Molecular medicine reports最新文献

{"title":"R‑loops in hepatocellular carcinoma: Bridging genomic instability and therapeutic opportunity (Review).","authors":"Ching-Hua Hsieh, Yueh-Wei Liu, Pei-Chin Chuang","doi":"10.3892/mmr.2025.13716","DOIUrl":"https://doi.org/10.3892/mmr.2025.13716","url":null,"abstract":"<p><p>R‑loops, three‑stranded nucleic acid structures composed of an RNA:DNA hybrid and displaced single‑stranded DNA, have emerged as important regulators of gene expression and genome maintenance. Although physiological R‑loops participate in normal cellular processes, their dysregulation can threaten genomic integrity by inducing DNA damage and replication stress. The present review explores the role of R‑loops in hepatocellular carcinoma (HCC), a malignancy characterized by marked genomic instability. In the present review, the formation mechanisms of R‑loops, their dual functions in transcriptional regulation and DNA damage, and their specific implications for HCC pathophysiology were discussed. HCC cells exhibit altered R‑loop homeostasis with aberrant accumulation linked to hepatitis B virus infection, inflammatory signaling and oncogene activation. The present review highlighted how HCC cells exploit or manage R‑loops to promote tumor progression, particularly through the epigenetic silencing of differentiation genes and modulation of replication stress responses. Furthermore, emerging therapeutic strategies targeting R‑loop biology were examined, including small molecules that induce synthetic lethality, gene‑based interventions and combination approaches that exploit R‑loop vulnerabilities. Challenges in targeting R‑loops and future directions, including multi‑omics profiling and biomarker development, were also addressed. Understanding the complex interplay between R‑loops and HCC offers promising avenues for novel diagnostic and therapeutic approaches for this malignancy.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"33 1","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145308713","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mitochondrial gatekeeper in hepatocellular carcinoma: Unraveling the multifaceted roles of VDAC in metabolic reprogramming, apoptosis evasion and therapeutic innovation (Review).","authors":"Jie Wang, Yu Liang, Xiaotao Jia, Xinmao Yang, Danning Shi, Yuanchun Wang, Yanfang Pan","doi":"10.3892/mmr.2025.13719","DOIUrl":"https://doi.org/10.3892/mmr.2025.13719","url":null,"abstract":"<p><p>Hepatocellular carcinoma (HCC), the predominant form of primary liver cancer, represents a substantial global health challenge with limited treatment options. The voltage‑dependent anion channel (VDAC), a critical mitochondrial outer membrane protein, has emerged as a pivotal regulator in HCC pathogenesis. Dysregulation of VDAC expression and function disrupts mitochondrial metabolism, confers resistance to apoptosis and promotes tumor proliferation. Mechanistically, VDAC facilitates HCC progression through metabolic reprogramming, evasion of programmed cell death and crosstalk with multiple oncogenic signaling pathways. Current VDAC‑targeted therapeutic approaches, including small‑molecule inhibitors and metabolic modulators, have demonstrated promising preclinical efficacy in inducing apoptosis and suppressing tumor growth. Notably, these agents may overcome therapeutic resistance and exhibit synergistic effects with conventional therapies. However, several challenges persist, particularly in elucidating isoform‑specific functions, optimizing pharmacokinetic profiles and identifying predictive biomarkers for patient stratification. The present comprehensive review critically evaluates the mechanistic involvement of VDAC in HCC progression, assesses emerging targeting strategies and proposes future research directions to establish VDAC as a viable precision medicine target for HCC management.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"33 1","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145355525","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Liquid‑liquid phase separation of PHLDB2 promotes oral squamous cell carcinoma metastasis through regulating epithelial mesenchymal transition and PIK3CA expression.","authors":"Kunyi Chen, Yuhong Wang, Jianing Cui, Qianrui Liu, Xiaoyong Liu, Wenjin Wang, Jinsong Hou","doi":"10.3892/mmr.2025.13720","DOIUrl":"https://doi.org/10.3892/mmr.2025.13720","url":null,"abstract":"<p><p>Liquid‑liquid phase separation (LLPS) contributes to multiple cellular bioprocesses; however, its clinicopathological relevance to oral squamous cell carcinoma (OSCC) remains largely unexplored. In the present study an integrative multi‑omics analysis investigating the prognostic value and molecular functions of LLPS‑related genes (LLPSRGs) in OSCC was conducted by leveraging transcriptomics and clinical data from 302 cases in The Cancer Genome Atlas database and LLPSRGs. A total of two prognostically distinct molecular subtypes were stratified by unsupervised clustering analysis, and a robust prognostic signature comprising seven key LLPSRGs was developed through LASSO regression and multivariate Cox analysis. Functional enrichment analysis highlighted