Molecular medicine reports最新文献

{"title":"[Retracted] The effect of foxp3‑overexpressing Treg cells on non‑small cell lung cancer cells.","authors":"Jiangzhou Peng, Zigang Yu, Lei Xue, Jiabin Wang, Jun Li, Degang Liu, Qiang Yang, Yihui Lin","doi":"10.3892/mmr.2025.13644","DOIUrl":"10.3892/mmr.2025.13644","url":null,"abstract":"<p><p>Following the publication of the above paper, it was drawn to the Editors' attention by a concerned reader that the western blot data shown in Fig. 2C on p. 5863, the cell adhesion assay data in Fig. 3C on p. 5864, and scratch‑wound assay data shown in Figs. 3D and 4B on p. 5865 were strikingly similar to data appearing in different form in other articles written by different authors at different research institutes that had already been published elsewhere prior to the submission of this paper to <i>Molecular Medicine Reports</i>. In view of the fact that the abovementioned data 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 17: 5860‑5868, 2018; DOI: 10.3892/mmr.2018.8606].</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"32 4","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12340747/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144799678","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Regulation of <i>Botulinum</i> neurotoxin half‑life through the ubiquitin‑proteasome system.","authors":"Hae-Seul Choi, Hye-Rim Seo, Miso Choi, Hwa-Yeong Kim, Sun-Kyu Jin, Myunghoon Lee, Kwang-Hyun Baek","doi":"10.3892/mmr.2025.13633","DOIUrl":"https://doi.org/10.3892/mmr.2025.13633","url":null,"abstract":"<p><p><i>Botulinum</i> neurotoxin (BoNT), renowned for its potency, is used in both therapeutic and cosmetic applications; however, it is constrained by a relatively short half‑life and limited duration of efficacy. The present study investigated the role of the ubiquitin‑proteasome system in BoNT degradation and evaluated strategies to extend its half‑life by targeting specific lysine residues. Ubiquitination was observed in the light chains of BoNT/A1 (K335 and K417), BoNT/A2 (K335) and BoNT/E (K62 and K288), which were identified as key ubiquitination sites. The substitution of these lysine residues to arginine inhibited ubiquitination, improving protein stability and extending the half‑life of BoNT. These findings offer a potential strategy to enhance the therapeutic efficacy of BoNT by prolonging its stability, paving the way for future advancements in BoNT‑based treatments.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"32 4","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144708207","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":"Differential expression of haematopoietic prostaglandin D synthase by POU2F3‑positive tuft cells in conventional bilayered oncocytic and metaplastic epithelia of Warthin tumours.","authors":"Kenta Hosomi, Akira Sato, Mitsuaki Ishida, Kensuke Nakanishi, Tetsuya Terada, Shin-Ichi Haginomori, Yoshinobu Hirose, Ko Fujimori","doi":"10.3892/mmr.2025.13624","DOIUrl":"10.3892/mmr.2025.13624","url":null,"abstract":"<p><p>Warthin tumours (WT), the second most common benign salivary gland tumour, are histopathologically composed of bilayered oncocytic epithelial cells with occasional metaplastic epithelium. Tuft cells, which are chemosensory epithelial cells, are present in WT. Tuft cells serve various roles by producing physiologically active substances, such as prostaglandins (PGs). PGD2 released from tuft cells is crucial for tissue repair and inhibiting pancreatic carcinogenesis. However, whether or not tuft cells in WT produce PGD2 has not yet been elucidated. The present study aimed to investigate the production of PGD₂ in POU class 2 homeobox 3 (POU2F3; a specific tuft cell marker)‑positive cells of WT and normal salivary glands. Consecutive patients with WT who underwent surgical resection were selected. Dual immunohistochemical staining for POU2F3 and haematopoietic PGD synthase (H‑PGDS) was performed. The present study included 28 patients with WT of the parotid gland (all male patients; median age, 68 years). The conventional bilayered oncocytic epithelium was present in all tumours; squamous metaplastic epithelium and conventional bilayered oncocytic epithelium were observed in 16 patients. Dual immunohistochemical analysis revealed that POU2F3+/H‑PGDS‑ cells were exclusively present in the striated duct of the normal salivary gland, and abundant POU2F3‑positive tuft cells were observed in both the conventional bilayered oncocytic and metaplastic squamous epithelia of WT. The median ratio of POU2F3‑positive cells expressing H‑PGDS was significantly higher in the conventional oncocytic epithelium (89.9%) than in the metaplastic squamous epithelium (10.6%) of WT (P=0.00044). The present results suggest a link between tissue injury to the striated duct and the pathogenesis of WT, and that PGD₂ released from POU2F3‑positive cells in the conventional bilayered oncocytic epithelium is associated with ongoing tissue injury. Further studies are warranted to clarify the function of tuft cells in WT and gain deeper insights into the pathogenesis of WT.