Aagaardestrada0785

An interested reader drew to our attention that, in the above paper, several of the figures appeared to contain strikingly similar data to those published in other articles by different authors from different research institutions, including (as examples) Fig. 8 (cf. Fig. 8 in Fang, K et al 'Antiproliferative effects of matricine in gemcitabine‑resistant human pancreatic carcinoma cells are mediated via mitochondrial‑mediated apoptosis, inhibition of cell migration, invasion suppression, and mammalian target of rapamycin (mTOR)‑TOR/PI3K/AKT signalling pathway', Med Sci Monit 25 2943‑2949, 2019), Fig. 4 (cf. Fig. 7 in He, W et al 'Arglabin is a plant sesquiterpene lactone that exerts potent anticancer effects on human oral squamous cancer cells via mitochondrial apoptosis and downregulation of the mTOR/PI3K/Akt signaling pathway to inhibit tumor growth in vivo', J BUON 23 1679‑1685, 2018) and Fig. 7 (cf. Fig. Selleck Zimlovisertib 7B in Yu, Y et al 'Globularifolin exerts anticancer effects on glioma U87 cells through inhibition of Akt/mTOR and MEK/ERK signaling pathways in vitro and inhibits tumor growth in vivo', Biochemie 42 144‑151, 2017). The authors also independently informed the Editorial Office that they were unable to repeat the experiments shown in Fig. 4, and requested a retraction. Given the overall problems that have come to light with this paper, the Editor of Molecular Medicine Reports has agreed with the authors that this article should be retracted from the publication. The Editor and the authors apologize for any inconvenience caused. [the original article was published in Molecular Medicine Reports 17 5652‑5657, 2018; DOI 10.3892/mmr.2018.8599].Isocitrate dehydrogenase1 (IDH1) mutation is the most important genetic change in glioma. The most common IDH1 mutation results in the amino acid substitution of arginine 132 (Arg/R132), which is located at the active site of the enzyme. IDH1 Arg132His (R132H) mutation can reduce the proliferative rate of glioma cells. Numerous diseases follow circadian rhythms, and there is growing evidence that circadian disruption may be a risk factor for cancer in humans. Dysregulation of the circadian clock serves an important role in the development of malignant tumors, including glioma. Brain‑Muscle Arnt‑Like protein 1 (BMAL1) and Circadian Locomotor Output Cycles Kaput (CLOCK) are the main biological rhythm genes. The present study aimed to further study whether there is an association between IDH1 R132H mutation and biological rhythm in glioma, and whether this affects the occurrence of glioma. The Cancer Genome Atlas (TCGA) database was used to detect the expression levels of the biological rhythm genes BMAL1 and CLd increased the expression levels of the G1 phase‑associated proteins Cyclin D3 and CDK4, but did not significantly change the expression levels of the G2/M phase‑associated protein Cyclin B1. The expression levels of the positive and negative rhythm regulation genes BMAL1, CLOCK, period (PER s (PER1, 2 and 3) and cryptochrom (CRY)s (CRY1 and 2) were significantly decreased, those of the Smad signaling pathway‑associated genes Smad2, Smad3 and Smad2‑3 were decreased, and those of phosphorylated (p)‑Smad2, p‑Smad3 and Smad4 were increased. Therefore, the present results suggested that the IDH1 R132H mutation may alter the cell cycle and biological rhythm genes in U87‑MG cells through the TGF‑β/Smad signaling pathway.Chaperone‑mediated autophagy (CMA) is a selective type of autophagy whereby a specific subset of intracellular proteins is targeted to the lysosome for degradation. link2 The present study investigated the mechanisms underlying the response and resistance to 5‑fluorouracil (5‑FU) in colorectal cancer (CRC) cell lines. In engineered 5‑FU‑resistant CRC cell lines, a significant elevation of lysosome‑associated membrane protein 2A (LAMP2A), which is the key molecule in the CMA pathway, was identified. High expression of LAMP2A was found to be responsible for 5‑FU resistance and to enhance PLD2 expression through the activation of NF‑κB pathway. Accordingly, loss or gain of function of LAMP2A in 5‑FU‑resistant CRC cells rendered them sensitive or resistant to 5‑FU, respectively. Taken together, the results of the present study suggested that chemoresistance in patients with CRC may be mediated by enhancing CMA. Thus, CMA is a promising predictor of chemosensitivity to 5‑FU treatment and anti‑CMA therapy may be a novel therapeutic option for patients with CRC.Proximal tubular epithelial cells (PTECs) have innate immune characteristics, and produce proinflammatory factors, chemokines and complement components that drive epithelial‑mesenchymal transition (EMT). Our previous studies revealed that human mesangial cells and podocytes were able to synthesize and secrete immunoglobulin (Ig)A and IgG, respectively. The aim of the present study was to evaluate the expression of Igs in PTECs. Firstly, IgG was detected in the cytoplasm, the cell membrane and the lumen of PTECs in the normal renal cortex by immunohistochemistry. Secondly, Igγ gene transcription and V(D)J recombination were detected in single PTECs by nested PCR and Sanger sequencing. Thirdly, Igγ, Igκ and Igλ were clearly detected in an immortalized PTEC line (HK‑2) by immunostaining and western blotting, in which RP215 (an antibody that predominantly binds to non‑B cell‑derived IgG) was used. In addition, Igγ, Igκ and Igλ gene transcripts, conservative V(D)J recombination in the Igγ variable region, recombination activating gene 1/2 and activation‑induced cytidine deaminase were all detected in HK‑2 cells. These data suggested that PTECs may express IgG in a similar manner to B cells. Furthermore, IgG expression was upregulated by TGF‑β1 and may be involved in EMT.Bone‑related diseases comprise a large group of common diseases, including fractures, osteoporosis and osteoarthritis (OA), which affect a large number of individuals, particularly the elderly. The progressive destruction and loss of alveolar bone caused by periodontitis is a specific type of bone loss, which has a high incidence and markedly reduces the quality of life of patients. With the existing methods of prevention and treatment, the incidence and mortality of bone‑related diseases are still gradually increasing, creating a significant financial burden to societies worldwide. To prevent the occurrence of bone‑related diseases, delay their progression or reverse the injuries they cause, new alternative or complementary treatments need to be developed. Melatonin exerts numerous physiological effects, including inducing anti‑inflammatory and antioxidative functions, resetting circadian rhythms and promoting wound healing and tissue regeneration. Melatonin also participates in the health management of bone and cartilage. In the present review, the potential roles of melatonin in the pathogenesis and progression of bone injury, osteoporosis, OA and periodontitis are summarized. Furthermore, the high efficiency and diversity of the physiological regulatory effects of melatonin are highlighted and the potential benefits of the use of melatonin for the clinical prevention and treatment of bone‑related diseases are discussed.Nasopharyngeal carcinoma (NPC) is a common disease with high prevalence worldwide, affecting hundreds of thousands of patients every year. Although its progress can be inhibited by concurrent chemoradiotherapy and platinum‑based agents, there is also a need for novel drugs to treat NPC. The present study identified tanshinone IIA as a potent drug that could suppress the proliferation of HK1 cells by enhancing pyroptosis via regulation of the miR‑125b/foxp3/caspase‑1 signaling pathway. Firstly, the effects of tanshinone IIA on HK1 cells were assessed and it was confirmed that treatment with tanshinone IIA significantly decreased the proliferation of HK1 cells, with increased activity of caspase‑3 and caspase‑9. Then, the pyroptosis levels after tanshinone IIA administration were detected. The results showed that tanshinone IIA enhanced pyroptosis in a dose‑dependent manner. link3 Furthermore, the mechanism underlying the effects of tanshinone IIA on HK1 cells were explored. It was found that transfection with a microRNA (miR)‑125b agomir and a small interfering RNA (si)‑foxp3 plasmid reversed the inhibitory effect induced by tanshinone IIA, accompanied by an increase in reactive oxygen species levels and lactate dehydrogenase release, indicating a critical role of miR‑125b/foxp3 signaling in pyroptosis in HK1 cells. In conclusion, the present study demonstrates that tanshinone IIA enhances pyroptosis and inhibits the proliferation of HK1 cells by modulating miR‑125b/foxp3/caspase‑1/GSDMD signaling. It is the first study to reveal the inhibitory effect of tanshinone IIA on HK1 cells and to demonstrate the critical role of miR‑125b/foxp3 signaling in mediating these effects, providing robust evidence for the treatment of NPC.Osteoblasts are sensitive to ionizing radiation. The small GTPase RhoA and its effector Rho‑associated protein kinase (ROCK) are critical to several cellular functions, including cytoskeleton reorganization, cell survival, and cell differentiation. However, whether the RhoA/ROCK signaling pathway is involved in the regulation of osteoblast cytoskeleton reorganization and differentiation induced by low‑dose X‑ray irradiation remains to be determined. The aim of the present study was to investigate the role of the RhoA/ROCK signaling pathway in mediating differentiation of osteoblasts and reorganization of the cytoskeleton under low‑dose X‑ray irradiation. Osteoblasts were pretreated with the ROCK kinase‑specific inhibitor (Y‑27632) before exposure to low‑dose X‑ray irradiation. The changes of F‑actin in MC3T3 cells were observed at different time points following X‑ray irradiation. Cell Counting Kit‑8 assay, alkaline phosphatase activity, Alizarin red staining and western blotting were used to detect the proliferation and differentiation of osteoblasts after 0.5‑Gy X‑ray irradiation. In the present study, low‑dose X‑ray irradiation promoted the expression of genes associated with the cytoskeleton reorganization. Indeed, the results showed that, 0.5‑Gy X‑ray irradiation can induce reorganization of cytoskeleton and promote differentiation of osteoblasts through the RhoA/ROCK signaling pathway. Additionally, inhibiting ROCK activity blocked low‑dose X‑ray irradiation‑induced LIMK2 phosphorylation, stress fiber formation and cell differentiation. Thus, these results demonstrated the excitatory effects of low‑dose X‑ray irradiation on MC3T3‑E1 cells, including reorganization of the cytoskeleton and differentiation of osteoblasts.Thyroid cancer (TC) is the most prevalent malignant tumor in the endocrine system. Serpin peptidase inhibitor clade E member 2 (SERPINE2) is closely associated with tumor metastasis. The aim of the present study was to investigate whether SERPINE2 forms a feedback loop with epidermal growth factor (EGF)/EGF receptor (EGFR) that regulates cellular processes in human papillary thyroid carcinoma (TPC‑1) cells. Reverse transcription‑quantitative PCR and western blotting were utilized to analyze the expression of SERPINE2. Cell proliferation ability was detected with a cell proliferation and cytotoxicity assay kit (MTT) and by clone formation assay. The proliferation markers, including proliferating cell nuclear antigen and Ki‑67, were also investigated to analyze the proliferative activity of TPC‑1 cells. Besides, cell migration and invasion were analyzed by wound healing and Transwell assays, respectively, while cell apoptosis was analyzed by TUNEL staining. The results showed that SERPINE2 expression was increased in TPC cells, and SERPINE2 and EGF/EGFR regulated each other.