Ashwagandha (Withania somnifera) targets liver cancer stem cells via inhibiting Hedgehog signaling pathway in hepatocellular carcinoma.

Samah E Ismail, Amany I Youssef, Esraa E Fawzy, Eman A Khalifa, Amani H Kazem, Marwa A Kholief, Zainab A Saleh

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Article in Medical oncology (Northwood, London, England), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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7 authors.

Samah E IsmailApplied Medical Chemistry Department, Medical Research Institute, Alexandria University, Alexandria, Egypt. Samah.diab@alexu.edu.eg.

Amany I YoussefApplied Medical Chemistry Department, Medical Research Institute, Alexandria University, Alexandria, Egypt.

Esraa E FawzyBotany and Microbiology Department, Faculty of Science, Alexandria University, Alexandria, Egypt.

Eman A KhalifaHistochemistry and Cell Biology Department, Medical Research Institute, Alexandria University, Alexandria, Egypt.

Amani H KazemPathology Department, Medical Research Institute, Alexandria University, Alexandria, Egypt.

Marwa A KholiefForensic Medicine and Clinical Toxicology Department, Faculty of Medicine, Alexandria University, Alexandria, Egypt.

Zainab A SalehApplied Medical Chemistry Department, Medical Research Institute, Alexandria University, Alexandria, Egypt.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ashwagandha (W. somnifera), known for its broad health benefits, has shown potential in cancer prevention and treatment. The aim of this study was to investigate the potential effect of ashwagandha aqueous extract (ASH-AE) on cell proliferation and therapy resistance markers in hepatocellular carcinoma (HCC). An in vitro study was conducted using the HepG2 cell line. The HepG2 cells were divided into 4 groups according to the treatment regimen received. ASH-AE was extracted from the whole plant and characterized by GC-MS and HPLC. HepG2 cell viability was determined for all groups. The protein expression of cluster of differentiation 90 (CD90) was determined by flow cytometry technique. Also, the gene expression of Sonic Hedgehog (SHH), Patched 1(PTCH1) and ATP-binding cassette subfamily C1 (ABCC1) was assayed by qRT-PCR. The protein expression and localization of glioma-associated oncogene 1 (Gli1) in HepG2 cells were determined by immunocytochemistry (ICC) assay. The results indicated that ASH-AE either alone or in combination with sorafenib (SOR) significantly reduced HepG2 cell viability in a concentration dependent manner (P ˂0.001) with IC50 was 6.65 mg/ml for ASH-AE, 11.3 µM for SOR, and 5.6 mg/ml + 18.6 µM for ASH-AE in combination with SOR. Moreover, SOR significantly increased the percentage of CD90

Indexed as

Carcinoma, HepatocellularHedgehog ProteinsLiver NeoplasmsNeoplastic Stem CellsPlant ExtractsSignal TransductionWithaniaATP-Binding Cassette, Sub-Family C ProteinsCell ProliferationCell SurvivalHep G2 CellsHumansPatched-1 ReceptorSorafenibZinc Finger Protein GLI1AshwagandhaATP-Binding Cassette, Sub-Family C ProteinsGLI1 protein, humanHedgehog Proteinsmultidrug resistance-associated protein 1Patched-1 ReceptorPlant ExtractsPTCH1 protein, humanSorafenibZinc Finger Protein GLI1AshwagandhaHedgehog signaling pathwayLiver cancer stem cellsSorafenib

Identifiers

PMID41642395

DOI10.1007/s12032-025-03215-0

PMCPMC12876520

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