International journal of molecular medicine最新文献

{"title":"[Retracted] Puerarin improves graft bone defect through microRNA‑155‑3p‑mediated p53/TNF‑α/STAT1 signaling pathway.","authors":"Yang Zhou, Hongyu Lian, Kexin Liu, Deli Wang, Xuelian Xiu, Zhang Sun","doi":"10.3892/ijmm.2024.5404","DOIUrl":"10.3892/ijmm.2024.5404","url":null,"abstract":"<p><p>Following the publication of the above paper, it has been drawn to the Editor's attention by a concerned reader that the immunohistochemical assay data shown in Fig. 4B on p. 245 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>International Journal of Biological Sciences</i> prior to the submission of this paper to <i>International Journal of Molecular Medicine</i>. In view of the fact that the contentious data had already apparently been published previously, the Editor of International Journal of Molecular Medicine has decided that this paper should be retracted from the Journal. After having been in contact with the authors, they agreed with the decision to retract the paper. The Editor apologizes to the readership for any inconvenience caused. [International Journal of Molecular Medicine 46: 239-251, 2020; DOI: 10.3892/ijmm.2020.4595].</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":null,"pages":null},"PeriodicalIF":5.7,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11315659/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141758519","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":"SPP1 promotes the polarization of M2 macrophages through the Jak2/Stat3 signaling pathway and accelerates the progression of idiopathic pulmonary fibrosis.","authors":"Xuelian Yang, Ziqin Liu, Jiawei Zhou, Jianqiang Guo, Tao Han, Yafeng Liu, Yunyun Li, Ying Bai, Yingru Xing, Jing Wu, Dong Hu","doi":"10.3892/ijmm.2024.5413","DOIUrl":"10.3892/ijmm.2024.5413","url":null,"abstract":"<p><p>Idiopathic pulmonary fibrosis (IPF) is a fatal pulmonary disease that requires further investigation to understand its pathogenesis. The present study demonstrated that secreted phosphoprotein 1 (SPP1) was aberrantly highly expressed in the lung tissue of patients with IPF and was significantly positively associated with macrophage and T‑cell activity. Cell localization studies revealed that SPP1 was primarily overexpressed in macrophages, rather than in T cells. Functionally, knocking down SPP1 expression <i>in vitro</i> inhibited the secretion of fibrosis‑related factors and M2 polarization in macrophages. Furthermore, knocking down SPP1 expression inhibited the macrophage‑induced epithelial‑to‑mesenchymal transition in both epithelial and fibroblastic cells. Treatment with SPP1 inhibitors <i>in vivo</i> enhanced lung function and ameliorated pulmonary fibrosis. Mechanistically, SPP1 appears to promote macrophage M2 polarization by regulating the JAK/STAT3 signaling pathway both <i>in vitro</i> and <i>in vivo</i>. In summary, the present study found that SPP1 promotes M2 polarization of macrophages through the JAK2/STAT3 signaling pathway, thereby accelerating the progression of IPF. Inhibition of SPP1 expression <i>in vivo</i> can effectively alleviate the development of IPF, indicating that SPP1 in macrophages may be a potential therapeutic target for IPF.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":null,"pages":null},"PeriodicalIF":5.7,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11335352/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141916676","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":"NCAPD2 augments the tumorigenesis and progression of human liver cancer via the PI3K‑Akt‑mTOR signaling pathway.","authors":"Jiang-Xue Gu, Ke Huang, Wei-Lin Zhao, Xiao-Ming Zheng, Yu-Qin Wu, Shi-Rong Yan, Yu-Gang Huang, Pei Hu","doi":"10.3892/ijmm.2024.5408","DOIUrl":"10.3892/ijmm.2024.5408","url":null,"abstract":"<p><p>Non‑SMC condensin I complex subunit D2 (<i>NCAPD2</i>) is a newly identified oncogene; however, the specific biological function and molecular mechanism of NCAPD2 in liver cancer progression remain unknown. In the present study, the aberrant expression of <i>NCAPD2</i> in liver cancer was investigated using public tumor databases, including TNMplot, The Cancer Genome Atlas and the International Cancer Genome Consortium based on bioinformatics analyses, and it was validated using a clinical cohort. It was revealed that NCAPD2 was significantly upregulated in liver