Evidence map›Paper›PMID 39699801›Full record

ArticleCellular oncology (Dordrecht, Netherlands)2024

Exploring tumor microenvironment interactions and apoptosis pathways in NSCLC through spatial transcriptomics and machine learning.

Huimin Li, Yuheng Jiao, Yi Zhang, Junzhi Liu, Shuixian Huang

Abstract read
In one paragraph

Article in Cellular oncology (Dordrecht, Netherlands), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Article
  2. Review
  3. Beyond the membrane: rethinking EGFR signaling in physiology and cancer.Cellular and molecular life sciences : CMLS · 2026
    Review
  4. Article
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.

Huimin LiDepartment of Internal Medicine Residency Training Base, Gongli Hospital of Shanghai Pudong New Area, Shanghai, 200135, China.
Yuheng JiaoDepartment of Heart Failure, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai, 200120, China.
Yi ZhangDepartment of Otolaryngology, Gongli Hospital of Shanghai Pudong New Area, Shanghai, 200135, China.
Junzhi LiuDepartment of Otolaryngology, Gongli Hospital of Shanghai Pudong New Area, Shanghai, 200135, China. junzhil97@163.com.
Shuixian HuangDepartment of Otolaryngology, Gongli Hospital of Shanghai Pudong New Area, Shanghai, 200135, China. enthsx@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe most common type of lung cancer is non-small cell lung cancer (NSCLC), accounting for 85% of all cases. Programmed cell death (PCD), an important regulatory mechanism for cell survival and homeostasis, has become increasingly prominent in cancer research in recent years. As such, exploring the role of PCD in NSCLC may help uncover new mechanisms for therapeutic targets.

methodsWe utilized the GEO database and TCGA NSCLC gene data to screen for co-expressed genes. To delve deeper, single-cell sequencing combined with spatial transcriptomics was employed to study the intrinsic mechanisms of programmed cell death in cells and their interaction with the tumor microenvironment. Furthermore, Mendelian randomization was applied to screen for causally related genes. Prognostic models were constructed using various machine learning algorithms, and multi-cohort multi-omics analyses were conducted to screen for genes. In vitro experiments were then carried out to reveal the biological functions of the genes and their relationship with apoptosis.

resultsCells with high programmed cell death activity primarily activate pathways related to apoptosis, cell migration, and hypoxia, while also exhibiting strong interactions with smooth muscle cells in the tumor microenvironment. Based on a set of programmed cell death genes, the prognostic model NSCLCPCD demonstrates strong predictive capabilities. Moreover, laboratory experiments confirm that SLC7A5 promotes the proliferation of NSCLC cells, and the knockout of SLC7A5 significantly increases tumor cell apoptosis.

conclusionsOur data indicate that programmed cell death is predominantly associated with pathways related to apoptosis, tumor metastasis, and hypoxia. Additionally, it suggests that SLC7A5 is a significant risk indicator for the prognosis of non-small cell lung cancer (NSCLC) and may serve as an effective target for enhancing apoptosis in NSCLC tumor cells.

Indexed as

ApoptosisCarcinoma, Non-Small-Cell LungLung NeoplasmsMachine LearningTranscriptomeTumor MicroenvironmentCell Line, TumorCell ProliferationGene Expression ProfilingGene Expression Regulation, NeoplasticHumansPrognosisSignal TransductionBiomarkerCell apoptosisSingle-cell RNA sequencingSLC7A5Spatial transcriptomics

Identifiers

PMID39699801
PMCPMC12973996

What Socratic 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 Socratic graph.