# Ethanol Extract of Adlay Hulls Suppresses Acute Myeloid Leukemia Cell Proliferation via PI3K/Akt Pathway Inhibition

**Authors:** Guangjie Li, Wenyuan Yang, Jiahui Xu, Ziqian Liu, Zhijian Li, Xiaoqiu Wu, Tongtong Li, Ruoxian Wang, Yamin Zhu, Ning Liu

PMC · DOI: 10.3390/cimb47050358 · Current Issues in Molecular Biology · 2025-05-13

## TL;DR

A natural extract from adlay hulls shows anti-leukemia effects by blocking a key cell growth pathway.

## Contribution

First identification of adlay hull bioactive components and their anti-AML mechanisms via PI3K/Akt pathway inhibition.

## Key findings

- AHE-EA-C inhibits AML cell proliferation and induces G0/G1 phase arrest and apoptosis.
- AHE-EA-C suppresses the PI3K/Akt pathway by reducing PI3K and Akt phosphorylation.
- 52 compounds with potential anti-AML activity were identified, including neohesperidin and cycloartanol.

## Abstract

Acute myeloid leukemia (AML) is a common hematologic malignancy in the elderly with frequent relapse and poor prognosis. Limited treatments highlight the need for novel natural anticancer compounds. Adlay, valued for its medicinal and dietary properties, exhibits anti-inflammatory and anticancer effects. However, research on adlay hulls, particularly their anti-AML bioactive molecules, remains insufficient. This study evaluated the effects of adlay hull ethanol extract (AHE) on AML cell proliferation and apoptosis. AHE was extracted with ethanol and fractionated using n-hexane, ethyl acetate, and n-butanol, followed by silica gel chromatography. Cytotoxicity was assessed via the CCK-8 assay, and mechanisms were analyzed by flow cytometry and Western blotting. The bioactive components were characterized by UPLC-IMS-QTOF-MS. AHE-EA-C (ethyl acetate fraction C) inhibited AML cell proliferation, induced G0/G1 phase arrest, and promoted apoptosis. It suppressed the PI3K/Akt pathway by reducing PI3K and Akt phosphorylation. Using UPLC-IMS-QTOF-MS analysis, a total of 52 compounds with potential anti-AML activity were identified in AHE-EA-C, among which neohesperidin and cycloartanol have been previously reported to exhibit anti-AML activity and thus hold promise as candidates for further development as AML inhibitors. This study is the first to identify adlay hull bioactive components and their anti-AML mechanisms via PI3K/Akt pathway inhibition, providing a foundation for developing natural anti-AML therapies.

## Linked entities

- **Proteins:** PIK3CA (phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha), AKT1 (AKT serine/threonine kinase 1)
- **Chemicals:** neohesperidin (PubChem CID 442439), cycloartanol (PubChem CID 12760132)
- **Diseases:** Acute myeloid leukemia (MONDO:0015667), AML (MONDO:0018874)

## Full-text entities

- **Genes:** PIK3CB (phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit beta) [NCBI Gene 5291] {aka P110BETA, PI3K, PI3KBETA, PIK3C1}, AKT1 (AKT serine/threonine kinase 1) [NCBI Gene 207] {aka AKT, PKB, PKB-ALPHA, PRKBA, RAC, RAC-ALPHA}
- **Diseases:** AML (MESH:D015470), inflammatory (MESH:D007249), Cytotoxicity (MESH:D064420), hematologic malignancy (MESH:D019337)
- **Chemicals:** ethyl acetate (MESH:C007650), n-butanol (MESH:D020001), silica (MESH:D012822), neohesperidin (MESH:C546526), n-hexane (MESH:C026385), Ethanol (MESH:D000431), AHE (-)
- **Cell lines:** AHE-EA-C — Homo sapiens (Human), Transformed cell line (CVCL_E575)

## Full text

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## Figures

7 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12109684/full.md

## References

35 references — full list in the complete paper: https://tomesphere.com/paper/PMC12109684/full.md

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Source: https://tomesphere.com/paper/PMC12109684