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"32 4","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12308854/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144668023","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of cellular prion protein in mouse granulosa cells and its effects on ovarian function in knockout mice.","authors":"Qinyue Cao, Hehua Wang, Jingjing Hu, Yan Wang, Tong Dai, Fen Liu, Xia Yang, Qinyu Yang, Chunhua Tu","doi":"10.3892/mmr.2025.13630","DOIUrl":"10.3892/mmr.2025.13630","url":null,"abstract":"<p><p>Cellular prion protein (PrP^c) regulates ovarian reserve maintenance through anti‑Müllerian hormone (AMH)‑dependent mechanisms. The present study explored the role of PrP^c in the ovarian function of mice using complementary <i>in vitro</i> and <i>in vivo</i> models. First, prion protein gene (PRNP) knockdown or overexpression was carried out in mouse ovarian granulosa cells. In vitro analyses conducted using flow cytometry and ELISA revealed that the depletion of PrP^c specifically hindered the secretion of AMH compared with control groups, while the levels of progesterone (P4) and estradiol (E2) remained unchanged across all experimental groups. Importantly, the reduction in AMH levels was reversed upon re‑expression of PrP^c. Additionally, neither the distribution of the cell cycle nor the rates of apoptosis were affected by the manipulation of PrP^c. Subsequently, a comparative analysis of mice with PRNP knockout (KO) vs. wild‑type mice was performed. However, PrP^c depletion did not alter the production of progesterone or estradiol. Whilst the ovarian histology remained intact in KO mice, an elevation in follicle‑stimulating hormone levels was observed, thereby suggesting a potential involvement of compensatory neuroendocrine regulation. These findings revealed that PrP^c may be a novel modulator for maintaining the ovarian reserve which depends on AMH. The present study redefined the molecular landscape of ovarian reserve depletion by identifying the dysfunction of the PrP^c‑AMH axis as a possible reason for diminished ovarian reserve syndromes.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"32 4","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12319384/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144708134","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bardoxolone methyl inhibits ferroptosis through the Keap1‑Nrf2 pathway in renal tubular epithelial cells.","authors":"Soyeon Yoo, Miyeon Kim, Ju Young Bae, Sang Ah Lee, Gwanpyo Koh","doi":"10.3892/mmr.2025.13632","DOIUrl":"10.3892/mmr.2025.13632","url":null,"abstract":"<p><p>Diabetic kidney disease (DKD), a primary cause of end‑stage kidney disease, involves ferroptosis in renal tubular epithelial cells (RTECs). Bardoxolone methyl (BM), known for its antioxidant and anti‑inflammatory properties, activates the Keap1‑Nrf2 pathway and has slows kidney function decline. 2‑Deoxy‑d‑ribose (dRib) can induce ferroptosis in RTECs by promoting the degradation of solute carrier family 7 member 11 (SLC7A11), a protein essential for cystine transport and glutathione (GSH) synthesis. The present study aimed to evaluate whether BM could inhibit dRib‑induced ferroptosis in RTECs and to elucidate the underlying mechanisms. Using NRK‑52E cells and primary RTECs, cystine uptake, GSH and iron levels, cell viability, lipid peroxidation and ferroptosis‑related markers were assessed. Co‑immunoprecipitation was used to assess Keap1‑Nrf2 interactions and confocal microscopy was employed to observe Nrf2 nuclear translocation. BM pretreatment dose‑dependently restored cystine uptake, increased GSH levels and improved cell viability, while reducing intracellular iron accumulation and lipid peroxidation triggered by dRib. These protective effects were attenuated by Nrf2 inhibitors, indicating that the activity of BM is Nrf2‑dependent. BM enhanced Nrf2 protein expression, upregulated SLC7A11 and increased the expression of Nrf2‑ARE target genes, including heme oxygenase‑1, NADPH quinone oxidoreductase 1, glutamate‑cysteine ligase catalytic subunit and glutamate‑cysteine ligase modifier subunit, while suppressing ferroptosis‑related markers (acyl‑CoA synthetase long chain family member 4, ChaC glutathione‑specific gamma‑glutamylcyclotransferase 1 and prostaglandin‑endoperoxide synthase 2). Furthermore, BM disrupted the Nrf2‑Keap1 interaction, promoting Nrf2 nuclear translocation. In conclusion, BM may disrupt the Keap1‑Nrf2 interaction in RTECs, upregulate SLC7A11 and mitigate dRib‑induced ferroptosis, thereby presenting a potential therapeutic option to prevent the progression of DKD by protecting RTECs from ferroptosis.