# Ampelopsis japonica enhances the effect of radiotherapy in non-small cell lung cancer

**Authors:** Zhaohua Liu, Peixia Cui, Qian Wu, Xiao Ji

PMC · DOI: 10.1007/s00066-024-02322-7 · Strahlentherapie Und Onkologie · 2024-12-04

## TL;DR

Ampelopsis japonica improves radiotherapy effectiveness in non-small cell lung cancer by inhibiting the PI3K-Akt signaling pathway.

## Contribution

This study demonstrates that Ampelopsis japonica enhances radiotherapy outcomes in NSCLC through modulation of the PI3K-Akt pathway.

## Key findings

- Ampelopsis japonica enhances radiotherapy's inhibition of NSCLC tumor growth in mice.
- AJ increases radiotherapy-induced apoptosis in NSCLC cells.
- AJ suppresses the PI3K-Akt signaling pathway in combination with radiotherapy.

## Abstract

Radiotherapy is widely used in the clinical treatment of non-small cell lung cancer (NSCLC); however, its effectiveness often proves unsatisfactory. Ampelopsis japonica (AJ) is a traditional Chinese herb with anti-inflammatory and anticancer activities. However, whether AJ could enhance the effect of radiotherapy in NSCLC needs to be further explored.

In vivo, BALB/c nude mice were used for a xenograft tumor model to explore whether AJ could enhance the effect of radiation therapy (RT) in NSCLC. In vitro, human NSCLC cell lines HCC827 and H1299 were used to explore the effect of AJ on the cell proliferation and apoptosis of RT-treated NSCLC. Moreover, bioinformatic analysis was performed to analyze the signaling pathways regulated by AJ.

Ampelopsis japonica enhanced the inhibitory effect of RT on NSCLC tumor growth in vivo. Simultaneously, AJ further enhanced the inhibitory effect of RT on NSCLC proliferation and the promoting effect of RT on NSCLC apoptosis. Bioinformatic analysis showed that AJ regulated the PI3K-Akt signaling pathway. We confirmed that AJ decreased the protein levels of the PI3K-Akt signaling pathway. Furthermore, the combination of AJ and RT suppressed activation of the PI3K-Akt signaling pathway.

Ampelopsis japonica augmented the inhibitory impact of RT on NSCLC cell proliferation and tumor growth by suppressing the PI3K-Akt signaling pathway.

## Linked entities

- **Proteins:** PIK3CA (phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha), AKT1 (AKT serine/threonine kinase 1)
- **Diseases:** non-small cell lung cancer (MONDO:0005233)
- **Species:** Homo sapiens (taxon 9606)

## Full-text entities

- **Genes:** AKT1 (AKT serine/threonine kinase 1) [NCBI Gene 207] {aka AKT, PKB, PKB-ALPHA, PRKBA, RAC, RAC-ALPHA}
- **Diseases:** inflammatory (MESH:D007249), NSCLC (MESH:D002289), tumor (MESH:D009369)
- **Chemicals:** herb (-)
- **Species:** Ampelopsis japonica (species) [taxon 714442], Mus musculus (house mouse, species) [taxon 10090], Homo sapiens (human, species) [taxon 9606]
- **Cell lines:** H1299 — Homo sapiens (Human), Lung large cell carcinoma, Cancer cell line (CVCL_0060), BALB/c — Mus musculus (Mouse), Spontaneously immortalized cell line (CVCL_0184), HCC827 — Homo sapiens (Human), Lung adenocarcinoma, Cancer cell line (CVCL_2063)

## Full text

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## Figures

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Source: https://tomesphere.com/paper/PMC12119655