Hereditas最新文献

{"title":"M2 macrophage-derived exosomes promote the malignant progression and glycolysis of cervical cancer via Msi1.","authors":"Liting Sun, Abudureyimu Tunishahan, Xiaowen Li","doi":"10.1186/s41065-026-00703-9","DOIUrl":"https://doi.org/10.1186/s41065-026-00703-9","url":null,"abstract":"<p><strong>Background: </strong>Cervical cancer is a common gynecologic malignancy characterized by high recurrence and metastasis rate. Exosomes derived from M2-polarized tumor-associated macrophages play a key role in promoting tumorigenesis and cancer progression. Additionally, musashi1 (Msi1) is a key oncoprotein across multiple malignancies. Therefore, this study aims to determine the role of M2 macrophage-derived exosomal Msi1 in cervical cancer progression and glycolysis and to clarify the underlying mechanism.</p><p><strong>Methods: </strong>M2 macrophages were identified using microscope, flow cytometry, and western blot. Gene mRNA and protein expression levels were analyzed via quantitative real-time polymerase chain reaction (qRT-PCR) and western blot. The cell proliferation, invasion, apoptosis, and sphere formation were assessed using 5-Ethynyl-2'-deoxyuridine (EdU) staining, Transwell, flow cytometry, and sphere formation assay, respectively. The glucose uptake and lactate production were determined using commercial kits. Exosomes were identified using western blot, transmission electron microscopy, and nanoparticle tracking analysis (NTA). Cellular uptake of exosomes was assessed by incubating SiHa and Ca Ski cells with PKH67-labeled exosomes. Cervical cancer xenograft mouse models were established to analyze the role of M2 macrophage-derived exosomal Msi1.</p><p><strong>Results: </strong>Msi1 expression was increased in M2 macrophages (**P < 0.01 and ***P < 0.001). Functionally, M2 macrophages enhanced cervical cancer cell proliferation, invasion, aerobic glycolysis, and stemness as well as suppressed cell apoptosis through secreting exosomes (*P < 0.05, **P < 0.01, and ***P < 0.001). Importantly, Msi1 expression was increased in M2 macrophage-derived exosomes (***P < 0.001). Mechanically, M2 macrophage-derived exosomes promoted malignancy and glycolysis by carrying Msi1 (*P < 0.01 and ***P < 0.001). In vivo, M2 macrophage-derived exosomal Msi1 accelerated cervical cancer progression (***P < 0.001).</p><p><strong>Conclusion: </strong>M2 macrophage-derived exosomes promote cervical cancer progression and glycolysis by delivering Msi1 to recipient cells.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148328800","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"KLF5 promotes proliferation, migration, and autophagy-/EMT‑associated molecular changes in lens epithelial cells via transcriptional activation of THBS1 in traumatic cataract.","authors":"Junjun Han, Tian Wang, Xin Yang, Xiaoli Li","doi":"10.1186/s41065-026-00701-x","DOIUrl":"https://doi.org/10.1186/s41065-026-00701-x","url":null,"abstract":"<p><strong>Purpose: </strong>Traumatic cataract is a common blinding eye disease after ocular trauma, and its pathogenesis is closely related to lens epithelial cell dysfunction, while the definite molecular regulatory mechanism between upstream transcription factor and downstream target gene remains poorly clarified. This study aimed to clarify the role and molecular mechanism of the krüppel-like factor 5 (KLF5)/ thrombosponin 1 (THBS1) axis in regulating proliferation, migration, epithelial-mesenchymal transition and autophagy of lens epithelial cells in traumatic cataract, and to explore its potential clinical therapeutic value.</p><p><strong>Methods: </strong>The GSE295383 dataset in the gene expression omnibus (GEO) database was downloaded, and the differentially expressed genes (DEGs) were screened by linear models for microarray data (limma) package of R language. Combined with Weighted gene co-expression network analysis (WGCNA), the gene co-expression network was constructed and the key modules were screened. Gene ontology (GO), kyoto encyclopedia of genes and genomes (KEGG) and gene set enrichment analysis (GSEA) combined with human transcription factor target (hTFtarget) and JASPAR databases were used to predict the upstream transcription factors of THBS1. Subsequently, SRA01/04 cells were induced with transforming growth factor-beta 2 (TGF-β2) to construct a cataract cell model.</p><p><strong>Results: </strong>THBS1 and KLF5 were highly expressed in LECs exposed to TGF-β2. KLF5 could activate THBS1 transcription by binding to THBS1 promoter - 174 to -165 sites. Knockdown of THBS1 inhibited TGF-β2-induced viability, proliferation, migration, and altered the expression of epithelial-mesenchymal transition (EMT)- and autophagy-related markers in LECs. Knockdown of KLF5 downregulated THBS1 expression and produced a similar inhibitory effect, while overexpression of THBS1 reversed the effect of KLF5 knockdown.