the involvement of this signature in epithelial‑mesenchymal transition (EMT), with PHLDB2 emerging as a core regulator. Notably, the PHLDB2 protein underwent LLPS and formed droplet condensates both outside and in OSCC cells. Moreover, functional experiments revealed that PHLDB2 depletion attenuated the malignant biological behavior of OSCC cells, including cell proliferation, stemness, invasion and migration, and PHLDB2 promoted OSCC progression by regulating the PI3K‑Akt signaling pathway and PIK3CA expression. Retrospective clinical cohort and public dataset analyses validated that high expression of PHLDB2 was significantly associated with lymph node metastasis, higher pathological grade and reduced survival in patients with OSCC. Collectively, the present study established an LLPS‑based prognostic signature for OSCC, and revealed that phase separation of PHLDB2 may drive OSCC progression through regulating EMT and PIK3CA.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"33 1","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145355530","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"<i>PLIN5</i> deficiency ameliorates metabolic dysfunction‑associated fatty liver disease by inhibiting ferroptosis.","authors":"Ya Li, Xiaohan Wang, Xuecui Yin, Xiaohui Zhu, Weiqi Cui, Lin Dong, Yu Xia, Ying Wang, Liu Liu, Pengyuan Zheng, Youcai Tang","doi":"10.3892/mmr.2025.13714","DOIUrl":"https://doi.org/10.3892/mmr.2025.13714","url":null,"abstract":"<p><p>Metabolic‑associated fatty liver disease (MAFLD) is widely recognized as the most common type of chronic liver disease. As a member of the perilipin (PLIN) family, PLIN5 serves an important role in the regulation of lipid metabolism. Ferroptosis is a form of iron‑dependent non‑apoptotic cell death characterized by lipid peroxidation. Notably, knockout of <i>PLIN5</i> can attenuate high‑fat diet (HFD)‑induced MAFLD; however, the specific underlying mechanism remains unclear. The present study induced <i>PLIN5</i> overexpression by transfecting AML12 cells with a pcDNA3.1‑<i>PLIN5</i> plasmid, and <i>PLIN5</i> knockdown was achieved using short hairpin RNA‑mediated interference. Subsequently, intracellular ferrous iron (Fe²⁺) levels were assessed via immunofluorescence staining. Furthermore, a MAFLD model was established in C57BL/6J mice by feeding them a HFD. To establish an <i>in vitro</i> model of hepatic steatosis, AML12 hepatocytes were treated with palmitic acid and oleic acid to induce intracellular lipid accumulation. To further explore the effects of PLIN5 on ferroptosis, liver single‑cell sequencing was conducted and cellular experiments were performed to assess changes in redox and ferroptosis‑related proteins. The current study investigated the effects of PLIN5 on MAFLD in animal and cellular experiments, including the changes in lipid accumulation, redox and ferroptosis‑related markers. The results revealed that genetic knockdown of <i>PLIN5</i> significantly attenuated lipid accumulation and intracellular Fe²⁺ levels in AML12 hepatocytes, whereas <i>PLIN5</i> overexpression markedly exacerbated these parameters. In addition, <i>PLIN5</i> deficiency substantially reduced malondialdehyde content while enhancing glutathione levels, indicating attenuated oxidative stress. The results of the <i>in vivo</i> studies demonstrated that <i>PLIN5</i> knockout effectively ameliorated MAFLD progression in mice by suppressing ferroptosis. In conclusion, PLIN5 knockout may delay the progression of MAFLD in mice via ferroptosis inhibition. Therefore, targeting PLIN5 could offer a novel therapeutic strategy to address MAFLD by modulating lipid metabolism and ferroptosis pathways.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"33 1","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145308682","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Retracted] Protective effect of erythropoietin against myocardial injury in rats with sepsis and its underlying mechanisms.","authors":"Xinliang Zhang, Shimin Dong, Yanjun Qin, Xiaohua Bian","doi":"10.3892/mmr.2025.13711","DOIUrl":"https://doi.org/10.3892/mmr.2025.13711","url":null,"abstract":"<p><p>Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that the histological data featured in Fig. 8A of this paper had already appeared in Fig. 3 in an article published by the same research group in the journal <i>World Journal of Emergency Medicine</i> in 2013. Subsequently, the Editorial Office performed an independent assessment of the overlapping data between these two papers, and even though additional experiments were performed in the article reported above, including the creation of an alternative sepsis model with Kunming mice and the inclusion of pathological data for the rats in organs other than the heart, it remained the case that Figs. 1‑3 of the <i>World Journal of Emergency Medicine</i> article and many of the data in Tables 1‑3 (albeit in graphical form) were included in the above paper. Given that almost all of the data featured in the <i>World Journal of Emergency Medicine</i> paper had apparently been included in the above article, the Editor of <i>Molecular Medicine Reports</i> has decided that this should be retracted on account of these data having been published previously. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes for any inconvenience caused to the readership of the Journal. [Molecular Medicine Reports 11: 3317‑3329, 2015; DOI: 10.3892/mmr.2015.3155].</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"33 1","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145308694","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MALT1 inhibition by MI‑2 suppresses epithelial‑to‑mesenchymal transition and fibrosis by inactivating the NF‑κB pathway in high glucose‑treated HK‑2 cells.","authors":"Yating Lan, Jian Ma, Huijun Chen, Chaohong Lan, Na Zhao","doi":"10.3892/mmr.2025.13712","DOIUrl":"https://doi.org/10.3892/mmr.2025.13712","url":null,"abstract":"<p><p>Mucosa‑associated lymphoid tissue lymphoma translocation protein 1 (MALT1) is a scaffold protein and protease that is associated with multiple biological processes, such as immune signaling transduction, inflammation and glucose variation. However, its implication in diabetic nephropathy (DN) is unclear. The present study aimed to investigate the dysregulation of MALT1 and the effect of its inhibition by MI‑2 in high glucose‑treated renal tubular epithelial cells. HK‑2 cells were treated with 15 mM D‑glucose [low‑concentration glucose (LG) group] and 30 mM D‑glucose [high‑concentration glucose (HG)]. The negative control (NC) group consisted of cells cultured only with the standard medium. Subsequently, HK‑2 cells under the HG condition were treated with 0, 1, 2 and 4 µM MI‑2, an inhibitor of MALT1. Cell migration rate, invasive cell count, and the expression levels of vimentin, α‑smooth muscle actin (α‑SMA), fibronectin (FN) and collagen I were increased, whereas E‑cadherin expression was decreased in the HG group compared with that in the NC group (all P<0.01), implying enhanced epithelial‑to‑mesenchymal transition (EMT) and fibrosis in the HG group. Furthermore, MALT1 was upregulated in the HG group compared with that in the NC group (P<0.01). Following MI‑2 treatment in cells under the HG condition, the inhibitory effects of MI‑2 on EMT, fibrosis and the NF‑κB pathway were dose‑dependent. Cell migration rate, invasive cell count and vimentin expression were reduced, whereas E‑cadherin expression was elevated; furthermore, the expression levels of α‑SMA, FN and collagen I were downregulated in the high concentration MI‑2 (HC‑MI‑2) group compared with those in the HG group (all P<0.01). In addition, the NF‑κB pathway was inactivated, as reflected by increased inhibitor of κB α expression and decreased phosphorylated-p65 expression in the HC‑MI‑2 group compared with in the HG group (both P<0.001). In conclusion, MALT1 inhibition by MI‑2 suppresses EMT and fibrosis by inactivating the NF‑κB pathway in HG‑treated HK‑2 cells, indicating its potency as a target for DN.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"33 1","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145308641","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Combining tadalafil and hyperbaric oxygen therapy protects against ovarian ischemia‑reperfusion damage in rats.","authors":"Mehmet Akif Baktir, Mustafa Ermis, Esra Balcioglu, Betul Yalcin, Enes Karaman, Ahmet Cumaoglu","doi":"10.3892/mmr.2025.13721","DOIUrl":"https://doi.org/10.3892/mmr.2025.13721","url":null,"abstract":"<p><p>A frequently occurring surgical emergency in gynecology is ovarian torsion, which occurs when the ovary twists on its ligamentous supports, which obstructs blood flow. The aim of the present study was to evaluate the protective effects of hyperbaric oxygen therapy (HBOT) and tadalafil against ischemia‑reperfusion (IR) injury in a rat model of ovarian torsion. Female Wistar albino rats were randomly assigned to five groups (n=8/group): Control, IR, IR + tadalafil, IR + HBOT and IR + tadalafil + HBOT. Ovarian torsion was induced under anesthesia for 2 h, followed by daily post‑operative treatments with tadalafil (10 mg/kg) and/or HBOT (2.4 atmospheres absolute for 1 h) for 7 days. Blood and ovarian tissue specimens were collected for analysis at the end of the treatment period. IR‑induced ovarian tissue injury significantly decreased the counts of primordial, primary and preantral follicles compared with those in the control group. In addition, serum ELISA and immunohistochemical analysis revealed that IR injury reduced anti‑Müllerian hormone (AMH) levels in serum and the granulosa cells of primary, preantral and secondary follicles. HBOT alone resulted in a significant increase in the counts of primordial, primary and preantral cells, as did the combination of HBOT with tadalafil. In addition, AMH immunoreactivity significantly increased in primary, preantral and secondary follicles following treatment with HBOT and tadalafil. Furthermore, all therapeutic interventions elevated serum AMH levels in the IR model rats. These findings suggest that tadalafil treatment combined with HBOT may help protect ovarian reserve and mitigate IR‑induced tissue damage in rat ovaries.