Molecular medicine reports最新文献

Hyperoside (Hyp), a naturally occurring flavonol glycoside derived from Crataegus, otherwise known as hawthorn, possesses potent antioxidant properties and has demonstrated therapeutic potential in various oxidative stress‑related diseases, including osteoporosis (OP). However, the precise molecular mechanisms underlying the anti‑osteoporotic effects of Hyp remain to be fully elucidated. The present study aimed to evaluate the therapeutic efficacy of Hyp against OP and to elucidate its underlying mechanisms. An osteoporotic mouse model was established via bilateral ovariectomy (OVX) to assess the in vivo efficacy of Hyp. Network pharmacology was employed to predict the potential therapeutic targets of Hyp in OP. In vitro experiments using bone marrow mesenchymal stem cells (BMSCs) were performed to validate the findings. Techniques including alkaline phosphatase staining, Alizarin red S staining, reverse transcription‑quantitative PCR and western blotting were used to assess osteogenic differentiation and molecular signaling pathways. Micro‑CT analysis revealed that Hyp significantly ameliorated OVX‑induced bone loss in mice. Network pharmacology identified the PI3K/AKT signaling pathway as a potential key target. In vitro, Hyp significantly reduced H2O2‑induced oxidative stress in BMSCs and promoted their osteogenic differentiation. Mechanistically, Hyp was found to activate the PI3K/AKT signaling pathway, suggesting its notable role in mediating the antioxidant and osteoinductive effects of Hyp. Summarily, Hyp may effectively alleviate OVX‑induced OP in mice, potentially by mitigating oxidative stress and promoting osteogenesis via activation of the PI3K/AKT signaling pathway. These findings provide novel insights into the therapeutic mechanism of Hyp and support its potential as a candidate agent for OP treatment.

Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that certain of the flow cytometric data shown in Figs. 2D and 4D, and western blot data shown in Fig. 5A, were strikingly similar to data that had already been published previously in articles submitted to different journals that were written by different authors at different research institutes, a few of which have been retracted. 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. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [Molecular Medicine Reports 19: 1491‑1500, 2019; DOI: 10.3892/mmr.2018.9775].

Chronic kidney disease (CKD) progression is driven by a harmful interplay between impaired mitophagy and sustained oxidative stress. Under normal conditions, mitophagy serves as a protective mechanism by removing damaged mitochondria and limiting the production of reactive oxygen species. However, in CKD, a self‑reinforcing cycle of mitochondrial dysfunction, defective mitophagy oxidative stress, and inflammation occurs, which promotes fibrosis. The present review examines the molecular mechanisms governing mitophagy, with a specific focus on the regulatory roles of core signaling pathways, namely the PTEN‑induced kinase l/Parkin, BCL2 interacting protein 3/Nip3‑like protein X and FUN14 domain‑containing protein l pathways, and how their disruption contributes to CKD. The mechanistic crosstalk between mitophagy and oxidative stress is highlighted as a central pathogenic axis in CKD progression. In addition, emerging therapeutic strategies that aim to restore mitophagy and enhance antioxidant capacity are discussed, suggesting new strategies for targeted CKD treatment.

Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that, regarding the TUNEL assay experiments shown in Fig. 2E on p. 5, the Merge panels for the shFLVCR1‑AS1 experiments shown for the Caco‑2 and SW480 cell lines appeared to have been inserted into this figure the wrong way around. The authors were contacted by the Editorial Office to offer an explanation for this apparent anomaly in the presentation of the data in this paper; however, up to this time, no response from them has been forthcoming. Owing to the fact that the Editorial Office has been made aware of potential issues surrounding the scientific integrity of this paper, we are issuing an Expression of Concern to notify readers of this potential problem while the Editorial Office continues to investigate this matter further. [Molecular Medicine Reports 23: 139, 2021; DOI: 10.3892/mmr.2020.11778].

As the first functional organ to form during vertebrate embryogenesis, the heart exhibits heightened susceptibility to developmental toxicity. Epigenetic regulatory mechanisms, including DNA methylation, histone modifications, non‑coding RNAs, N6‑methyladenosine methylation and chromatin accessibility alterations, mediate cardiac developmental toxicity induced by exogenous compounds including environmental chemicals and pharmaceuticals. The present review comprehensively summarizes the current understanding of the molecular mechanisms through which these compounds exert cardiac developmental toxicity through epigenetic regulation. An in‑depth analysis of research progress and technical challenges across diverse epigenetic pathways is provided. By summarizing recent evidence, the present review proposes candidate epigenetic biomarkers for cardiac developmental toxicity monitoring and explores potential intervention strategies targeting these pathways. Future research should prioritize multi‑omics integration technologies and clinical translation system development. These advances are anticipated to foster innovation in both mechanistic research and preventive strategy development for cardiac developmental toxicity.

Following the publication of the above paper, a concerned reader drew to the Editor's attention that, within the left‑hand and centre data panels of Fig. 6 on p. 5735, apparent anomalies were identifiable, including unexpectedly similar‑looking cells and repeated patternings of these cells in terms of their layout/arrangement, albeit with inversions of the cells in certain cases. In addition, it was noted that some of the data featured in Table I and in Fig. 4B were strikingly similar to data that had previously appeared in a paper published in the journal Cell Biochemistry and Biophysics that was written by different authors at different research institutes. After having conducted an independent investigation of this paper in the Editorial Office, the Editor of Molecular Medicine Reports has determined that it should be retracted from the Journal on account of a lack of confidence in the authenticity of the data. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor regrets any inconvenience that has been caused to the readership of the Journal. [Molecular Medicine Reports 12: 5730‑5736, 2015; DOI: 10.3892/mmr.2015.4169].