</p><p><strong>Conclusions: </strong>This study demonstrated that KLF5 promoted the proliferation, migration, and EMT‑associated molecular changes of LECs in traumatic cataract through transcriptional activation of THBS1, and regulated the expression of autophagy‑related markers in LECs, suggesting that KLF5/THBS1 axis might be a potential target for the treatment of traumatic cataract.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148316999","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Development and validation of palmitoylation-related genes characteristics for prediction of prognosis and immune landscape in endometrial cancer.","authors":"Chuchu Zhao, Guiying Zhang","doi":"10.1186/s41065-026-00699-2","DOIUrl":"10.1186/s41065-026-00699-2","url":null,"abstract":"<p><strong>Background: </strong>Endometrial cancer (EC) is the most common cancer of the female reproductive system. Palmitoylation dysregulation is linked to various diseases. However, there is still insufficient research on its use as a prognostic marker for EC.</p><p><strong>Methods: </strong>This research utilized transcriptomic data and clinical characteristics from EC patients sourced from the TCGA database. Key palmitoylation-related genes (PRGs) were identified through a series of bioinformatics analyses, followed by the construction of a prognostic model. The mRNA expression levels of characteristic genes in EC cells and clinical samples were investigated through reverse transcription quantitative polymerase chain reaction (RT-qPCR). Immune infiltration analysis was performed using ssGSEA and CIBERSORT. The molecular subtypes of EC were identified by consensus clustering.</p><p><strong>Results: </strong>This study identified six PRGs, and the results of bioinformatic analysis of their mRNA expression patterns were consistent with experimental validation. A risk stratification model constructed based on these six PRGs was able to significantly distinguish between high-risk and low-risk patients in terms of survival prognosis, with patients in the low-risk group having a better prognosis than those in the high-risk group. Furthermore, immune characteristic heterogeneity was observed among different risk subgroups. Through consensus clustering analysis, EC samples were classified into two molecular subtypes with significant differences.</p><p><strong>Conclusion: </strong>This study constructed and validated a prognostic risk model for EC based on PRGs, which demonstrated potential for stratifying patient survival rates and characterizing immune microenvironment features in a retrospective dataset.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-06-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13540888/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148301305","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of miR-557 in modulating cervical cancer malignancy by targeting TAOK1.","authors":"Yilin Yin, Yingying Huang, Li Lin, Mingxiu Cui, Linge Zhong","doi":"10.1186/s41065-026-00695-6","DOIUrl":"10.1186/s41065-026-00695-6","url":null,"abstract":"<p><strong>Background: </strong>Cervical cancer (CC) remains a major threat to women's health globally. Although miR-557 is a tumor suppressor in multiple cancers, its role in CC remains unclear.</p><p><strong>Objective: </strong>This study investigated whether miR-557 regulates CC progression by targeting TAOK1.</p><p><strong>Methods: </strong>This study collected 113 pairs of cervical cancer tissues and adjacent tissues. The expression of miR-557 was detected by qRT-PCR, and its relationship with clinicopathological features and prognosis was analyzed. In HeLa and SiHa cell lines, we performed functional assays (CCK-8, Transwell) and measured ferroptosis-related indicators (Fe²⁺, GSH, GSH-Px) after transfecting miR-557 mimic or TAOK1 overexpression vectors. The miR-557/TAOK1 targeting relationship was validated by dual-luciferase reporter assay and rescue experiments.</p><p><strong>Results: </strong>miR-557 was significantly downregulated in CC tissues and cell lines. Low miR-557 expression correlated with advanced FIGO stage, LNM, and poor prognosis. Functionally, miR-557 overexpression inhibited CC cell proliferation, migration, and invasion, accompanied by increased Fe²⁺ levels and decreased GSH and GSH-Px activity. TAOK1 was identified as a direct target of miR-557, and its overexpression reversed the tumor-suppressive effects and ferroptosis-related changes induced by miR-557.</p><p><strong>Conclusions: </strong>miR-557 is significantly downregulated in CC and exerts tumor-suppressive functions. By targeting TAOK1, it inhibits the malignant progression of CC cells and may act as a promising biomarker for CC.