# Regulatory mechanism and expression level of PRPS2 in lung cancer

**Authors:** Ying Meng, Hua Zhang, Mingling Xu, Zhenzhen Chen, Lei Wei

PMC · DOI: 10.1111/1759-7714.15302 · Thoracic Cancer · 2024-05-12

## TL;DR

This study shows that PRPS2 is overactive in lung cancer and that reducing its levels can slow cancer growth and spread, suggesting it could be a new target for treatment.

## Contribution

The study identifies PRPS2 as a potential novel biomarker for lung cancer treatment and diagnosis.

## Key findings

- PRPS2 is upregulated in lung cancer tissues compared to normal tissues.
- PRPS2 silencing inhibits cancer cell proliferation, migration, invasion, and tumor growth in vivo.
- PRPS2 knockdown increases apoptosis in lung cancer cells.

## Abstract

Lung cancer, with high morbidity and mortality, is the commonest respiratory system neoplasm, which seriously endangers the life safety of patients. In this study, the effect of PRPS2 on cell progression was preliminarily investigated.

Immunohistochemical staining, western blot and reverse transcription‐quantitative polymerase chain reaction (RT‐qPCR) were performed to verify the expression level of PRPS2 in lung cancer. Lung cancer cell lines with stable downregulation of PRPS2 were constructed in A549 cells and NCIH460 cells. The function of PRPS2 silencing on the proliferation ability was verified by the EdU and cell colony formation experiment. Scratch and transwell tests were conducted to verify the role of PRPS2 silencing on the migratory and invasive ability of cells. The impact of PRPS2 silencing on cell apoptosis and cell cycle was verified by flow cytometry test. The effects of PRPS2 silencing on apoptosis‐associated proteins were assessed by western blot assay. The function of PRPS2 silencing on tumor growth in vivo was studied through xenograft tumor experiment.

In comparison with normal tissues, PRPS2 was upregulated in lung cancer tissues. PRPS2 knockdown notably hindered the migratory ability, invasive ability and proliferation, but accelerated cell apoptosis. In vivo experiments confirmed that PRPS2 silencing blocked the growth of transplanted tumors.

In lung cancer, PRPS2 silencing suppressed the malignant progression, indicating that PRPS2 might be a novel biomarker for lung cancer treatment and diagnosis.

PRPS2 knockdown significantly accelerated the apoptosis of lung cancer cells, but inhibited the proliferation, migration and invasion of lung cancer cells in vitro and the growth of transplanted tumors in vivo.

## Linked entities

- **Genes:** PRPS2 (phosphoribosyl pyrophosphate synthetase 2) [NCBI Gene 5634]
- **Diseases:** lung cancer (MONDO:0005138)

## Full-text entities

- **Genes:** PRPS2 (phosphoribosyl pyrophosphate synthetase 2) [NCBI Gene 5634] {aka PRSII}
- **Diseases:** Lung cancer (MESH:D008175), tumor (MESH:D009369), respiratory system neoplasm (MESH:D012142)
- **Species:** Homo sapiens (human, species) [taxon 9606]
- **Cell lines:** NCIH460 — Homo sapiens (Human), Lung large cell carcinoma, Cancer cell line (CVCL_0459), A549 — Homo sapiens (Human), Lung adenocarcinoma, Cancer cell line (CVCL_0023)

## Full text

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## Figures

5 figures with captions in the complete paper: https://tomesphere.com/paper/PMC11194120/full.md

## References

25 references — full list in the complete paper: https://tomesphere.com/paper/PMC11194120/full.md

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Source: https://tomesphere.com/paper/PMC11194120