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07 September 2019 : Laboratory Research

[Retracted: 25 Mar 2021] Anticancer Action of Psilostachyin-A in 5-Fluorouracil-Resistant Human Liver Carcinoma are Mediated Through Autophagy Induction, G2/M Phase Cell Cycle Arrest and Inhibiting Extracellular-Signal-Regulated Kinase/Mitogen Activated Protein Kinase (ERK/MAPK) Signaling Pathway

Jun Liu1CDE, Yan Liu1ABC, Yan Liu1BCD, Lei Huang1EF, Guoliang Wang1BCD, Jun Wang1DEF, Xiangang Xu1DEF, Chengxian Shi1CEF, Jianzhao Huang1ACDG*

DOI: 10.12659/MSM.916635

Med Sci Monit 2019; 25:6711-6718

An editorial decision has been made to retract this manuscript due to breach of publishing guidelines, following the identification of non-original and manipulated figures. Reference: Jun Liu, Yan Liu, Yan Liu, Lei Huang, Guoliang Wang, Jun Wang, Xiangang Xu, Chengxian Shi, Jianzhao Huang: Anticancer Action of Psilostachyin-A in 5-Fluorouracil-Resistant Human Liver Carcinoma are Mediated Through Autophagy Induction, G2/M Phase Cell Cycle Arrest and Inhibiting Extracellular-Signal-Regulated Kinase/Mitogen Activated Protein Kinase (ERK/MAPK) Signaling Pathway. Med Sci Monit 2019; 25:6711-6718. 10.12659/MSM.916635

Abstract

BACKGROUND: Liver cancer is one of the most common malignancies around the world and one of the major causes of cancer related mortality. The objective of this study was to evaluate the anticancer effect of the natural compound psilostachyin-A on 5-fluorouracil-resistant human liver carcinoma cells and its effects on autophagy, cell cycle, caspase activation, and the ERK/MAPK signaling pathway.

MATERIAL AND METHODS: Cell Counting Kit 8 (CCK-8) assay was used to evaluate the effects on HepG2 cell viability at different doses of psilostachyin-A. Cell cycle analysis was performed using flow cytometry, and Transwell assay was used to check effects on cell invasion. Transmission electron microscopic studies were done to evaluate autophagy induced by psilostachyin-A, and the western blot method was carried out to evaluate the effects on autophagy and the ERK/MAPK signaling pathway.

RESULTS: CCK-8 assay revealed that the psilostachyin-A reduced the cell viability of HepG2 cancer cells in a dose dependent manner. Psilostachyin-A also reduced the colony forming potential of HepG2 cells, concentration dependently. The IC50 of psilostachyin was found to be 25 µM. The anticancer effects of psilostachyin-A were due to the induction of autophagy which was accompanied by enhancement of LC3B II expression. Psilostachyin also caused cell cycle arrest by enhancing the accumulation of HepG2 cells in the G2/M phase. Transwell assay showed that psilostachyin-A suppressed the invasion of HepG2 cells. The results also showed that psilostachyin-A could block the ERK/MAPK pathway, indicative of the cytotoxic effects of psilostachyin-A on liver cancer.

CONCLUSIONS: These preliminary observations suggested that psilostachyin-A might prove beneficial in the treatment of liver cancer.

Keywords: Retracted Publication

Retraction note

Med Sci Monit 2021; 27:e932375     https://medscimonit.com/abstract/index/idArt/932375
 
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Medical Science Monitor eISSN: 1643-3750
Medical Science Monitor eISSN: 1643-3750