Evidence map›Paper›PMID 39261409›Full record

ArticleMolecular and cellular biochemistry2025

Transcription factor Yin Yang 1 enhances epithelial-mesenchymal transition, migration, and stemness of non-small cell lung cancer cells by targeting sonic hedgehog.

Tonghai Huang, Kangqi Ren, Xiean Ling, Zeyao Li, Lin Chen

Abstract read
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In one paragraph

Article in Molecular and cellular biochemistry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

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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

1 citing paper in PubMed.

  1. 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.

Tonghai HuangDepartment of Thoracic Surgery, Shenzhen People's Hospital, 1st Affiliated Hospital of Southern University of Science and Technology, 2, Clinical Medical College of Jinan University, No.1017, East Gate Rd, Shenzhen, 518020, Guangdong, China. tonghaihuang@aliyun.com.
Kangqi RenDepartment of Thoracic Surgery, Shenzhen People's Hospital, 1st Affiliated Hospital of Southern University of Science and Technology, 2, Clinical Medical College of Jinan University, No.1017, East Gate Rd, Shenzhen, 518020, Guangdong, China.
Xiean LingDepartment of Thoracic Surgery, Shenzhen People's Hospital, 1st Affiliated Hospital of Southern University of Science and Technology, 2, Clinical Medical College of Jinan University, No.1017, East Gate Rd, Shenzhen, 518020, Guangdong, China.
Zeyao LiDepartment of Thoracic Surgery, Shenzhen People's Hospital, 1st Affiliated Hospital of Southern University of Science and Technology, 2, Clinical Medical College of Jinan University, No.1017, East Gate Rd, Shenzhen, 518020, Guangdong, China.
Lin ChenDepartment of Thoracic Surgery, Shenzhen People's Hospital, 1st Affiliated Hospital of Southern University of Science and Technology, 2, Clinical Medical College of Jinan University, No.1017, East Gate Rd, Shenzhen, 518020, Guangdong, China.

Funding

Natural Science Foundation of Shenzhen JCYJ20190806154601642
6 · The paper itself

Abstract

Non-small cell lung cancer (NSCLC) is a frequent type of lung cancer. Transcription factor Yin Yang 1 (YY1), an endogenous transcription factor containing zinc finger structure, can accelerate NSCLC progression. However, the impact of YY1 on the stemness of NSCLC cells and the mechanism of promoting NSCLC cell progression is unclear. YY1 and Sonic hedgehog (Shh) expressions were monitored by RT-qPCR, western blot, and immunohistochemistry. Overall survival was tested through Kaplan-Meier analysis. The interaction between YY1 and Shh was confirmed. Then, cell migration, stemness, and epithelial-mesenchymal transition (EMT) were assessed with functional experiments in vitro and in vivo. YY1 and Shh were highly expressed in NSCLC tissues and positively correlated with the poor OS of NSCLC patients. Functional experiments denoted that YY1 or Shh overexpression could accelerate EMT, migration, and stemness of NSCLC cells, and YY1 or Shh knockdown played the opposite role to its overexpression. Mechanism analysis disclosed that Shh, as a target gene of YY1, was positively related to YY1. The rescued experiment manifested that Shh silencing could reverse the induction effect of YY1 overexpression on EMT, migration, and stemness of NSCLC cells. In vivo experiments also confirmed that YY1 could accelerate tumor growth and EMT and weaken apoptosis. YY1 promotes NSCLC EMT, migration, and stemness by Shh, which might be novel diagnostic markers and therapeutic targets for NSCLC therapy.

Indexed as

Carcinoma, Non-Small-Cell LungCell MovementEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticHedgehog ProteinsLung NeoplasmsNeoplasm ProteinsNeoplastic Stem CellsYY1 Transcription FactorA549 CellsAnimalsCell Line, TumorFemaleHumansMaleMiceHedgehog ProteinsNeoplasm ProteinsSHH protein, humanYY1 protein, humanYY1 Transcription FactorEMTNSCLCShhStemnessYY1

Identifiers

PMID39261409

What Socratic 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 Socratic graph.