Dihydroartemisinin inhibits the Raf/ERK/MEK and PI3K/AKT pathways in glioma cells
Authors: Wei DU
Qingjun Zhang
Yake Xue
Changhe Pang
Xinting Wei
Journal: Oncology Letters (2015)
Discipline: CLINICAL MEDICINE
Keywords: PI3K/AKT; Raf/MEK/ERK; dihydroartemisinin; dual pathway inhibitor; glioma.
Affiliations: Department of Neurosurgery, The First Affiliated Hospital, Zhengzhou University, Zhengzhou, Henan 450052, P.R. China.

Abstract:  It has previously been reported that dihydroartemisinin (DHA) is an effective novel anticancer compound in a number of types of tumor cells. Previous studies have demonstrated the anticancer activity of DHA in gioma cells. However, its underlining mechanism remains unclear. In the present study, the anticancer activity of DHA was examined in the glioma cell lines BT325 and C6. Western blot analysis was also employed to determine the signaling pathway changes. It was demonstrated that DHA effectively inhibited cell growth and induced apoptosis in glioma cells. Moreover, western blot analysis indicated that DHA-induced apoptosis was accompanied by inactivation of the Raf/MEK/ERK and PI3K/AKT signaling pathways, in addition to the downregulation of anti-apoptotic proteins Mcl-1 and Bcl-2 expression levels. 

Retracted: No

PubPeer comments:
 This paper was found during a systematic search of papers in this journal with possible duplicated images. Fifteen papers in this journal (n=98 examined) were found to contain inappropriately duplicated images. These papers have all been reported to the journal publisher in 2017. The editors promised to  investigate promptly but no action has been taken as of today. Figures 3 and 5. * Red boxes: Lane 1 of the pMEK BT325 cells panel in Figure 3A looks similar to lane 1 of the BCL-2 C6 cells panel in Figure 5B, albeit upside down. * Green boxes: Lanes 1-3 of the MEK C6 cells panel in Figure 3B look similar to lanes 1-3 of the GAPDH BT325 cells panel in Figure 5A. ![file] , 
 Corrigendum [15 March 2021] . ------------------------------------- Following the publication of the above article, an interested reader drew to the authorsu2019 attention that lane 1 of the pMEK BT325 cells panel in Fig. 3A appeared strikingly similar to lane 1 of the BCL-2 C6 cells panel in Fig. 5B, albeit the protein band was inverted. Furthermore, lanes 1u20133 of the MEK C6 cells panel in Fig. 3B looked strikingly similar to lanes 1u20133 of the GAPDH BT325 cells panel in Fig. 5A. The authors re-examined their original data, and realized that some of the data featured in Fig. 3 had been assembled incorrectly owing to the large number of proteins that had been investigated, and given the fact that not only one person was responsible for generating these data. The corrected version of Fig. 3 is shown opposite. Note that the corrections made to this figure do not affect the overall conclusions reported in the paper. The authors are grateful to the Editor of Oncology Letters for allowing them the opportunity to publish this corrigendum, and apologize to the readership for any inconvenience caused. ![] Figure 3. - DHA inhibits RAF MEK ERK and PI3K AKT signaling pathways in (A) BT325 and (B) C6 cells. Cells were treated with the indicated concentrations of DHA for 24 h. Western blot analysis was performed using specific antibodies against the indicated proteins. ,