Anticancer activity of 23,24-dihydrocucurbitacin B against the HeLa human cervical cell line is due to apoptosis and G2/M cell cycle arrest Retraction in /10.3892/etm.2021.10033

Zhang,Jun‑Xiao; Wei‑Tan,Hong; Hu,Chun‑Yan; Wang,Wei‑Qiang; Chu,Guang‑Hua; Wei,Li‑Hui; Chen,Liu

doi:10.3892/etm.2018.5710

Anticancer activity of 23,24-dihydrocucurbitacin B against the HeLa human cervical cell line is due to apoptosis and G2/M cell cycle arrest

Retraction in 10.3892/etm.2021.10033

Authors:
- Jun‑Xiao Zhang
- Hong Wei‑Tan
- Chun‑Yan Hu
- Wei‑Qiang Wang
- Guang‑Hua Chu
- Li‑Hui Wei
- Liu Chen
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Affiliations: Department of Gynecology, Northwest Women and Children's Hospital, Xi'an, Shaanxi 710061, P.R. China, Department of Gynecology, Peking University People's Hospital, Beijing 100044, P.R. China
Published online on: January 5, 2018 https://doi.org/10.3892/etm.2018.5710
Pages: 2575-2582

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Abstract

Cervical cancer is one of the primary causes of cancer‑associated mortality worldwide. Due to the increasing incidence of cervical cancer, multiple treatment options are required. Initial responses to chemotherapy and surgical interventions are generally positive, however patients often experience relapse and tumor recurrence. Currently, the effects of cucurbitacins on different types of cancer are being investigated, as they exhibit a wide variety of bioactivities. The anticancer activity of the cucurbitacin 23,24‑dihydrocucurbitacin B against a panel of human cervical cancer cell lines was investigated in the current study. Cell viability was determined using an MTT assay and apoptosis was detected using DAPI staining. The proportion of apoptotic cells, cell cycle distribution, mitochondrial membrane potential (ΔΨm) and reactive oxygen species (ROS) levels were estimated using flow cytometry. Protein expression was determined using western blot analysis. The results of the current study indicated that 23,24‑dihydrocucurbitacin B inhibited the viability of human cervical cancer cell lines and had an IC50 of 40‑60 µM. However, its cytotoxic effects were much less pronounced in normal epithelial fr2 and HerEpiC cells, where it had an IC50 of 125 µM. The underlying mechanisms of this were further studied and the results demonstrated that 23,24‑dihydrocucurbitacin B induced apoptosis in HeLa cells and caused ROS‑mediated shifts in the ΔΨm. Additionally, it caused the cell cycle arrest of HeLa cells at the G2/M checkpoint. The phosphoinositide 3 kinase/protein kinase B/mechanistic target of rampamycin (PI3K/AKT/mTOR) cascade may serve an important role in cancer tumorigenesis, progression and resistance to chemotherapy. The results indicated that 23,24‑dihydrocucurbitacin B significantly decreased the expression of important proteins in the PI3K/Akt/mTOR cascade. Taken together, these results suggest that 23,24‑dihydrocucurbitacin B may be novel method of treating cervical cancer.

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