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"32 4","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12319272/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144708204","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Activation of toll‑like receptors by non‑coding RNAs and their fragments (Review).","authors":"Ruth Ruiz Esparza-Garrido, Miguel Ángel Velázquez-Flores","doi":"10.3892/mmr.2025.13650","DOIUrl":"10.3892/mmr.2025.13650","url":null,"abstract":"<p><p>Non‑coding RNAs are a diverse group of RNAs that are generally not translated into proteins, and control gene expression and other cellular processes through a myriad of mechanisms. Non‑coding RNAs are fragmented to regulate cellular processes such as ribosomal RNA maturation, reverse transcription and degradation of nascent transcripts, among other functions. Non‑coding RNAs and their fragments interact with Toll‑like receptors (TLRs) to induce the activation of the innate and adaptative immune system, which are important for counteracting viral and bacterial infections as well as for triggering ischemia‑related cytotoxic effects in the brain. As the study of these interactions progresses, novel functions are being elucidated, such as their participation in viral reactivation in the brain. Due to their importance as pattern recognition receptor families, TLRs may be potential therapeutic targets for the treatment of autoimmune diseases, viral diseases and cancer. TLR activators are currently used for the treatment of different types of cancer and several other biomolecules are still under investigation to progress towards clinical use. The ncRNAs and their fragments also function as ligands for TLRs, but further study of non‑coding RNAs and their action on TLRs will allow the elucidation of new TLR agonists and antagonists to establish successful immunotherapies. The aim of the present review is to show the existing evidence on TLR activation by ncRNAs and their fragments, with special emphasis on the diseases in which they are involved and on the potential of the study of these interactions for the identification of therapeutic targets and development of therapies.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"32 4","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12365740/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144847588","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"O‑GlcNAcylation: The crosstalk between infection immunity and autophagy in sepsis (Review).","authors":"Zhenzhen Huang, Xin Liu, Ling Zhang, Yujie Lin, Xiangli Ma, Peiwu Li","doi":"10.3892/mmr.2025.13646","DOIUrl":"10.3892/mmr.2025.13646","url":null,"abstract":"<p><p>Sepsis is a life‑threatening condition triggered by dysregulated host immune responses, involving complex interactions among immune cell dysfunction, metabolic reprogramming and impaired autophagy. As a dynamic post‑translational modification of serine/threonine residues, the attachment of N‑acetylglucosamine (GlcNAc) via an oxygen linkage (O‑GlcNAcylation) serves as a central hub in the pathogenesis of sepsis by integrating immunometabolic adaptation and autophagy regulation. This modification, dynamically controlled by O‑GlcNAc transferase and O‑GlcNAcase, modulates immune cell activation, inflammatory signaling and pathogen clearance. In sepsis, aberrant O‑GlcNAcylation exacerbates organ damage by promoting pro‑inflammatory cytokine release and suppressing protective autophagy. Studies have highlighted its dual role: Enhancing O‑GlcNAcylation can bolster antiviral immunity, while targeted inhibition could mitigate bacteria‑induced hyperinflammation. Furthermore, O‑GlcNAcylation regulates the initiation, elongation and lysosomal fusion stages of autophagy by modifying key proteins, including beclin1, unc‑51‑like kinase 1 and synaptosome-associated protein 29, thereby influencing immune cell function. The present review also explores the mechanisms by which O‑GlcNAcylation modulates immune responses across diverse pathogens, namely bacteria, fungi, viruses and parasites, via signaling pathways such as NF‑κB and STAT, emphasizing the importance of site‑specific interventions and biomarker development. In conclusion, targeting O‑GlcNAcylation offers a potential novel direction for sepsis treatment. However, further exploration of its dynamic equilibrium in the precise regulation of the immune‑autophagy network is necessary.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"32 4","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12340768/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144799581","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ER‑α36 knockdown is associated with lysosomal dysfunction and proliferation inhibition in liver cancer cells.","authors":"Huanhuan He, Xuan Wang, Zhixuan Wei, An Wang, Xiangyue Fang, Hanbo He, Zhuorui Wu, Xiji Shu, Binlian Sun, Qiongxia Chen, Xuan Huang, Hongyan Zhou, Yuchen Liu, Zhengqi Fu","doi":"10.3892/mmr.2025.13649","DOIUrl":"10.3892/mmr.2025.13649","url":null,"abstract":"<p><p>Estrogen receptor (ER)‑α36 and autophagy have each independently been reported to promote the proliferation of liver cancer cells; however, the association between them has not been explored. Therefore, the present study aimed to investigate the role and the underlying mechanism of ER‑α36 in the regulation of autophagy in liver cancer cells. The proliferation of liver cancer cell variants was examined by colony formation assay. A xenograft tumor model in nude mice was used to examine the role of ER‑α36 in malignant proliferation of liver cancer cells <i>in vivo</i>. Autophagic flux and lysosomal localization were assessed with immunofluorescence and confocal microscopy. The levels of