Evidence map›Paper›PMID 37518006›Full record

ArticleHereditas2023

Elevated HMGB1 promotes the malignant progression and contributes to cisplatin resistance of non-small cell lung cancer.

Ying Ma, Qin Feng, Bateer Han, Rong Yu, Zhiyong Jin

Open access · goldAbstract read
In one paragraph

Article in Hereditas, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

8 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. HMGB1: A Central Node in Cancer Therapy Resistance.International journal of molecular sciences · 2025
    Review
  5. Article
  6. Review
  7. Article
  8. 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

5 authors at 1 institution in 1 country.

Ying Ma *Department of Thoracic Surgery, Affiliated People's Hospital of Inner Mongolia Medical University, No.1 Tong Dao Bei Road, Hohhot, 010059, China.
Qin Feng *Inner Mongolia Cancer Hospital and Affiliated People's Hospital of Inner Mongolia Medical University, Hohhot, 010020, China.
Bateer HanInner Mongolia Cancer Hospital and Affiliated People's Hospital of Inner Mongolia Medical University, Hohhot, 010020, China.
Rong YuInner Mongolia Cancer Hospital and Affiliated People's Hospital of Inner Mongolia Medical University, Hohhot, 010020, China.
Zhiyong JinDepartment of Thoracic Surgery, Affiliated People's Hospital of Inner Mongolia Medical University, No.1 Tong Dao Bei Road, Hohhot, 010059, China. nyfyjinzhiyong@163.com.ORCID http://orcid.org/0000-0003-2808-5934
Inner Mongolia Medical University · CN

Funding

Autonomous region health science and technology plan projects of Health Commission of Inner Mongolia(2022) 202201289Autonomous region health science and technology plan projects of Health Commission of Inner Mongolia(2022) 202201363Million-dollar joint projects of Inner Mongolia Medical University YKD2021LH035
6 · The paper itself

Abstract

backgroundHMGB1 (high mobility group box B-1) exhibits crucial role in tumor genesis and development, including lung cancer. Whereas, more HMGB1-related details in non-small cell lung cancer (NSCLC) are still largely unclear.

methodsThe HMGB1 and inflammatory factors in malignant (MPE) and non-malignant pleural effusion (BPE) were determined by ELISA. Additionally, qRT-PCR, western blot, or immunohistochemistry were used to determine HMGB1, drug-resistant and apoptotic proteins' expressions in NSCLC A549, A549-DDP cell lines, and xenograft model. Cell viability, migration/ invasion, and apoptosis were analyzed using MTT, Transwell, and flow cytometry assays, respectively.

resultsInflammatory factors and HMGB1 expressions in MPE were significantly higher than BPE of NSCLC. Compared with preoperative and adjacent tissues, significantly higher HMGB1, drug-resistant protein, and anti-apoptotic protein expressions were observed in recurrent tissues. Overexpressed HMGB1 induced NSCLC cells to exhibit stronger aggressive, proliferative, and drug-resistant features. The related abilities were reversed when HMGB1 was interfered. Overexpressed HMGB1 showed a similar co-localization with drug resistant protein P-gp in cytoplasm in xenograft model, while low HMGB1 expression localized in cell nucleus.

conclusionsHMGB1 overexpression significantly promoted the malignant progression and cisplatin resistance of NSCLC in vitro and in vivo.

Indexed as

Carcinoma, Non-Small-Cell LungHMGB1 ProteinLung NeoplasmsMicroRNAsAnimalsApoptosisCell Line, TumorCisplatinDrug Resistance, NeoplasmHumansCisplatinHMGB1 ProteinHMGB1 protein, humanMicroRNAsCisplatinHigh mobility group B1 (HMGB1)Multidrug resistance (MDR)Non-small cell lung cancer (NSCLC)

Identifiers

PMID37518006
PMCPMC10388484
OpenAlexW4385397713

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.