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13491869/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148239264","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comprehensive molecular analyses of a circadian rhythm-related gene diagnostic model and immune infiltration using machine learning methods in sepsis-associated acute kidney injury.","authors":"Yuzhen Luo, Tangjuan Liu, Yiqiang Chen","doi":"10.1186/s41065-026-00698-3","DOIUrl":"10.1186/s41065-026-00698-3","url":null,"abstract":"<p><strong>Background: </strong>This study aimed to explore hub circadian rhythm-related genes (CRRGs) associated with sepsis-associated acute kidney injury (saAKI) using machine learning algorithms to provide novel ideas for the diagnosis and treatment of this disease.</p><p><strong>Materials: </strong>Two AKI datasets (GSE30718 and GSE139061) were obtained from the Gene Expression Omnibus (GEO) database. We initially identified differentially expressed genes (DEGs) and performed WGCNA to identify candidate CRRGs. Following this, diagnostic CRRGs were identified on the basis of machine learning algorithms. The ssGSEA method was used to measure the link between hub CRRGs and immune cells. GSEA and GSVA were used to understand the relevant functions and pathways. The hub CRRGs were validated using the GSE255281 dataset and RT‒qPCR of clinical blood samples.</p><p><strong>Results: </strong>On the basis of the DEGs and WGCNA results, a total of 21 candidate CRRGs were obtained for saAKI. Seven diagnostic CRRGs were identified via the Lasso, random forest (RF) and SVM-RFE algorithms. We then constructed a predictive nomogram using the diagnostic CRRGs, and the calibration, decision and ROC curves revealed that it had high diagnostic efficiency. Through the evaluation of 2 subdatasets, 4 hub CRRGs (DEFB1, EGF, REN and PTPRD) were ultimately identified. Immune cell infiltration analysis indicated that there might be immune dysregulation in saAKI. GSEA and GSVA revealed different biological functions and pathways related to immunity, inflammation, metabolism and material transport that might exist in different subgroups of hub CRRGs. The validation dataset GSE255281 and RT‒qPCR analysis verified the expression of EGF and PTPRD.</p><p><strong>Conclusion: </strong>Our research utilized comprehensive machine learning methods to construct a CRRG-based diagnostic model for saAKI. The identified CRRGs may be potential biomarkers of saAKI, and this study may provide new strategies for the diagnosis and treatment of saAKI.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13491666/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148224540","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MIR9-3HG/let-7c-5p/THBS1 axis promotes hepatocellular carcinoma progression.","authors":"Jinmin Su, Jiaoling Gu, Zhizhong Lu","doi":"10.1186/s41065-026-00694-7","DOIUrl":"10.1186/s41065-026-00694-7","url":null,"abstract":"<p><strong>Background: </strong>Long non-coding RNAs (lncRNA) are key regulators in hepatocellular carcinoma (HCC). However, the role of MIR9-3HG in HCC remained unclear.</p><p><strong>Objective: </strong>This study investigated the expression, clinical significance, and molecular mechanism of MIR9-3HG in HCC.</p><p><strong>Methods: </strong>MIR9-3HG, hsa-let-7c-5p, and THBS1 levels were quantified via RT-qPCR in 179 paired HCC tissues and cell lines. Associations between MIR9-3HG expression and clinicopathological features were analyzed using χ² test. The prognostic value was assessed using Kaplan-Meier and Cox regression analyses. The biological functions of MIR9-3HG were evaluated through CCK-8, Transwell assays. The competing endogenous RNA (ceRNA) targeting relationship was validated using dual-luciferase reporter.</p><p><strong>Results: </strong>MIR9-3HG was significantly upregulated in HCC tissues and cell lines. High MIR9-3HG expression correlated with advanced TNM stage, higher Edmondson-Steiner grade, vascular invasion, and poor overall survival, and was identified as an independent prognostic factor. Hsa-let-7c-5p expression was negatively correlated with MIR9-3HG and THBS1in HCC tissues. In vitro experiments, silencing MIR9-3HG inhibited HCC cell proliferation, migration, and invasion. Luciferase reporter assays demonstrated that MIR9-3HG functioned as a ceRNA to sponge hsa-let-7c-5p. In turn, hsa-let-7c-5p directly targeted and negatively regulated THBS1.</p><p><strong>Conclusion: </strong>MIR9-3HG promoted HCC aggressiveness by acting as a ceRNA for hsa-let-7c-5p to upregulate THBS1. These findings highlighted its potential as a prognostic biomarker.