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"33 1","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145355599","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role and relevance of exosome-mediated epigenetic regulation in the pathogenesis, diagnosis and treatment of  cardiovascular diseases (Review).","authors":"Yishuo Zhang, Shanshan Zhang, Yijing Li, Wenqi Jin, Liya Zhou, Jing Lu","doi":"10.3892/mmr.2025.13715","DOIUrl":"https://doi.org/10.3892/mmr.2025.13715","url":null,"abstract":"<p><p>Cardiovascular diseases (CVDs) are among the main factors impacting negatively human health on a global scale. Every year, there is an increase in the prevalence of CVDs despite advancements in therapy for managing traditional risk factors. Research on exosomes is has garnered great interest due to their role in regulating intercellular communication. Exosome‑mediated epigenetic regulation is involved in the interaction between circulating cells and blood arteries, as well as in intercellular communication processes, and exosomes serve as biomarkers of cell activation. The present study aimed to summarize the recent research on exosome‑mediated epigenetic regulation mechanisms, as well as the roles of exosomes in the pathology and diagnosis of CVDs, which may increase the current understanding of the precise functions that exosomes play in the development of CVDs.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"33 1","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145308716","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploring the role of cytochrome P450 family 1 subfamily B member 1 and quercetin in modulating neuropathic pain after spinal cord injury.","authors":"Pengyu Zhou, Lu Li, Yu Cao, Jiahao Chen, Chuyin Chen, Xiangsheng Zhang, Jiurong Chen, Yingdong Deng, Ziqiang Lin, Yupei Lai, Suo Wang, Simin Tang, Wenqi Zhang, Peng Sun, Jun Zhou","doi":"10.3892/mmr.2025.13717","DOIUrl":"https://doi.org/10.3892/mmr.2025.13717","url":null,"abstract":"<p><p>Spinal cord injury (SCI) represents a notable global health challenge, with neuropathic pain (NP) being a common complication that intensifies patient suffering. Existing research tends to overlook the temporal aspects of NP and fails to offer targeted treatment options. To tackle this issue, the present study initially examined genome‑wide association study summaries related to NP, incorporating expression quantitative trait locus (eQTL) from blood samples through summary‑based Mendelian randomization. This allowed the investigation of the association between NP and eQTL, facilitating the identification of genes linked to the risk of NP. Following this, weighted gene co‑expression network analysis of a Gene Expression Omnibus dataset was utilized to identify SCI‑related module genes, resulting in the detection of 218 shared genes across these analyses. Subsequent functional enrichment assessments, protein‑protein interaction evaluations and machine learning technique analyses, including least absolute shrinkage and selection operator regression, random forest and support vector machine recursive feature elimination analyses, highlighted three central genes: Glycerol‑3‑phosphate dehydrogenase 1‑like, epoxide hydrolase 2 and cytochrome P450 family 1 subfamily B member 1 (CYP1B1). Additionally, network pharmacology and molecular docking analyses confirmed CYP1B1 as a viable therapeutic target. A analysis of single‑cell RNA sequencing datasets demonstrated an increase in CYP1B1 expression within spinal cord fibroblasts following SCI. Furthermore, quercetin (Que) was shown to inhibit CYP1B1 expression and reduce NP (based on mechanical paw withdrawal threshold and thermal paw withdrawal latency) in murine models. The results of the present study highlight the important role of spinal cord fibroblast CYP1B1 as a notable contributor to NP following SCI and suggest that Que may serve as a promising mechanism‑based therapeutic option.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"33 1","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145308692","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Retracted] Knockdown of ubiquitin‑specific protease 51 attenuates cisplatin resistance in lung cancer through ubiquitination of zinc‑finger E‑box binding homeobox 1.","authors":"Feng Zhou, Chunling Du, Donghui Xu, Jinchang Lu, Lei Zhou, Chaomin Wu, Bo Wu, Jianan Huang","doi":"10.3892/mmr.2025.13718","DOIUrl":"https://doi.org/10.3892/mmr.2025.13718","url":null,"abstract":"<p><p>Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that the control GAPDH western blotting data shown in Fig. 2B on p. 1385 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 <i>Biomedicine & Pharmacotherapy</i>. Certain of the other western blot data featured in Figs. 2 and 4 were likewise very similar to data which subsequently appeared in other articles that were unrelated to this one. In view of the fact that the abovementioned data in Fig. 2C had already apparently been published previously, the Editor of <i>Molecular Medicine Reports</i> 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: 1382‑1390, 2020; DOI: 10.3892/mmr.2020.11188].</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"33 1","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145355580","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}