Following the publication of this paper, it was drawn to the Editor\'s attention by a concerned reader that the colony formation assay data shown in Fig. 4C on p. 6 were strikingly similar to data appearing in different form in other articles written by different authors at different research institutes, which had already been published. Owing to the fact that the contentious data in the above article had already been published 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 accepted the decision to retract the paper. The Editor apologizes to the readership for any inconvenience caused. [Molecular Medicine Reports 24: 685, 2021; DOI: 10.3892/mmr.2021.12325].

The aim of the present study was to investigate the role of estrogen receptor (ER)α and ERβ, and galectin‑3 (GAL‑3) in migration and invasion of androgen‑independent DU‑145 prostate cancer cells, and to examine the regulation of the expression of GAL‑3 by the activation of these receptors. Wound healing and cell invasion assays were performed using the control (basal level of cellular function) and treated DU‑145 cells. At 24 h of treatment, 17β‑estradiol (E2), the ERα‑selective agonist, 4,4\',4\"‑(4‑propyl‑(1H)‑pyrazole‑1,3,5‑triyl)trisphenol (PPT), or the ERβ‑selective agonist, 2,3‑bis(4‑hydroxyphenyl)‑propionitrile (diarylprepionitrile; DPN), increased the migration and invasion of the DU‑145 cells. Pre‑treatment with the ERα‑ and ERβ‑selective antagonists blocked these effects, indicating that ERα and ERβ are upstream receptors regulating these processes. Western blot analysis and immunofluorescence staining for the detection of the GAL‑3 were performed using the control and treated DU‑145 cells. Treatment of the DU‑145 cells with E2, PPT or DPN for 24 h increased the expression of the GAL‑3 compared to the control. Furthermore, a specific inhibitor of GAL‑3 (VA03) inhibited the migration and invasion of DU‑145 cells, indicating the involvement of the complex ERα/GAL‑3 and ERβ/GAL‑3 in the regulation of these processes. On the whole, the present study demonstrates that the activation of both ERs increases the expression and signaling of GAL‑3, and promotes the migration and invasion of DU‑145 cells. The findings of the present study provide novel insight into the signatures and molecular mechanisms of ERα and ERβ in DU‑145 cells.

Oral squamous cell carcinoma (OSCC) is a cancer associated with high mortality (accounting for 3.1/100,000 deaths per year in Brazil in 2013) and a high frequency of amplification in the expression of the epidermal growth factor receptor (EGFR). Treatment with the EGFR inhibitor cetuximab leads to drug resistance in patients with OSCC due to unknown mechanisms. Galectin‑3 (Gal‑3) is a β‑galactoside binding lectin that regulates multiple signaling pathways in cells. The present study aimed to investigate the effect of Gal‑3 in cetuximab‑resistant (cet‑R) OSCC. The OSCC HSC3 cell line was selected to establish a mouse xenograft model, which was treated with cetuximab to induce resistance. Subsequently, a Gal‑3 inhibitor was used to treat cet‑R tumors, and the tumor volume was monitored. The expression of Gal‑3, phosphorylated (p)‑ERK1/2 and p‑Akt was assessed using immunohistochemistry. The combined effect of cetuximab and the Gal‑3 inhibitor on HSC3 tumor xenografts was also investigated. HSC3 cells were cultured in vitro to investigate the regulatory effects of Gal‑3 on ERK1/2 and Akt via western blotting. In addition, the effects of the Gal‑3 inhibitor on the proliferation, colony formation, invasion and apoptosis of HSC3 cells were investigated by performing Cell Counting Kit‑8, colony formation, Transwell and apoptosis assays, respectively. In cet‑R OSCC tumors, increased expression of Gal‑3, p‑ERK1/2 and p‑Akt was observed. Further research demonstrated that Gal‑3 regulated the expression of both ERK1/2 and Akt in HSC3 cells by promoting phosphorylation. Moreover, the Gal‑3 inhibitor decreased the proliferation and invasion, but increased the apoptosis of cet‑R HSC3 cells. In addition, the Gal‑3 inhibitor suppressed the growth of cet‑R tumors. Collectively, the results indicated that the Gal‑3 inhibitor and cetuximab displayed a synergistic inhibitory effect on OSCC tumors. In summary, the present study demonstrated that Gal‑3 may serve an important role in cet‑R OSCC. The combination of cetuximab and the Gal‑3 inhibitor may display a synergistic antitumor effect, thereby inhibiting the development of cetuximab resistance in OSCC.

Nasopharyngeal carcinoma (NPC) is an epithelial carcinoma originating from the nasopharyngeal mucosal tissue and is highly prevalent in southeast Asia. Galectin‑3 (gal‑3) serves crucial roles in many cancers but its role in NPC remains to be elucidated. The aim of the present study was to investigate the role of gal‑3 in NPC. Immunohistochemistry and ELISA were used to determine the expression level of gal‑3 in patients with NPC or chronic rhinitis (CR). Gal‑3 short hairpin (sh)RNA was established to knockdown gal‑3 in 5‑8F and 6‑10B cells, allowing for the evaluation of the roles of gal‑3 in proliferation, migration and apoptosis in NPC cell lines. Immunohistochemistry staining of IL‑6 and IL‑8 was applied to access the inflammatory state of tumor tissues, and the correlation between the inflammatory state and gal‑3 was analyzed. The results demonstrated that gal‑3 was upregulated in patients with NPC compared with patients with CR. Knockdown of gal‑3 inhibited proliferation and migration in 5‑8F and 6‑10B cells, as well as promoted apoptosis in these cells. The expression levels of MMP‑9 and IL‑8 were also decreased in 5‑8F and 6‑10B cells after transfection with gal‑3 shRNA. A positive correlation was identified between the expression level of gal‑3 and the inflammatory state of NPC. The phosphorylation levels of ERK1/2 and Akt were downregulated after knockdown of gal‑3 in 5‑8F and 6‑10B cells. In conclusion, the expression level of gal‑3 was upregulated in patients with NPC and was positively correlated with the inflammatory state of NPC. The results suggested that gal‑3 promoted the proliferation and migration of 5‑8F and 6‑10B cells, while inhibiting the apoptosis of these cells. Moreover, activation of ERK1/2 and Akt may be the underlying mechanism of the effects of gal‑3 on NPC.

Galectin-3 is an important mediator of cardiac fibrosis and heart failure. Cell viability of cardiomyocytes was measured using a CCK‑8 assay; flow cytometry was employed for the detection of the cell cycle and cardiomyocytes apoptosis. Reverse transcription‑quantitative polymerase chain reaction and western blotting was performed to examine the expression of associated genes and proteins. The present study demonstrated that overexpression of galectin‑3 significantly decreased the viability of cardiomyocytes in a time‑dependent manner, with simultaneous arrest of the cell cycle and induction of apoptosis. The expression levels of proliferating cell nuclear antigen (PCNA) and B‑cell lymphoma 2 (Bcl‑2) were decreased and Bcl‑2‑associated X protein (Bax) was increased in cardiomyocytes with galectin‑3 overexpression. However, inhibition of galectin‑3 by intravenous tail vein injection of a galectin‑3‑targeting short hairpin RNA‑expressing vector during hypertension‑induced heart failure in Dahl hypertensive rats increased rat survival and body weight. Inhibition of galectin‑3 also increased the expression of PCNA and Bcl‑2 and reduced the expression of Bax in the cardiac tissue of hypertensive rats. These results demonstrate the therapeutic potential of targetinggalectin‑3 for the treatment of cardiac disease.