[Retracted] Arnebin‑1 promotes angiogenesis by inducing eNOS, VEGF and HIF‑1α expression through the PI3K‑dependent pathway
Affiliations: Department of Pharmacology, Cardiac and Cerebral Vascular Research Centre, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, Guangdong 510080, P.R. China
- Published online on: April 3, 2023 https://doi.org/10.3892/ijmm.2023.5241
- Article Number: 38
Copyright : © Zeng et al. This is an open access article distributed under the terms of Creative Commons Attribution License [CC BY 4.0].
This article is mentioned in:
Int J Mol Med 36: [Related article:] 685-697, 2015; DOI: 10.3892/ijmm.2015.2292
Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that the α-tubulin protein bands shown in Fig. 2A on p. 689 were strikingly similar to data appearing in different form in the following paper: Tian R, Li Y and Gao M: Shikonin causes cell-cycle arrest and induces apoptosis by regulating the EGFR-NF-κB signalling pathway in human epidermoid carcinoma A431 cells. Biosci Rep 35: e00189, 2015. Moreover, there were a pair of overlapping data panels shown in the cell invasion and migration assay data in Fig. 5B on p. 692, one identified instance of western blot data being shared between Figs. 3D and 4F, and a pair of overlapping data panels in Fig. 5D, such that all these data, which were intended to have shown the results from differently performed experiments, may have been derived from a smaller number of original sources.
Owing to the fact that the contentious data in the above article were already under consideration for publication prior to its submission to International Journal of Molecular Medicine and an overall lack of confidence in the presented data, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a satisfactory reply. The Editor apologizes to the readership for any inconvenience caused.