Recurrence and metastasis are the leading causes of poor prognosis and death in lung cancer, and the mechanism of cancer metastasis has not yet been fully elucidated. As a gut-specific homeobox (HOX) transcription factor, intestine-specific HOX (ISX) is a proto-oncogene induced by the inflammatory factor IL-6. Notably, ISX overexpression can induce the epithelial-mesenchymal transition (EMT) response, and promotes tumor cell migration and invasion. In the present study, a lung cancer cell model with overexpression of ISX was established by infecting lung cancer cells with lentivirus. Reverse transcription-quantitative polymerase chain reaction was first used to verify the expression of the EMT-related gene induced by ISX overexpression. Furthermore, transcriptome sequencing and analysis showed that the overexpression of ISX induced significant changes in the gene expression profile of human lung cancer cells. In addition, type I collagen α1 chain (COL1A1), a highly expressed gene in various tumor tissues and cells, was shown to promote tumor cell migration and invasion, possibly by promoting EMT, and was significantly upregulated in human lung cancer cells overexpressing ISX. These results suggested that ISX may promote lung cancer migration and invasion by increasing the expression of COL1A1. In addition, four drugs that are currently used to treat lung cancer were screened. Of these, Iressa® (gefitinib) was revealed to significantly inhibit the viability, migration and invasion of lung cancer cells that stably overexpress ISX by downregulating the expression of COL1A1. In conclusion, these findings may help to prevent tumor metastasis and spread, and the potential molecular mechanism by which ISX promotes the development and migration of lung cancer was suggested. The current findings provide novel targets, and a scientific basis for the prevention and treatment of lung cancer, which may reduce costs for patients, their families and society.

Infantile hemangioma (IH), a common vascular tumor, occurs in childhood; however, its pathogenesis has not been fully elucidated. In the present study, the roles and detailed mechanisms of long non‑coding RNA (lncRNA) NEAT1 in the progression of hemangioma were further explored. The NEAT1‑interacting proteins were selected by analyzing the catRAPID database and lactate dehydrogenase B (LDHB) was predicted to bind with NEAT1. The binding between NEAT1 and LDHB was validated using an RNA immunoprecipitation assay and it was further found that knocking down NEAT1 expression destabilized LDHB by regulating the proteasome pathway. The knocking down of lncRNA NEAT1 also inhibited cellular protein lactylation and downregulated β‑catenin. Furthermore, blockade of lactylation via 2‑DG and oxamate attenuated the viability and colony formation of hemangioma cells. NEAT1 promoted the lactylation of H3K18 in the promoter region of β‑catenin, and blockade of lactylation downregulated β‑catenin expression in hemangioma cells. The lactyltransferases alanyl‑tRNA synthetase 1 and P300 were regulated by NEAT1 and also positively regulated β‑catenin. The levels of β‑catenin mRNA and H3K18 lactylation were also found to be elevated in IH tissues. Taken together, the results of the present study revealed that lncRNA NEAT1, which is upregulated in hemangioma, binds with and stabilizes LDHB, subsequently elevates the levels of cellular lactate and H3K18 lactylation, potentiates β‑catenin transcription and ultimately enhances the proliferation of hemangioma cells.

Subsequently to the publication of this paper, an interested reader drew to the authors' attention that, in the "Identification of hub genes for CRC" subsection of the Results on p. 8263, the left‑hand column, in the first sentence the reference to Matthew's correlation coefficient algorithm should perhaps have been written as the Maximal Clique Centrality algorithm. The authors have replied to confirm that, upon carefully reviewing the paper, the Maximal Clique Centrality algorithm from the CytoHubba plugin was indeed used to identify the top 20 hub genes, and that, during the manuscript preparation, the full name of "MCC" was incorrectly written as "Matthews correlation coefficient" due to an oversight on their part. Therefore, the first sentence in this subsection of the Results section should have read as follows: "To identify potential hub genes among the 306 genes previously identified, the Maximal Clique Centrality (MCC) algorithm from the CytoHubba software plug‑in was used." The authors sincerely apologize for any confusion or misunderstanding this error may have caused for the readers, and are grateful to the Editor of Molecular Medicine Reports for granting them the opportunity to publish this corrigendum. [Molecular Medicine Reports 17: 8260‑8268, 2018; DOI: 10.3892/mmr.2018.8862].

Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that certain of the cell apoptotic data shown in Fig. 5A were strikingly similar to data appearing in different form in another article written by different authors at different research institutes that had already been published in the journal Cell Cycle; moreover, the lens smudging patterns underlying the neurite outgrowth experimental data shown in Figs. 2D and 5C matched that of data shown in other figures of the same article published in journal Cell Cycle, suggesting these data may have been derived from the same original source. Owing to the fact that the contentious data mentioned above had already apparently been published previously, the Editor of Molecular Medicine Reports 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 reply. The Editor apologizes to the readership for any inconvenience caused. [Molecular Medicine Reports 22: 1489‑1497, 2020; DOI: 10.3892/mmr.2020.11203].