Biomedical subjects

Min Xiao

Publications and source records attributed to Min Xiao.

3 recordsLinked to original sources

PubMed2026

DNA hypermethylation of abscisic-acid-related genes helps enhance the cold tolerance of tetraploid rice.

Polyploid plants exhibit enhanced stress resistance and superior adaptability to extreme environments, but the underlying molecular mechanisms remain incompletely understood. Here we confirm that tetraploid rice exhibits stronger cold tolerance than diploid rice. This improved tolerance is mediated by reduced malondialdehyde accumulation, elevated antioxidant enzyme activity, and epigenetic regulation of genes involved in abscisic acid (ABA) biosynthesis and signaling. Under cold stress, tetraploid rice induces stress-responsive genes (especially in the ABA pathway) more rapidly and to higher levels than diploid rice. This enhanced gene expression coincides with increased endogenous ABA accumulation. Furthermore, polyploidization and cold stress synergistically induce high methylation at CG, CHG, and CHH sites in genes and transposons (TEs). Notably, the methylation level of class II TEs in tetraploid rice is significantly higher than in diploid rice under low temperatures. To suppress TE activation in gene promoter regions under cold stress, tetraploid rice enhances the methylation level of ABA pathway-related gene promoters, thereby silencing TEs and maintaining genome stability. Collectively, these results enrich the theoretical understanding of the strong stress tolerance in polyploid plants and provide theoretical support for breeding cold-tolerant polyploid rice varieties.

ABA↗

PubMed2026

miR-2116-5p functions as a tumor suppressor in lung adenocarcinoma by targeting ADAM12 and serves as a prognostic biomarker.

BACKGROUND: MicroRNAs play key roles in tumor progression. miR-2116-5p is downregulated in lung adenocarcinoma (LUAD), and this study investigated its prognostic value and functional role in the disease. MATERIALS AND METHODS: A total of 125 LUAD patients contributed tissue samples. miR-2116-5p and ADAM12 expression in tissues and cell lines were detected by RT‑qPCR. Clinicopathological correlations of miR-2116-5p were analyzed using the chi-square test. Kaplan‑Meier and Cox regression were employed to assess prognostic significance. CCK‑8, Transwell, and dual‑luciferase reporter assays were performed to investigate miR‑2116-5p function and its targeting of ADAM12. Rescue experiments validated the functional involvement of ADAM12. RESULTS: Significant downregulation of miR-2116-5p was observed in LUAD tissues and cell lines. Low expression was markedly linked to lymph node metastasis (P = 0.013) and advanced TNM stage (P = 0.002). Patients exhibiting reduced miR-2116-5p levels showed worse overall survival, and it was identified as an independent prognostic factor (HR = 2.521, 95% CI: 1.129-5.628, P = 0.020). Functional experiments showed that increasing miR-2116-5p expression suppressed LUAD cell proliferation, migration, and invasion, whereas its knockdown promoted these processes. ADAM12 was confirmed as a direct target, with expression inversely correlated in LUAD tissues (r = -0.749, P < 0.001). ADAM12 overexpression effectively counteracted the ability of miR-2116-5p to suppress proliferation, migration, and invasion. CONCLUSION: miR‑2116-5p suppresses LUAD progression by targeting ADAM12, suggesting it may serve as a prognostic biomarker and therapeutic target.

Humans↗

PubMed2025

Lactate dehydrogenase a is a crucial biomarker that affects the prognosis, chemotherapy effect, and immune infiltration of breast cancer.

PURPOSE: Lactate dehydrogenase A (LDHA) is a key node in tumor growth, metabolism, and invasion and is upregulated across multiple cancers. However, the molecular mechanisms by which LDHA influences breast cancer (BC) remain unclear. We analyzed public datasets and an institutional cohort to clarify the relationship between LDHA and BC, with the aim of informing future therapeutic strategies. PATIENTS AND METHODS: Using The Cancer Genome Atlas (TCGA), we assessed LDHA expression in BC and examined its associations with tumor mutational burden (TMB), immune cell infiltration, immune checkpoint molecules, and drug sensitivity. We integrated multiple databases and used Kaplan-Meier analyses to evaluate prognostic value. To explore biological functions of LDHA, we performed Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and Gene Set Enrichment Analysis (GSEA). We then analyzed BC patients receiving neoadjuvant chemotherapy (NAC) at Harbin Medical University Cancer Hospital to test the relationship between serum lactate dehydrogenase (LDH) and pathological complete response (pCR). Finally, we used National Health and Nutrition Examination Survey (NHANES) data to examine the association between serum LDH and mortality. RESULTS: LDHA was upregulated in BC tissues, and higher expression was significantly associated with worse overall survival (OS), recurrence-free survival (RFS), and distant metastasis-free survival (DMFS). Functional analyses indicated enrichment of metabolic pathways, such as glycolysis. LDHA expression correlated with multiple immune cell populations, suggesting involvement in the tumor immune microenvironment. Lower LDHA expression was associated with greater sensitivity to several chemotherapeutic agents. In our institutional cohort, patients with lower serum LDH were more likely to achieve pCR, and LDH was an independent predictor of pCR. In NHANES, elevated serum LDH was linked to increased mortality risk. CONCLUSION: Our findings suggest that LDHA expression and serum LDH levels are promising prognostic biomarkers for survival and may predict chemotherapy response in BC patients. These results highlight the clinical relevance of LDHA-mediated metabolic pathways. However, as a correlational study, our findings warrant further validation through functional experiments to confirm LDHA's role as a potential therapeutic target.

Humans↗