ABSTRACT
The objective of this study is to elucidate the role of Partitioning-defective 3 (Par3) in the development of gastric cancer and its correlation with different gastric cancer tissue types, particularly considering the health implications for athletes and fitness enthusiasts. From January 2019 to January 2022, 180 gastric cancer specimens, post-surgical resection, were analyzed (group B), with gastric mucosa tissue serving as a control (group A). Immunohistochemical methods assessed Par3 expression across various parameters, including tissue layer, invasion depth, tissue type, and lymph node metastasis. Key findings include a significant decrease in Par3 expression in cancer tissues compared to controls (P<0.05), no significant difference in Par3 expression between early (T1+T2) and advanced (T3+T4) stage patients (P>0.05), and similar findings regarding lymph node metastasis. Notably, Par3 expression was markedly lower in gastric type cancer than in intestinal or mixed types (P<0.05). Kappa consistency analysis indicated a significant correlation between Par3 down-regulation and gastric-type cancer (kappa=0.416), but not with other types (kappa=-0.270, -0.087). The study concludes that Par3 down-regulation is vital in gastric cancer development, particularly in gastric-type cancer, suggesting its potential as an auxiliary diagnostic marker. For athletes and fitness enthusiasts, these findings underscore the importance of monitoring gastric health, as disruptions in gastric function can significantly impact physical performance and overall well-being (AU)
Subject(s)
Humans , Male , Female , Middle Aged , Aged , Aged, 80 and over , Stomach Neoplasms/metabolism , Athletes , Physical Functional Performance , ImmunohistochemistryABSTRACT
The outcome of colon adenocarcinoma (COAD) patients remains dismal, and lactate metabolism has been characterized to promote tumor development and immune evasion. Based on the above background, it is worthwhile to explore novel prognostic and therapeutic biomarkers for COAD patients from the aspect of lactate metabolism. Above all, 228 available lactate-metabolism-related genes (LMRGs) were acquired, and the landscape of copy number variation and the expression difference of mRNA levels between colon normal and tumor samples were investigated among these LMRGs. Importantly, eight overall survival (OS)-involved LMRGs were then distinguished by means of univariate Cox regression analysis in both GSE40967 and TCGA-COAD data sets. Subsequently, prognostic risk scores were established, integrating seven OS-related LMRGs by LASSO Cox regression analysis in the GSE40967 set, and then verified in the TCGA-COAD cohort. From the comprehensive analyses, COAD patients with high risk had comparatively more inferior survival probability in all populations of the study, and they tended to have more severe clinicopathological features with the risk score increasing. Moreover, by integrating age, AJCC T and pathological stage, and risk score, we constructed a prognostic nomogram that demonstrated great prediction effectiveness for OS of COAD patients. Furthermore, the potential effect of various risk score on tumor immune was assessed from enrichment of immune-related pathways, tumor-infiltrating immune cells, and expression levels of immune checkpoints separately. We could draw a conclusion that COAD patients with higher lactate-metabolism-related risk scores may acquire an immunosuppressive tumor microenvironment, which subsequently led to immune escapes and poor prognoses. Conclusively, all findings in the present study illustrate a great prognostic value of the lactate-metabolism-related risk signature, providing more in-depth insights into the indispensable function of lactate metabolism in prognosis and tumor immunity of COAD.
ABSTRACT
Cholangiocarcinoma (CCA) is a type of cancer with a relatively low morbidity, but poor prognosis. Aberrant long non-coding RNA (lncRNA) expression has been observed in the pathological development of CCA. In the present study, lncRNA long intergenic non-protein coding RNA 630 (LINC00630) was found to be significantly upregulated in CCA tissues and cultured cells. LINC00630 expression was positively associated with histological differentiation, TNM stage and lymph node invasion. Short hairpin RNA (sh)-LINC00630 transfection could effectively decrease CCA cell proliferation, migration and invasion. Further investigations found that LINC00630 could interact with microRNA (miR)-199a, which specifically targeted fibroblast growth factor 7 (FGF7) for degradation. FGF7 overexpression restored the sh-LINC00630 transfection-induced decrease in CCA cell proliferation, migration and invasion. In conclusion, LINC00630 significantly promoted CCA cell proliferation, migration and invasion by upregulating FGF7 through miR-199a sponging.