cancer tissues compared with in control liver tissues, and <i>NCAPD2</i> served as an independent prognostic factor and predicted poor prognosis in liver cancer. In addition, the expression of NCAPD2 was positively correlated with the percentage of Ki67⁺ cells. Finally, single‑cell sequencing data, gene‑set enrichment analyses and <i>in</i> <i>vitro</i> investigations, including cell proliferation assay, Transwell assay, wound healing assay, cell cycle experiments, cell apoptosis assay and western blotting, were carried out in human liver cancer cell lines to assess the biological mechanisms of NCAPD2 in patients with liver cancer. The results revealed that the upregulation of NCAPD2 enhanced tumor cell proliferation, invasion and cell cycle progression at the G₂/M‑phase transition, and inhibited apoptosis in liver cancer cells. Furthermore, NCAPD2 overexpression was closely associated with the phosphatidylinositol 3‑kinase (PI3K)‑Akt‑mammalian target of rapamycin (mTOR)/c‑Myc signaling pathway and epithelial‑mesenchymal transition (EMT) progression in HepG2 and Huh7 cells. In addition, upregulated <i>NCAPD2</i> was shown to have adverse effects on overall survival and disease‑specific survival in liver cancer. In conclusion, the overexpression of NCAPD2 was shown to lead to cell cycle progression at the G₂/M‑phase transition, activation of the PI3K‑Akt‑mTOR/c‑Myc signaling pathway and EMT progression in human liver cancer cells.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":null,"pages":null},"PeriodicalIF":5.7,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11315656/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141874769","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":"Luteolin enhances drug chemosensitivity by downregulating the FAK/PI3K/AKT pathway in paclitaxel‑resistant esophageal squamous cell carcinoma.","authors":"Zhenzhen Yang, Hongtao Liu, Yinsen Song, Na Gao, Pan Gao, Yiran Hui, Yueheng Li, Tianli Fan","doi":"10.3892/ijmm.2024.5401","DOIUrl":"10.3892/ijmm.2024.5401","url":null,"abstract":"<p><p>Drug resistance is a key factor underlying the failure of tumor chemotherapy. It enhances the stem‑like cell properties of cancer cells, tumor metastasis and relapse. Luteolin is a natural flavonoid with strong anti‑tumor effects. However, the mechanism(s) by which luteolin protects against paclitaxel (PTX)‑resistant cancer cell remains to be elucidated. The inhibitory effect of luteolin on the proliferation of EC1/PTX and EC1 cells was detected by cell counting kit‑8 assay. Colony formation and flow cytometry assays were used to assess clonogenic capacity, cell cycle and apoptosis. Wound healing and Transwell invasion tests were used to investigate the effects of luteolin on the migration and invasion of EC1/PTX cells. Western blotting was used to detect the protein levels of EMT‑related proteins and stem cell markers after sphere formation. Parental cells and drug‑resistant cells were screened by high‑throughput sequencing to detect the differential expression of RNA and differential genes. ELISA and western blotting were used to verify the screened PI3K/Akt signaling pathway, key proteins of which were explored by molecular docking. Hematoxylin and eosin staining and TUNEL staining were used to observe tumor xenografts on morphology and apoptosis in nude mice. The present study found that luteolin inhibited tumor resistance (inhibited proliferation, induced cell cycle arrest and apoptosis and hindered migration invasion, EMT and stem cell spherification) <i>in</i> <i>vitro</i> in PTX‑resistant esophageal squamous cell carcinoma (ESCC) cells. In addition, luteolin enhanced drug sensitivity and promoted the apoptosis of drug‑resistant ESCC cells in combination with PTX. Mechanistically, luteolin may inhibit the PI3K/AKT signaling pathway by binding to the active sites of focal adhesion kinase (FAK), Src and AKT. Notably, luteolin lowered the tumorigenic potential of PTX‑resistant ESCC cells but did not show significant toxicity <i>in</i> <i>vivo</i>. Luteolin enhanced drug chemosensitivity by downregulating the FAK/PI3K/AKT pathway in PTX‑resistant ESCC and could be a promising agent for the treatment of PTX‑resistant ESCC cancers.