ER‑α36, LAMP1, AKT, p62 and LC3‑Ⅱ/Ⅰ in liver cancer cell variants, and tumors formed by HepG2 cell variants in the nude mice were examined using Western blot and immunohistochemistry. The results revealed that ER‑α36 knockdown impaired autophagic flux by increasing lysosomal membrane permeabilization (LMP) and blocking lysosomal degradation. ER‑α36 knockdown also significantly inhibited the proliferation of liver cancer cells and orthotopic liver xenograft tumors. In addition, decreased AKT phosphorylation and the juxtanuclear clustering of lysosomes were observed in the liver cancer cells with ER‑α36 knockdown. <i>In vitro</i> experiments using the AKT inhibitor MK‑2206 indicated that AKT is involved in the ER‑α36 knockdown‑induced changes in LMP and lysosomal localization in liver cancer cells. In summary, the present study revealed that ER‑α36 plays a role in regulating the autophagy and proliferation of liver cancer cells, which is associated with the modulation of AKT signaling, LMP and lysosome localization. These findings highlight an important role of ER‑α36 in liver tumorigenesis.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"32 4","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12365738/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144847589","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Anti‑inflammatory and anti‑migratory properties of wild‑grape‑derived ε‑viniferin in human endometrial cells:  A potential therapy for endometriosis.","authors":"Yinzhi Lin, Yoshikazu Naiki, Shiori Kojima, Masatoshi Hakamata, Hitomi Fukatsu, Yoshiaki Hasegawa, Akihiko Wakatsuki, Naoki Koide, Kazuo Umezawa","doi":"10.3892/mmr.2025.13648","DOIUrl":"10.3892/mmr.2025.13648","url":null,"abstract":"<p><p>Endometriosis is a chronic gynecological disorder characterized by the ectopic growth and proliferation of endometrial tissue outside the uterine cavity, leading to inflammation. Although low‑dose contraceptive pills are widely used for its treatment, these therapies are associated with side effects and are contraindicated in women trying to conceive. ε‑viniferin is a resveratrol dimer found in wild grapes (<i>Ampelopsis brevipedunculata</i>) with demonstrated antioxidant properties and an anti‑migratory effect in lung cancer cells. Because abnormal cell migration is a key process in endometriosis, we hypothesized that ε‑viniferin could also exhibit anti‑migratory effects in endometriotic cells, which remain to be elucidated. To test this hypothesis, the present study investigated the anti‑inflammatory and anti‑endometriotic effects of ε‑viniferin and wild‑grape extract. RAW264.7 and THP‑1 were used to evaluate the anti‑inflammatory effects of wild‑grape extract and ε‑viniferin by assessing cytotoxicity; nitric oxide (NO), reactive oxygen species and interleukin‑6 (IL‑6) production; and NF‑κB activity. Additionally, human endometrial stromal cells (HESCs) were used to investigate the anti‑endometriotic effects of ε‑viniferin, including its impact on cell migration, invasion and gene expression, using PCR array analysis. Both ε‑viniferin and wild‑grape extract significantly reduced lipopolysaccharide‑induced NO and IL‑6 production, indicating an anti‑inflammatory activity. Inhibition of NF‑κB activity at the cellular level further supported these findings. Moreover, both ε‑viniferin and wild‑grape extract effectively suppressed the migration and invasion of HESCs, indicating their potential to alleviate endometriosis symptoms. These findings suggest that ε‑viniferin is a promising therapeutic candidate for endometriosis, exhibiting both anti‑inflammatory and anti‑migratory effects. Our results present a novel approach for developing effective anti‑endometriotic therapies.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"32 4","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12365741/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144799679","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Retracted] Fisetin inhibits migration, invasion and epithelial‑mesenchymal transition of LMP1‑positive nasopharyngeal carcinoma cells.","authors":"Rong Li, Yinhai Zhao, Jin Chen, Songjun Shao, Xiujuan Zhang","doi":"10.3892/mmr.2025.13628","DOIUrl":"10.3892/mmr.2025.13628","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 cell migration and invasion assay data shown in Fig. 1A and B on p. 415 contained a number of overlapping data sections, such that data which were intended to show the results from differently performed experiments had apparently been derived from the same original sources. In view of the large number of panels containing overlapping sections of data that were identified in Fig. 1, the Editor of <i>Molecular Medicine Reports</i> has decided that this paper should be retracted from the Journal due to a lack of confidence in the presented data. 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 9: 413‑418, 2014; DOI: 10.3892/mmr.2013.1836].</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"32 4","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12311558/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144708202","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}