Evidence map›Paper›PMID 37423604›Full record

ArticleThoracic cancer2023

Salidroside suppresses the multiple oncogenic activates and immune escape of lung adenocarcinoma through the circ_0009624-mediated PD-L1 pathway.

Guilin Jin, Mi Ma, Chunyan Yang, Luo Zhen, Mingke Feng

Open access · goldAbstract read
In one paragraph

Article in Thoracic cancer, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

3 citing papers in PubMed, 7 citations in OpenAlex.

  1. Open life sciences · 2025
    Article
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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

5 authors at 1 institution in 1 country.

Guilin JinUniversity of Tibetan Medicine, Lhasa, China.
Mi MaUniversity of Tibetan Medicine, Lhasa, China.
Chunyan YangUniversity of Tibetan Medicine, Lhasa, China.
Luo ZhenUniversity of Tibetan Medicine, Lhasa, China.
Mingke FengUniversity of Tibetan Medicine, Lhasa, China.ORCID 0009-0006-5393-0617
Tibetan Traditional Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLung adenocarcinoma (LUAD) is a fatal malignancy all over the world. Salidroside (SAL) is an active component extracted from Rhodiola rosea that has been reported to exert antitumor activity against several human cancers, containing lung adenocarcinoma (LUAD). The purpose of this study was to explore the effect and underlying mechanism of SAL in LUAD.

methodsCell viability, proliferation, migration, and invasion were measured using cell counting kit-8 (CCK-8), 5-ethynyl-2'-deoxyuridine (EdU), and transwell assays. Effects of LUAD cells on the cytotoxicity, percentage, and death of CD8

resultsSAL restrained LUAD cell proliferation, migration, invasion, and immune escape in vitro via modulating PD-L1. Circ_0009624 expression was increased in LUAD. Applying SAL repressed circ_0009624 and PD-L1 expression in LUAD cells. SAL treatment hindered suppressed various oncogenic activates and immune escape of LUAD cells by regulating the circ_0009624/PD-L1 pathway. SAL blocked LUAD xenograft growth in vivo.

conclusionApplying SAL might constrain malignant phenotypes and immune escape of LUAD cells partially through the circ_0009624-mediated PD-L1 pathway, providing a novel insight for LUAD treatment.

Indexed as

Adenocarcinoma of LungLung NeoplasmsB7-H1 AntigenCell Line, TumorCell ProliferationGlucosidesHumansPhenolsB7-H1 AntigenGlucosidesPhenolsrhodiolosideCirc_0009624LUADPD-L1salidroside

Identifiers

PMID37423604
PMCPMC10447170
OpenAlexW4383682732

What OpenQuestion 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 OpenQuestion graph.