# GATA6 inhibits the biological function of non-small cell lung cancer by modulating glucose metabolism

**Authors:** Weiwei Ju, Lijuan Lin, Qifang Zhang, Xiumei Lv, Shaohui Teng, Yu Hong, Zhixiang Shao, Hanyun Na, Shengjin Yu

PMC · DOI: 10.1007/s00432-024-05664-y · Journal of Cancer Research and Clinical Oncology · 2024-03-14

## TL;DR

GATA6 reduces lung cancer cell growth by affecting glucose metabolism, offering a new target for treatment.

## Contribution

This study identifies GATA6 as a novel regulator of glucose metabolism in non-small cell lung cancer.

## Key findings

- GATA6 is significantly down-regulated in lung cancer tissues and linked to poor prognosis.
- Increased GATA6 levels inhibit cancer cell proliferation and migration.
- GATA6 suppresses c-Myc mRNA, disrupting glucose metabolism in lung cancer cells.

## Abstract

This study aims to explore the role of GATA6 in lung cancer, with a focus on its impact on metabolic processes.

We assessed GATA6 expression in lung cancer tissues and its association with patient prognosis. In vitro cell function experiments were conducted to investigate the effects of altered GATA6 levels on lung cancer cell proliferation and migration. Mechanistic insights were gained by examining GATA6's influence on glucose metabolism-related genes, particularly its effect on c-Myc mRNA expression.

Our study revealed significant down-regulation of GATA6 in lung cancer tissues, and this down-regulation was strongly correlated with unfavorable patient prognosis. Elevating GATA6 levels effectively inhibited the proliferation and migration of lung cancer cells in our cell function experiments. Mechanistically, we found that GATA6 suppressed the expression of c-Myc mRNA, impacting genes related to glucose metabolism. As a result, glucose uptake and metabolism in lung cancer cells were disrupted, ultimately impeding their malignant behaviors.

Our study provides crucial insights into the metabolic regulation of GATA6 in lung cancer cells. These findings have the potential to offer a solid theoretical foundation for the development of novel clinical treatments for lung cancer.

## Linked entities

- **Genes:** GATA6 (GATA binding protein 6) [NCBI Gene 2627], MYC (MYC proto-oncogene, bHLH transcription factor) [NCBI Gene 4609]
- **Diseases:** lung cancer (MONDO:0005138), non-small cell lung cancer (MONDO:0005233)

## Full-text entities

- **Genes:** MYC (MYC proto-oncogene, bHLH transcription factor) [NCBI Gene 4609] {aka MRTL, MYCC, bHLHe39, c-Myc}, GATA6 (GATA binding protein 6) [NCBI Gene 2627]
- **Diseases:** lung cancer (MESH:D008175), non-small cell lung cancer (MESH:D002289)
- **Chemicals:** glucose (MESH:D005947)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

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## References

27 references — full list in the complete paper: https://tomesphere.com/paper/PMC10940364/full.md

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Source: https://tomesphere.com/paper/PMC10940364