Antitumor effect of resveratrol on chondrosarcoma cells via phosphoinositide 3-kinase/AKT and p38 mitogen-activated protein kinase pathways
Authors: Yihe Hu
Zixun Dai
Jie Xie
Pengfei Lei
Journal: Molecular Medicine Reports (2015)
Discipline: CLINICAL MEDICINE
Keywords: Chondrosarcoma; Resveratrol; proliferation; apoptosis; invasion
Affiliations: Department of Orthopedics, Xiangya Hospital of Central South University, Changsha, Hunan 410008, P.R. China.

Abstract:  Chondrosarcoma is one of the most common types of primary bone cancer that develops in cartilage cells. Resveratrol (Res), a natural polyphenol compound isolated from various fruits, has a suppressive effect on various human malignancies. It has been shown that Res inhibits matrix metalloproteinase (MMP)-induced differentiation in chondrosarcoma cells. However, the effects of Res on cell proliferation, apoptosis and invasion of chondrosarcoma cells, as well as the underlying mechanisms, remain largely unknown. To the best of our knowledge, the present study showed for the first time that Res inhibited proliferation and induced apoptosis in chondrosarcoma cells in a dose-dependent manner. Furthermore, it was shown that Res also suppressed chondrosarcoma cell invasion in a dose-dependent manner, probably via the inhibition of MMP2 and MMP9 protein expression. Molecular mechanism investigations revealed that Res could inhibit the activity of phosphoinositide 3-kinase/AKT and p38 mitogen-activated protein kinase signaling pathways, which has been demonstrated to be important in the regulation of proliferation, apoptosis and invasion in various cancer cell types. In conclusion, this study suggests that Res may serve as a promising agent for the treatment of chondrosarcoma. 

Retracted: Yes

PubPeer comments:
 Fig 2.  Apoptosis analysis was performed to examine the effect of Res on cell apoptosis in JJ012 chondrosarcoma cells.   Colored rectangles mark the appearances of the same  hockey sticks in papers by otherwise-unrelated authors. Figs 2C; 4B from [He, Tang Tian (2015)] .  A cell apoptosis assay was performed to examine the cell proliferation of CNE1 cells transfected with miR-214 mimics or the miR-214 inhibitor ;  A cell apoptosis assay was performed to determine the apoptotic rate of CNE1 cells transfected with the miR-214 inhibitor or co-transfected with the miR-214 inhibitor and Bax siRNA .  *[above]* Fig 4A from [Peng et al (2013)] .  Flow cytometry was used to determine the apoptotic rate of U87 and CHG-5 cells after forced downregulation of RACK1.  *[below[* Fig 4B from [Lai, Chen Li (2015)] .  ... a Transwell assay were performed to examine the cell proliferation of AGS cells transfected with miR-133a mimics, miR-133a inhibitor, or co-transfected with miR-133a mimics and FSCN1 plasmid. Control: AGS cells without any transfection.  , 
 Fig 3A.  A Transwell assay was performed to determine the effect of Res on cell invasion of JJ012 chondrosarcoma cells .  For comparison, Figs 4B and 5B from [Lei et al (2015)] .  Cell invasion assay was performed on MG63 cells with or without transfection with galectin-3-specific siRNA ;  Transwell assay was performed to examine the invasive capacity of MG63 cells transfected with galectin-3 siRNA, with or without pre-treatment of curcumin .  , 
 Dear Hoya: Thanks for your comments. I will investigate this and discuss with my team. , 
 Retracted [23 June 2021] . -------------------------------- Following the publication of this paper, it was drawn to the Editors attention by a concerned reader that the cell apoptotic data shown in Fig. 2 were strikingly similar to data appearing in different form in other articles by different authors. Owing to the fact that the contentious data in the above article had already been published elsewhere, or were already under consideration for publication, prior to its submission to *Molecular Medicine Reports*, the Editor has decided that this paper should be retracted from the Journal. After having been in contact with the authors, they agreed with the decision to retract the paper. The Editor apologizes to the readership for any inconvenience caused. ,