Molecular medicine reports最新文献

Following the publication of the above paper, a concerned reader drew to the Editor's attention that, concerning the western blots shown in Fig. 2 on p. 340, the protein bands representing the LC3 II data in the two left‑hand lanes of Fig. 2A were strikingly similar to the two blots representing the P62 data in the left‑hand lanes of the gel slice shown in Fig. 2C, albeit the bands appeared to have been horizontally flipped, with horizontal and vertical resizing. After assessing this issue in the Editorial Office, the Editor  of Molecular Medicine Reports has determined that the concerns of the reader were well founded; therefore, this paper has been retracted from the Journal on account of a lack of confidence in the authenticity of the presented data. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a satisfactory reply. The Editor regrets any inconvenience that may have been caused to the readership of the Journal. [Molecular Medicine Reports 22: 337‑343, 2020; DOI: 10.3892/mmr.2020.11080].

Renal interstitial fibrosis is a common pathological outcome of acute and chronic kidney disease. Within the present study, the aim was to explore whether long non‑coding RNA (lncRNA) NKILA regulates TGF‑β1‑induced renal tubular epithelial fibrosis through the JAK‑2/STAT3 pathway and its underlying mechanisms. A renal fibrosis model was established by treating HK‑2 cells with TGF‑β1. RNA sequencing revealed marked dysregulation of the cis‑regulated lncRNA NKILA, associated with the JAK2/STAT3 pathway. Functional studies involved overexpressing NKILA using lentivirus in HK‑2 cells with TGF‑β1‑treated cells as a control and knocking it down in the fibrotic model. The JAK2 inhibitor AG490 was employed for rescue experiments. Protein and mRNA levels of epithelial‑mesenchymal transition (EMT) markers [fibronectin, collagen I, epithelial (E)‑cadherin, α‑smooth muscle actin and vimentin] and JAK2/STAT3 pathway components were assessed using western blotting, immunofluorescence and reverse transcription‑quantitative PCR. Findings revealed that lncRNA NKILA overexpression promoted fibrosis of TGF‑β1‑treated HK‑2 cells by activating the JAK2/STAT3 pathway. While knockdown of lncRNA NKILA alleviated the TGF‑β1‑induced EMT damage in HK‑2 cells, downregulated EMT markers and upregulated E‑cadherin expression by suppressing the activation of the JAK2/STAT3 pathway. Of note, AG490 prevented the damaging effects of lncRNA NKILA or TGF‑β1‑induced HK‑2 cells. Mechanistically, lncRNA NKILA promoted TGF‑β1‑induced renal injuries by activating the JAK2/STAT pathway. Overall, this suggests that lncRNA NKILA functions as an independent fibrogenic factor and affects the progression of renal interstitial fibrosis by regulating the JAK2/STAT3 signaling pathway.

Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that most of the flow cytometric (FCM) assay data featured in Figs. 2C and 6C were strikingly similar to FCM data which were ultimately published in a number of other papers in different journals that were written by different authors at different research institutes, including a paper that was submitted on an earlier date to the same journal (Molecular Medicine Reports). Owing to the fact that the contentious data in the above article were found to be strikingly similar to data that have appeared elsewhere in other papers in the scientific literature, 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 21: 1145‑1153, 2020; DOI: 10.3892/mmr.2019.10903].

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. 3D and 5D on p. 3625 and p. 3626 respectively were strikingly similar to data that had appeared previously in other papers written by different authors at different research institutes, which had already been accepted for publication. In view of the fact that the abovementioned data had already apparently 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 22: 3621‑3628, 2020; DOI: 10.3892/mmr.2020.11483].

Liver X receptors (LXRs), transcription factors belonging to the nuclear receptor superfamily, exist as two isoforms, LXRα (NR1H3) and LXRβ (NR1H2), that orchestrate cholesterol absorption, transport and excretion. Beyond their canonical roles in lipid homeostasis, LXRs modulate glucose metabolism, inflammatory responses and cellular proliferation. Emerging evidence implicates dysregulated LXRs activity in the pathogenesis of chronic liver diseases (CLDs), including viral hepatitis, metabolic dysfunction‑associated steatotic liver disease and hepatocellular carcinoma. However, the therapeutic potential of LXRs modulation remains paradoxical: While activation mitigates hepatic injury by maintaining cholesterol homeostasis and suppressing inflammation, concurrent upregulation of sterol regulatory element‑binding protein 1c exacerbates lipogenesis, potentially aggravating hepatosteatosis. The present review synthesized current insights into the dual regulatory mechanisms of LXRs in CLDs, critically evaluates their context‑dependent roles and highlights the imperative to balance therapeutic efficacy with metabolic side effects in future drug development.

Following the publication of the above article, an interested reader drew to the authors' attention that, concerning the TUNEL assay data shown in Fig. 5A on p. 6, the images shown for the H₂O₂ and PU+H₂O₂ groups were remarkably similar, suggesting that these data had been derived from the same original source where the results of differently performed experiments were intended to have been portrayed. After having re‑examined their original data, the authors have realized that an unintentional error was made during the assembly of the images in Fig. 5A; specifically, the representative images for the H₂O₂ and PU+H₂O₂ groups were inadvertently duplicated. A revised version of Fig. 5, now showing the correct data for the H₂O₂ group in Fig. 5A, is shown on the next page. Note that the error made in assembling the data in Fig. 5 did not significantly affect either the results or the conclusions reported in this paper. All the authors agree with the publication of this Corrigendum, and are grateful to the Editor of Molecular Medicine Reports for allowing them the opportunity to publish this; moreover, they apologize to the readership for any inconvenience caused. [Molecular Medicine Reports 24: 851, 2021; DOI: 10.3892/mmr.2021.12491].