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":null,"pages":null},"PeriodicalIF":5.7,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11265837/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141590266","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 autophagy and ferroptosis in the development of endometriotic cysts (Review).","authors":"Hiroshi Kobayashi, Shogo Imanaka, Chiharu Yoshimoto, Sho Matsubara, Hiroshi Shigetomi","doi":"10.3892/ijmm.2024.5402","DOIUrl":"10.3892/ijmm.2024.5402","url":null,"abstract":"<p><p>It is considered that the etiology of endometriosis is retrograde menstruation of endometrial tissue. Although shed endometrial cells are constantly exposed to a challenging environment with iron overload, oxidative stress and hypoxia, a few cells are able to survive and continue to proliferate and invade. Ferroptosis, an iron‑dependent form of non‑apoptotic cell death, is known to play a major role in the development and course of endometriosis. However, few papers have concentrated on the dynamic interaction between autophagy and ferroptosis throughout the progression of diseases. The present review summarized the current understanding of the mechanisms underlying autophagy and ferroptosis in endometriosis and discuss their role in disease development and progression. For the present narrative review electronic databases including PubMed and Google Scholar were searched for literature published up to the October 31, 2023. Autophagy and ferroptosis may be activated at early stages in endometriosis development. On the other hand, excessive activation of intrinsic pathways (e.g., estrogen and mechanistic target of rapamycin) may promote disease progression through autophagy inhibition. Furthermore, suppression of ferroptosis may cause further progression of endometriotic lesions. In conclusion, the autophagy and ferroptosis pathways may play a dual role in disease initiation and progression. The present review discussed the temporal transition of non‑apoptotic cell death regulation during disease progression from retrograde endometrium to early lesions to established lesions.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":null,"pages":null},"PeriodicalIF":5.7,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11265838/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141590267","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":"Triptonide protects retinal cells from oxidative damage via activation of Nrf2 signaling.","authors":"Jinjing Li, Jiajun Li, Yuan Cao, Jin Yuan, Yaming Shen, Linyi Lei, Keran Li","doi":"10.3892/ijmm.2024.5400","DOIUrl":"10.3892/ijmm.2024.5400","url":null,"abstract":"<p><p>Age‑related macular degeneration (AMD) is an ocular disease that threatens the visual function of older adults worldwide. Key pathological processes involved in AMD include oxidative stress, inflammation and choroidal vascular dysfunction. Retinal pigment epithelial cells and Müller cells are most susceptible to oxidative stress. Traditional herbal medicines are increasingly being investigated in the field of personalized medicine in ophthalmology. Triptonide (Tn) is a diterpene tricyclic oxide, the main active ingredient in the extract from the Chinese herbal medicinal plant <i>Tripterygium wilfordii</i>, and is considered an effective immunosuppressant and anti‑inflammatory drug. The present study investigated the potential beneficial role of Tn in retinal oxidative damage in order to achieve personalized treatment for early AMD. An oxidative stress model of retinal cells induced by H₂O₂ and a retinal injury model of mice induced by light and N‑Methyl‑D‑aspartic acid were constructed. <i>In vitro</i>, JC‑1 staining, flow cytometry and apoptosis assay confirmed that low concentrations of Tn effectively protected retinal cells from oxidative damage, and reverse transcription‑quantitative PCR and western blotting analyses revealed that Tn reduced the expression of retinal oxidative stress‑related genes and inflammatory factors, which may depend on the PI3K/AKT/mTOR‑induced Nrf2 signaling pathway. <i>In vivo</i>, by retinal immunohistochemistry, hematoxylin and eosin staining and electroretinogram assay, it was found that retinal function and structure improved and choroidal neovascularization was significantly inhibited after Tn pretreatment. These results suggested that Tn is an efficient Nrf2 activator, which can be expected to become a new intervention for diseases such as AMD, to inhibit retinal oxidative stress damage and pathological neovascularization.