Biomedical subjects

Ming Liu

Publications and source records attributed to Ming Liu.

3 recordsLinked to original sources

PubMed2026

Genome-Wide Identification of the PAL Gene Family in Idesia polycarpa and Transcriptomic Responses to Botryosphaeria dothidea Infection.

Idesia polycarpa is a woody oil tree threatened by stem canker caused by Botryosphaeria dothidea, yet the organization and infection-responsive behavior of its phenylalanine ammonia-lyase (PAL) gene family remain poorly understood. Here, we identified five IpPAL genes and characterized their phylogenetic relationships, conserved features, duplication patterns, promoter cis-elements, and infection-associated expression profiles. Segmental and tandem duplication contributed to IpPAL family evolution, and all duplicated pairs showed Ka/Ks ratios below 1, consistent with purifying selection. RNA sequencing (RNA-seq) of contrasting Chengdu and Zhangjiajie provenances revealed distinct temporal responses. In Chengdu, IpPAL2-IpPAL4 were significantly upregulated at 24 h after inoculation, whereas all five genes were upregulated at 96 h. In Zhangjiajie, all five IpPAL genes were significantly upregulated at 24 h, while IpPAL2-IpPAL5 remained upregulated at 96 h. No IpPAL gene met the differential-expression criteria between provenances under mock conditions or at 24 h; at 96 h, IpPAL1 and IpPAL3 were lower and IpPAL5 was higher in Zhangjiajie than in Chengdu. Scanning electron microscopy (SEM) provided complementary qualitative evidence of provenance-associated tissue responses. These findings demonstrate time- and gene-specific IpPAL responses to B. dothidea and identify candidate genes for further functional analysis.

Ascomycota↗

PubMed2026

PLK1/FOXM1-associated tumor-cell state and macrophage-related immune features in endometrial cancer.

BACKGROUND: Polo-like kinase 1 (PLK1) and forkhead box M1 (FOXM1) have been widely studied in various cancers; however, their expression characteristics in endometrial cancer (EC) and their potential association with tumor microenvironment remodeling remain insufficiently characterized. METHODS: This study integrated The Cancer Genome Atlas uterine corpus endometrial carcinoma cohort, Gene Expression Omnibus, pan-cancer transcriptomic data, Human Protein Atlas/Clinical Proteomic Tumor Analysis Consortium, and local immunohistochemistry data to evaluate PLK1 expression and clinicopathological relevance across transcriptomic, proteomic, and histopathological data. Differential expression, survival, gene-set enrichment, transcription-factor enrichment, and immune-infiltration analyses characterized PLK1-associated features. In vitro experiments combined EC cell lines AN3CA and HEC-1A with co-immunoprecipitation, Western blotting, Transwell assays, and a THP-1 conditioned-medium model. Drug-response prediction and structure-based analysis prioritized candidate therapeutic hypotheses. RESULTS: PLK1 was consistently upregulated at both mRNA and protein levels in EC and was associated with higher tumor grade and International Federation of Gynecology and Obstetrics (FIGO) stage. In survival analysis, higher PLK1 expression was associated with poorer overall survival in univariable models but not after adjustment for age, tumor grade, and FIGO stage. Functional enrichment analysis showed that PLK1-associated genes were mainly involved in cell-cycle and mitotic processes. FOXM1 was identified as a potential candidate component of the PLK1-associated transcriptional program and was positively correlated with PLK1 expression and cell-cycle-related features. In vitro experiments supported an interaction between PLK1 and FOXM1 and suggested that FOXM1 Thr600 phosphorylation-related alterations were associated with migration and invasion phenotypes. Furthermore, the PLK1/FOXM1-associated tumor-cell state was linked to macrophage-related immune features and changes in the M2-like marker profile of THP-1-derived macrophage-like cells. Drug response analyses suggested differential predicted sensitivity patterns in PLK1-high tumors, providing candidate therapeutic hypotheses for further validation. CONCLUSION: The PLK1/FOXM1-associated tumor-cell state may represent a distinct molecular feature associated with proliferative activity, invasive phenotypes, and macrophage-related immune features in EC. This study provides preliminary evidence supporting the biological relevance of this molecular feature and highlights potential therapeutic directions for future investigation.

FoxM1↗

PubMed2026

Sugar rationing during the first 1000 days and early onset cancer: a natural experiment.

BACKGROUND: The "first 1000 days" of life is a critical window for metabolic programming, while the long-term oncological consequences of nutritional exposures during this period remain understudied. OBJECTIVES: We aimed to evaluate whether restricted sugar intake in utero and during early childhood reduces risk of early onset cancer diagnosis and mortality in adulthood, utilizing a natural experiment. METHODS: We analyzed 63,819 United Kingdom Biobank participants born between October 1951 and March 1956, spanning the end of United Kingdom sugar rationing (September 1953). Leveraging a quasi-experimental birth cohort design, we compared participants exposed to sugar rationing in utero and during infancy with those unexposed. Early onset cancer incidence (≤50 y) and mortality were ascertained via integrated national Cancer Registry and hospital inpatient records. Multivariable Cox proportional hazards models (including Gompertz distribution) were used to estimate hazard ratios (HRs), with exploratory site-specific analyses. RESULTS: Among 63,819 participants (56.3% female), 40,397 were exposed to rationing and 23,422 were unexposed. Early life sugar restriction significantly reduced early onset cancer risk (HR: 0.66; 95% confidence interval: 0.53, 0.81; P < 0.001). A dose-response relationship was observed, with peak protection in individuals exposed for ≤24 mo postnatally. This protection was observed systemically across solid tumors, independent of specific cancer sites. Specificity was corroborated by null associations with negative controls (herpes zoster and cataract). No significant difference was found for cancer-specific mortality. CONCLUSIONS: Restricting sugar intake during the first 1000 days is associated with a reduced risk of early onset cancer, extending the disease-free lifespan. The divergence between reduced incidence and unchanged mortality suggests early life metabolic environments primarily influence tumor latency rather than biological aggressiveness. These findings highlight the potential long-term public health implications of early life dietary guidelines against the rising burden of early onset cancer.

Humans↗