Following the publication of this paper, it was drawn to the Editors' attention by a concerned reader that the cell cycle assay data shown in Fig. 4A, and the western blotting assay data shown in Fig. 4B, were strikingly similar to data appearing in different form in other articles by different authors; furthermore, there were other possible anomalies associated with these data. 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. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive any reply. The Editor apologizes to the readership for any inconvenience caused. [the original article was published in Molecular Medicine Reports 11 379‑385, 2015; DOI 10.3892/mmr.2014.2684].Following the publication of the above review article, the authors have realized that they overlooked including the funding information in the Declarations section. Therefore, the following text should also have been included with the review Funding The present review was supported by the National Research Foundation of Korea grant funded by the Korean government (grant no. 2020R1F1A1061122) and Gachon University Research fund of 2018 (GCU-2018-0670) to SH. The authors regret their oversight, apologize to the funding bodies concerned, and regret any inconvenience caused. [the original article was published in International Journal of Oncology 58 344‑358, 2021; DOI 10.3892/ijo.2021.5175].Leukemia is a group of malignant diseases of clonal hematopoietic stem‑progenitor cells and its pathological mechanisms remain to be elucidated. Genetic and epigenetic abnormalities, as well as microenvironmental factors, including cytokines, serve critical roles in leukaemogenesis. Macrophage migration inhibitory factor (MIF) has been presented as one of the key regulators in tumorigenesis, angiogenesis and tumor metastasis. This article focuses on the functional role of MIF and its pathway in cancer, particularly in leukemia. MIF/CD74 interaction serves prominent roles in tumor cell survival, such as upregulating BCL‑2 and CD84 expression, and activating receptor‑type tyrosine phosphatase ζ. Furthermore, MIF upregulation forms a pro‑tumor microenvironment in response to hypoxia‑induced factors and promotes pro‑inflammatory cytokine production. Additionally, polymorphisms of the MIF promoter sequence are associated with leukemia development. MIF signal‑targeted early clinical trials show positive results. Overall, these efforts provide a promising means for intervention in leukemia.Banxia xiexin decoction (BXXX) is a classic preparation used to treat gastrointestinal diseases, and also has certain therapeutic effects on gastrointestinal tumors. BXXX has been reported to regulate the expression of proteins associated with drug resistance and sensitivity in tumors, and thus, the aim of the present study was to investigate the mechanisms of BXXX drug sensitivity in gastric cancer (GC). The expression levels of programmed cell death 1 ligand 1 (PD‑L1), 6‑O‑methylguanine‑DNA methyltransferase (MGMT) and STAT3 were immunohistochemically detected in the cancer and adjacent non‑cancer tissues of patients with GC, and in vitro experimentation was conducted using drug‑resistant and ‑sensitive GC cells. The expression levels of PD‑L1, MGMT and STAT3 were determined using reverse transcription‑quantitative PCR. FHT-1015 research buy Different concentrations of BXXX drug serum were used to treat the cells and the cellular inhibition rate was assessed using a Cell Counting Kit‑8 assay. Flow cytometry was used to detect apX on drug‑resistant GC cells, and significantly reversed the effect of BXXX on PD‑L1 expression. In conclusion, BXXX was found to influence the drug sensitivity of GC cells by regulating the expression of MGMT. This process functions viaPD‑L1, which was itself mediated by IL‑6/JAK/STAT3 signaling.Following the publication of this paper, it was drawn to the Editors' attention by a concerned reader that certain of the Transwell cell migration data shown in Figs. 2D and 4C 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 International Journal of Molecular Medicine, 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 any reply. The Editor apologizes to the readership for any inconvenience caused. [the original article was published in International Journal of Molecular Medicine 38 1587‑1595, 2016; DOI 10.3892/ijmm.2016.2754].Endometrial cancer (EC) is widely known as an aggressive malignancy. Due to the limited therapeutic options and poor prognosis of patients with advanced‑stage EC, there is a need to identify effective alternative treatments. Chrysin is a naturally active flavonoid (5,7‑dihydroxyflavone), which has been demonstrated to exert anticancer effects and may present a novel strategy for EC treatment. However, the role of chrysin in EC remains largely unclear. The aim of the present study was to examine the anticancer effects of chrysin on EC. The results revealed that, in addition to apoptosis, chrysin increased the LC3II expression levels and markedly accelerated the autophagic flux, suggesting that chrysin induced both the autophagy and apoptosis of EC cells. Furthermore, the inhibition of autophagy by chloroquine enhanced the inhibitory effect on cell proliferation and the promotion of the chrysin‑induced apoptosis of EC cells, indicating that chrysin‑induced autophagy was a cytoprotective mechanism. Additionally, chrysin led to the production of intracellular reactive oxygen species (ROS). N‑acetylcysteine (NAC) pretreatment significantly inhibited chrysin‑induced autophagy, suggesting that ROS activated autophagy induced by chrysin in EC cells. Furthermore, the phosphorylated (p‑)Akt and p‑mTOR levels were significantly decreased in a concentration‑dependent manner following treatment with chrysin, while NAC blocked these effects. Taken together, these findings demonstrated that chrysin‑induced autophagy via the inactivation of the ROS‑mediated Akt/mTOR signaling pathway in EC cells.