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":null,"pages":null},"PeriodicalIF":5.7,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11265836/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141590268","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":"PANoptosis: Novel insight into regulated cell death and its potential role in cardiovascular diseases (Review).","authors":"Xinyu Gao, Cuixue Ma, Shan Liang, Meihong Chen, Yuan He, Wei Lei","doi":"10.3892/ijmm.2024.5398","DOIUrl":"10.3892/ijmm.2024.5398","url":null,"abstract":"<p><p>PANoptosis, a complex form of proinflammatory programmed cell death, including apoptosis, pyroptosis and necroptosis, has been an emerging concept in recent years that has been widely reported in cancer, infectious diseases and neurological disorders. Cardiovascular diseases (CVDs) are an important global health problem, posing a serious threat to individuals' lives. An increasing body of research shows that inflammation has a pivotal role in CVDs, which provides an important theoretical basis for PANoptosis to promote the progression of CVDs. To date, only sporadic studies on PANoptosis in CVDs have been reported and its role in the field of CVDs has not been fully explored. Elucidating the various modes of cardiomyocyte death, the specific molecular mechanisms and the links among the various modes of death under various stressful stimuli is of notable clinical significance for a deeper understanding of the pathophysiology of CVDs. The present review summarizes the molecular mechanisms of apoptosis, pyroptosis, necroptosis and PANoptosis and their prospects in the field of CVDs.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":null,"pages":null},"PeriodicalIF":5.7,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11254103/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141498038","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":"Salusin‑α alleviates lipid metabolism disorders via regulation of the downstream lipogenesis genes through the LKB1/AMPK pathway.","authors":"Jintong Pan, Chao Yang, Aohong Xu, Huan Zhang, Ye Fan, Rong Zeng, Lin Chen, Xiang Liu, Yuxue Wang","doi":"10.3892/ijmm.2024.5397","DOIUrl":"10.3892/ijmm.2024.5397","url":null,"abstract":"<p><p>Lipid metabolism disorders are a major cause of several chronic metabolic diseases which seriously affect public health. Salusin‑α, a vasoactive peptide, has been shown to attenuate lipid metabolism disorders, although its mechanism of action has not been reported. To investigate the effects and potential mechanisms of Salusin‑α on lipid metabolism, Salusin‑α was overexpressed or knocked down using lentiviral vectors. Hepatocyte steatosis was induced by free fatty acid (FFA) after lentiviral transfection into HepG2 cells. The degree of lipid accumulation was assessed using Oil Red O staining and by measuring several biochemical indices. Subsequently, bioinformatics was used to analyze the signaling pathways that may have been involved in lipid metabolism disorders. Finally, semi‑quantitative PCR and western blotting were used to verify the involvement of the liver kinase B1 (LKB1)/AMPK pathway. Compound C, an inhibitor of AMPK, was used to confirm this mechanism's involvement further. The results showed that Salusin‑α significantly attenuated lipid accumulation, inflammation and oxidative stress. In addition, Salusin‑α increased the levels of LKB1 and AMPK, which inhibited the expression of sterol regulatory element binding protein‑1c, fatty acid synthase and acetyl‑CoA carboxylase. The addition of Compound C abrogated the Salusin‑α‑mediated regulation of AMPK on downstream signaling molecules. In summary, overexpression of Salusin‑α activated the LKB1/AMPK pathway, which in turn inhibited lipid accumulation in HepG2 cells. This provides insights into the potential mechanism underlying the mechanism by which Salusin‑α ameliorates lipid metabolism disorders while identifying a potential therapeutic target.