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13520333/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148163054","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MiR-766-3P promotes degenerative lumbar disc disease by regulating SIRT6 to aggravate the inflammatory response of human nucleus pulposus cells.","authors":"Dongwei An, Pan Yang","doi":"10.1186/s41065-026-00696-5","DOIUrl":"10.1186/s41065-026-00696-5","url":null,"abstract":"<p><strong>Background: </strong>Lumbar degenerative disc disease (LDD) is a disabling condition which was associated with progressive degeneration of the intervertebral discs. The miR-766-3p and its modulation of SIRT6 remains unclear in LDD.</p><p><strong>Purpose: </strong>This study aims to explored the regulated function of miR-766-3p and SIRT6 during LDD.</p><p><strong>Methods: </strong>Human nucleus pulposus cells (HNPCs) were treated with lipopolysaccharide (LPS) to construct a model of LDD to simulate inflammatory conditions. RT-qPCR and ELISA assays were employed to measure the expression of miR-766-3p and SIRT6. Additionally, we evaluated the levels of TNF‑α, IL‑1β, IL‑6, aggrecan, and collagen II by ELISA. Dual-luciferase reporter assays validated direct targeting between miR-766-3p and SIRT6.</p><p><strong>Results: </strong>We observed that miR-766-3p was upregulated in LDD patients, and SIRT6 was downregulated. It is consistent with the changes in LPS-induced HNPCs. Additionally, when we inhibited the miR-766-3p and overexpressed SIRT6, inflammatory cytokines decreased, whereas aggrecan and collagen II increased. Moreover, the inhibition of miR-766-3p increased SIRT6, which was decreased by LPS. And the binding relationship between miR-766-3p and SIRT6 was confirmed by luciferase activity. MiR-766-3p mimic reversed the effects of elevated SIRT6 expression.</p><p><strong>Conclusion: </strong>The findings identify the miR-766-p/SIRT6 axis as a critical regulator mediating inflammatory responses and driving extracellular matrix degradation during LDD. Targeting this molecular pathway would offer novel therapeutic strategies for mitigating tissue damage of LDD.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13455219/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148149669","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TLE1 as a key regulator of osimertinib resistance and EMT in lung adenocarcinoma: implications for prognosis and immunotherapy response.","authors":"Na Chen, Tianlin Wang, Yi Li, Ruixia Zhang, Xiduan Wei, Zhenglu Wang","doi":"10.1186/s41065-026-00690-x","DOIUrl":"10.1186/s41065-026-00690-x","url":null,"abstract":"<p><strong>Background: </strong>Acquired resistance to epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) poses a considerable challenge for the long-term treatment of non-small cell lung cancer (NSCLC). This study aims to identify a novel biomarker associated with osimertinib resistance and explore its role in EGFR-TKI resistance in lung adenocarcinoma (LUAD).</p><p><strong>Methods: </strong>Comprehensive bioinformatics analysis were done using transcriptomic data from the TCGA and GEO databases to identify genes associated with osimertinib tolerance. Candidate genes were further screened against a histone modification-related gene set from MSigDB, leading to the identification of TLE1. The hub gene, TLE1, was further evaluated through survival analysis, GSEA and CIBERSORT analyses. Loss-of-function experiments performed in vitro were utilized to assess the impact of TLE1 on osimertinib resistance in LUAD.</p><p><strong>Results: </strong>TLE1 was of particularly noteworthy, exhibiting elevated expression in LUAD, especially in stage IV patients, and was associated with poor prognosis. GSEA results showed that mTOR, VEGF and HIF-1 signaling pathways were notably activated in the high TLE1 expression group. CIBERSORT analysis markedly elevated levels of regulatory T cells (Tregs) in the TLE1 high expression group. Additionally, epithelial-mesenchymal transition (EMT) scores were significantly elevated in osimertinib tolerant groups and exhibited a positive correlation with TLE1 expression. Furthermore, TLE1 expression was significantly higher in osimertinib-resistant PC9 cells compared to parental PC9 cells. Downregulation of TLE1 enhanced the sensitivity of osimertinib-resistant PC9 cells to osimertinib.</p><p><strong>Conclusions: </strong>TLE1 was identified as a critical gene associated with osimertinib tolerance, influencing LUAD progression, potentially serving as a novel therapeutic target.</p><p><strong>Clinical trial number: </strong>Not applicable.