mouse xenograft model, the combination of a Gal-3 inhibitor and PD-L1 blockade synergistically suppressed tumor growth. Furthermore, the administration of a Gal-3 inhibitor enhanced T-cell infiltration and granzyme B release in tumors. Collectively, our results show that Gal-3 increases PD-L1 expression in lung cancer cells and that the administration of a Gal-3 inhibitor as an adjuvant enhanced the antitumor activity of PD-L1 blockade.

Indexed as

A549 CellsAnimalsB7-H1 AntigenCarcinoma, Non-Small-Cell LungCell Line, TumorCell MovementCell ProliferationGalectin 3Gene Expression Regulation, NeoplasticHumansImmune Checkpoint InhibitorsLung NeoplasmsMicePhosphorylationSmall Molecule LibrariesSTAT3 Transcription FactorB7-H1 AntigenCD274 protein, humanGalectin 3Immune Checkpoint InhibitorsSmall Molecule LibrariesSTAT3 protein, humanSTAT3 Transcription Factorgalectin-3immunotherapylung cancerNSCLCPD-L1tumor

Identifiers

PMID33455075
PMCPMC7931229
OpenAlexW3122904380

What OpenQuestion 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 OpenQuestion graph.