Lung cancer remains a significant global health challenge, largely due to difficulties in early detection and the lack of effective therapeutic strategies for more advanced‑stage disease. Elucidating the molecular mechanisms underlying lung carcinogenesis and identifying reliable biomarkers is of urgent importance. Long non‑coding RNAs (lncRNAs), a class of transcripts of >200 nucleotides without protein‑coding potential, have recently emerged as key regulators of tumor cell invasion, metastasis, proliferation, apoptosis and angiogenesis. Accumulating evidence suggests that lncRNAs hold notable promise as diagnostic and prognostic biomarkers in lung cancer. However, a comprehensive overview that integrates their mechanistic roles, clinical potential and the technological advances in their detection, while critically addressing the associated challenges, is lacking, to the best of the authors' knowledge. In the present review, a summary of recent advances in the mechanistic roles of lncRNAs during lung cancer progression and their involvement in therapy response and chemoresistance was provided, along with an up‑to‑date discussion of emerging detection technologies and their implications for clinical translation. The advantages, limitations and challenges of using lncRNAs as diagnostic or prognostic biomarkers in lung cancer are discussed. By synthesizing these aspects, the present review aimed to highlight the novel insights into lncRNAs and outline future research directions, thereby addressing a critical gap in the current literature.

Subsequently to the publication of this paper, and following the publication of an expression of concern statement (doi: 10.3892/mmr.2025.13679) that was published after an interested reader had noted that, regarding the confocal microscopic images shown in Fig. 3 on p. 2240, the top (Sham) and bottom (SCI) data panels appeared to show a small overlapping section such that data which were intended to show the results from differently performed experiments had apparently been derived from the same original source, the authors have now replied to the Editorial Office. After re‑examining their original data, the authors have realized that the data in Fig. 3 were inadvertently assembled incorrectly. The revised version of Fig. 3, now showing alternative data from one of the repeated experiments, is shown below. Note that this error did not significantly affect either the results or the conclusions reported in this paper, and all the authors agree with the publication of this corrigendum. Furthermore, the authors thank the Editor of Molecular Medicine Reports for granting them the opportunity to publish this corrigendum, and apologize to the readership for any inconvenience caused. [Molecular Medicine Reports 18: 2237‑2244, 2018; DOI: 10.3892/mmr.2018.9194].

Truncated‑cadherin (T‑cadherin) is a distinct glycosylphosphatidylinositol‑anchored atypical cadherin that differs from classical cadherins since it does not have transmembrane and intracellular domains. It primarily functions as a dual receptor, serving as a physiological receptor for low‑density lipoprotein (LDL) and a specific receptor for high‑molecular‑weight (HMW) adiponectin. Upon binding to LDL, T‑cadherin activates calcium signaling, thereby promoting cell proliferation and migration and contributing to the development of atherosclerotic plaques. Conversely, its interaction with HMW adiponectin mediates cardiovascular protective effects through various mechanisms, such as increased exosome secretion, reduced intracellular ceramide accumulation, improved insulin sensitivity and anti‑inflammatory actions. T‑cadherin is predominantly expressed in cardiovascular tissues, such as endothelial cells, smooth muscle cells, pericytes and cardiomyocytes. Genetic polymorphisms in cadherin‑13, the gene encoding T‑cadherin, are notably associated with the risk of hypertension, type 2 diabetes and end‑stage renal disease. In cancer, T‑cadherin generally has tumor‑suppressive effects, particularly in gastric, ovarian and breast cancers. This function is often compromised by promoter region hypermethylation, which leads to gene silencing and subsequently inhibits key signaling pathways, such as the PI3K/Akt, Wnt/β‑catenin and epithelial‑mesenchymal transition pathways. The present review provided a comprehensive overview of the molecular mechanisms, regulation of expression and potential clinical importance of T‑cadherin as a diagnostic biomarker and therapeutic target for cardiovascular diseases, including atherosclerosis, hypertension and heart failure, metabolic disorders, such as diabetes, and various cancers. Further research is required to fully elucidate the signal transduction pathways and competitive dynamics of T‑cadherin ligand binding.

Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that certain of the scratch‑wound assay data within Fig. 10A, and the Transwell assay data shown in Figs. 2C and 10B, contained duplicated data panels within the figure parts, and also comparing between the figures in the case of Figs. 2C and 10B; moreover, Transwell assay data shown in Fig. 3B were strikingly similar to data that had already been submitted for publication to the journal International Journal of Molecular Medicine in a paper written by different authors at different research institutes. In view of the fact that the abovementioned data had already apparently been submitted 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 a reply. The Editor apologizes to the readership for any inconvenience caused. [Molecular Medicine Reports 20: 81‑94, 2019; DOI: 10.3892/mmr.2019.10222].