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13425785/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148054340","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeted knockout of barley Ycf54 demonstrates its essential function in the Mg-protoporphyrin IX monomethyl ester cyclase involved in chlorophyll biosynthesis.","authors":"Helmy M Youssef, Iris Hoffie, Otto Nordling, David Stuart, Shakhira Zakhrabekova, Radwa Y Helmi, Jochen Kumlehn, Mats Hansson","doi":"10.1186/s41065-026-00693-8","DOIUrl":"10.1186/s41065-026-00693-8","url":null,"abstract":"<p><strong>Background: </strong>The Mg-protoporphyrin IX monomethyl ester cyclase is one of the 15 enzymes required for biosynthesis of chlorophyll in plants. The Ycf54 protein is a component associated with this enzyme and probably functions as a chaperone. Due to the lack of mutants in the Ycf54 gene, we targeted this gene in barley (Hordeum vulgare L.) by RNA-guided Cas9 genome editing to dissect its role in chlorophyll biosynthesis.</p><p><strong>Results: </strong>Two guide RNAs were designed and delivered via Agrobacterium-mediated transformation. We generated four homozygous mutant alleles harboring deletions of 1, 2, 6 and 27 base pairs. The 27 bp deletion mutant also had a silent C-to-G point mutation before the deletion and a CC-to-AG mutation following the deletion changing a serine residue to glutamate. The mutants exhibited three distinct phenotypes: completely yellow leaves, green leaves with yellow stripes, and fully green leaves. Yellow-leafed plants were classified as Xantha mutants, characterized by an absence of chlorophyll but presence of carotenoids. The striped phenotype represented chimeric individuals with severe mutations in meristematic tissues. Yellow mutants carried homozygous 1 or 2 bp deletions, both of which caused translational reading frame shifts and premature truncation of the Ycf54 protein, likely disrupting chlorophyll biosynthesis and resulting in lethality. These mutations could only be stored in heterozygous lines. In contrast, the 6 and 27 bp deletions were in-frame and did not have any observed effect on the green phenotype, demonstrating that these mutations, and the CC-to-AG mutation, preserve Ycf54 functionality with maintained chlorophyll synthesis and plant viability.</p><p><strong>Conclusions: </strong>Previous studies have implicated Ycf54 in the folding and maturation of the cyclase enzyme. Our findings provide direct genetic evidence that Ycf54 is essential for chlorophyll biosynthesis. Loss-of-function mutations result in a lethal, chlorophyll-deficient phenotype, underscoring the critical role of Ycf54 in photosynthetic development.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13221752/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148054383","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"miR-4513 promotes the proliferation and metastasis of non-small cell lung cancer cells by targeting VIPR1.","authors":"Zhonghao Pang, Bing Huang, Ying Cui, Shanwu Ma, Bin Zheng, Xuhua Zhang, Ying Liu","doi":"10.1186/s41065-026-00688-5","DOIUrl":"10.1186/s41065-026-00688-5","url":null,"abstract":"<p><strong>Objectives: </strong>The pathogenesis of non-small cell lung cancer (NSCLC) is complex. This research focuses on the expression, function, and molecular mechanisms of miR-4513 in NSCLC.</p><p><strong>Method: </strong>A total of 126 matched tissue pairs (NSCLC and adjacent normal) were collected, along with assessment of miR-4513 and VIPR1 expression in multiple cell lines (A549, H1299, BEAS-2B) by qRT-PCR. In vitro, the influence of miR-4513 on cellular phenotypes was assessed by determining proliferation rates through CCK-8 assay and quantifying migration/invasion capacities via Transwell systems. Targetscan predicted the targeting relationship between miR-4513 and VIPR1, which was subsequently confirmed by dual-luciferase.</p><p><strong>Results: </strong>The expression of miR-4513 is upregulated in NSCLC tissues. The high expression of miR-4513 is associated with pathological features. Survival analysis revealed that high expression of miR-4513 was an independent predictor of unfavorable clinical outcomes in NSCLC patients. In vitro, overexpression of miR-4513 can promote the proliferation, migration and invasion of NSCLC cells, while inhibition of its expression has the opposite effect. VIPR1 overexpression significantly inhibited the proliferation and invasion of NSCLC cells, confirming its tumor-suppressive role. Furthermore, miR-4513 can directly bind to the 3'UTR region of the VIPR1 gene and show a negative correlation with it.</p><p><strong>Conclusions: </strong>High expression of miR-4513 may serve as a potential biomarker for poor prognosis in NSCLC patients. In addition, miR-4513 may promote the malignant progression of NSCLC by targeting VIPR1.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13425973/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148054331","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}