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":null,"pages":null},"PeriodicalIF":5.7,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11254102/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141498039","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":"[Corrigendum] All‑<i>trans</i> retinoic acid alters the expression of the tight junction proteins Claudin‑1 and ‑4 and epidermal barrier function‑associated genes in the epidermis.","authors":"Jing Li, Qianying Li, Songmei Geng","doi":"10.3892/ijmm.2024.5399","DOIUrl":"10.3892/ijmm.2024.5399","url":null,"abstract":"<p><p>Following the publication of the above article, the authors contacted the Editorial Office to explain that they had identified a pair of duplicate images in the control (Vehicle) group of mouse images in Fig. 1A on p. 1792. Specifically, the same image (corresponding correctly to the 'Day 5' experiment) was inadvertently chosen to represent the cutaneous manifestations of mice in the Vehicle group on 'Day 3' and 'Day 5' in Fig. 1A. This error arose as a consequence of repetitive application and duplication procedures within the image set, resulting in the inadvertent reuse of the same photo. Additionally, due to minimal alterations observed in the skin condition of mice from the control group following treatment, each mouse exhibited a similar appearance; this similarity further contributed to the delayed identification of this error during the paper revision stage. Consequently, this duplication of the same image was made as a result of insufficient scrutiny. The revised version of Fig. 1, showing the correct image for the 'Day 3' experiment in Fig. 1A, is shown on the next page. The authors can confirm that the error associated with the assembly of this figure did not have any significant impact on either the results or the conclusions reported in this study, and all the authors agree with the publication of this Corrigendum. The authors are grateful to the Editor of <i>International Journal of Molecular Medicine</i> for allowing them the opportunity to publish this; furthermore, they apologize to the readership of the Journal for any inconvenience caused. [International Journal of Molecular Medicine 43: 1789‑1805, 2019; DOI: 10.3892/ijmm.2019.4098].</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":null,"pages":null},"PeriodicalIF":5.7,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11254101/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141590265","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":"Improved efficacy of cisplatin delivery by peanut agglutinin‑modified liposomes in non‑small cell lung cancer.","authors":"Ben Yang, Rongguan Kou, Hui Wang, Anping Wang, Lili Wang, Sipeng Sun, Mengqi Shi, Shouzhen Zhao, Yubing Wang, Yi Wang, Jingliang Wu, Fei Wu, Fan Yang, Meihua Qu, Wenjing Yu, Zhiqin Gao","doi":"10.3892/ijmm.2024.5394","DOIUrl":"10.3892/ijmm.2024.5394","url":null,"abstract":"<p><p>Globally, non‑small cell lung cancer (NSCLC) is a significant threat to human health, and constitutes >80% of lung cancer cases. Cisplatin (CDDP), a commonly used drug in clinical treatment, has been the focus of research aiming to mitigate its potent toxicity through encapsulation within liposomes. However, challenges, such as a reduced drug loading efficiency and nonspecific release, have emerged as obstacles. The present study aimed to improve the encapsulation efficiency of CDDP within liposomes by pre‑preparation of CDDP and modifying the liposome surface through the incorporation of peanut agglutinin (PNA) as a ligand [CDDP‑loaded PNA‑modified liposomes (CDDP‑PNA‑Lip)]. This strategy was designed to enhance the delivery of CDDP to tumour tissues, thereby reducing associated side effects. The effect of CDDP‑PNA‑Lip on the proliferation and migration of NSCLC cell lines with high MUC1 expression was elucidated through <i>in vitro</i> studies. Additionally, the capacity of PNA modification to augment the targeted anti‑tumour efficacy of liposomes was assessed through xenograft tumour experiments. The results indicated that in an in vitro uptake assay Rhodamine B (RhB)‑loaded PNA‑modified liposomes were taken up by cells with ~50% higher efficiency compared with free RhB. In addition, CDDP‑PNA‑Lip resulted in a 2.65‑fold enhancement of tumour suppression <i>in vivo</i> compared with free CDDP. These findings suggested that the encapsulation of CDDP within ligand‑modified liposomes may significantly improve its tumour‑targeting capabilities, providing valuable insights for clinical drug development.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":null,"pages":null},"PeriodicalIF":5.7,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11232663/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141498035","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}