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Peer-reviewedCC BY 4.0Biomolecules

Quinaldic Acid Inhibits A549 Lung Cancer Cell Growth Through S-Phase Accumulation and Apoptosis

  • Songyuan Li1
  • Lingmin Wang1
  • Liangliang Bao2
  • Hanwen He1
  • Yuting Zhao1
  • Yi Qu1
  • Lele Zhang1
  • Min Ma1
  • Huirong Liu1
  1. 1College of Life Sciences, Inner Mongolia Agricultural University, No. Zhaowuda Road, Saihan District, Hohhot 010008, China
  2. 2College of Science, Inner Mongolia Agricultural University, Hohhot 010008, China
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Abstract

Myxobacteria are prolific producers of structurally diverse secondary metabolites and represent a valuable source of anticancer lead compounds. In this study, quinaldic acid (QA) was putatively annotated from a myxobacterial metabolite extract by LC–MS/MS spectral matching and evaluated for its antitumor activity against non-small cell lung cancer (NSCLC) cells. QA inhibited the viability of four tumor cell lines in a concentration-dependent manner, with A549 lung adenocarcinoma cells displaying the highest sensitivity, with an IC50 of 1.07 mM after 24 h of treatment. QA also significantly suppressed clonogenic growth in A549 cells. Network pharmacology analysis suggested that QA may regulate NSCLC-related targets and pathways involved in cell-cycle control, apoptosis, p53, JAK–STAT, and NF-κB signaling. Experimental validation showed that QA induced S-phase accumulation in A549 cells, increasing the S-phase population by 14.70 percentage points at 4 mM. This effect was accompanied by increased cyclin A1 expression and decreased cyclin B1 and CDK1 expression. QA also promoted apoptosis in a concentration-dependent manner, increasing the apoptotic population by 40.40 percentage points at 2 mM. Apoptosis was associated with elevated BAX and caspase-3 expression and reduced BCL-2 expression. These findings suggest that QA suppresses A549 cell growth by inducing S-Phase accumulation and apoptosis, supporting its potential as a myxobacteria-derived anticancer scaffold.

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Cite

BibTeXRIS
BibTeX
@article{li2026quinaldic,
  title = {{Quinaldic Acid Inhibits A549 Lung Cancer Cell Growth Through S-Phase Accumulation and Apoptosis}},
  author = {Songyuan Li and Lingmin Wang and Liangliang Bao and Hanwen He and Yuting Zhao and Yi Qu and Lele Zhang and Min Ma and Huirong Liu},
  journal = {Biomolecules},
  year = {2026},
  month = oct,
  doi = {10.3390/biom16111551},
  url = {https://www.mdpi.com/2218-273X/16/11/1551},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Quinaldic Acid Inhibits A549 Lung Cancer Cell Growth Through S-Phase Accumulation and Apoptosis
AU  - Songyuan Li
AU  - Lingmin Wang
AU  - Liangliang Bao
AU  - Hanwen He
AU  - Yuting Zhao
AU  - Yi Qu
AU  - Lele Zhang
AU  - Min Ma
AU  - Huirong Liu
PY  - 2026
DA  - 2026/10/23
JO  - Biomolecules
DO  - 10.3390/biom16111551
UR  - https://www.mdpi.com/2218-273X/16/11/1551
AB  - Myxobacteria are prolific producers of structurally diverse secondary metabolites and represent a valuable source of anticancer lead compounds. In this study, quinaldic acid (QA) was putatively annotated from a myxobacterial metabolite extract by LC–MS/MS spectral matching and evaluated for its antitumor activity against non-small cell lung cancer (NSCLC) cells. QA inhibited the viability of four tumor cell lines in a concentration-dependent manner, with A549 lung adenocarcinoma cells displaying the highest sensitivity, with an IC50 of 1.07 mM after 24 h of treatment. QA also significantly suppressed clonogenic growth in A549 cells. Network pharmacology analysis suggested that QA may regulate NSCLC-related targets and pathways involved in cell-cycle control, apoptosis, p53, JAK–STAT, and NF-κB signaling. Experimental validation showed that QA induced S-phase accumulation in A549 cells, increasing the S-phase population by 14.70 percentage points at 4 mM. This effect was accompanied by increased cyclin A1 expression and decreased cyclin B1 and CDK1 expression. QA also promoted apoptosis in a concentration-dependent manner, increasing the apoptotic population by 40.40 percentage points at 2 mM. Apoptosis was associated with elevated BAX and caspase-3 expression and reduced BCL-2 expression. These findings suggest that QA suppresses A549 cell growth by inducing S-Phase accumulation and apoptosis, supporting its potential as a myxobacteria-derived anticancer scaffold.
SN  - 2218-273X
ER  -