Use of a Carbon Nanoparticle Tracer to Detect Sentinel Lymph Nodes for the Precise Treatment of Endometrial Carcinoma

This study aimed to investigate the role of Non-SMC condensin I complex subunit G (NCAPG) in endometrial cancer (EC) progression and prognosis. The researchers utilized various techniques, including analysis of The Cancer Genome Atlas (TCGA) database, immunohistochemistry, qRT-PCR, Western blotting, and functional assays to assess the impact of NCAPG on EC cells. The TCGA analysis revealed that NCAPG was significantly associated with overall survival and disease-free survival in EC patients. Immunohistochemistry analysis further confirmed a positive correlation between NCAPG expression, histological grade, and myometrial invasion in EC tissues. In vitro experiments demonstrated that NCAPG promoted EC cell proliferation, invasion, and influenced the G1/S cell cycle transition. Additionally, NCAPG was found to regulate the expression of FANCD2 and RAD51 in the homologous recombination repair pathway, and its knockdown sensitized EC cells to poly (ADP-ribose) polymerase inhibitors. The study also revealed the involvement of the PI3K/AKT signaling pathway in mediating the effects of NCAPG on EC cells’ proliferation, invasion, and homologous recombination repair. In conclusion, NCAPG acts as an oncogene in EC, driving proliferation, invasion, and homologous recombination repair through the PI3K/AKT pathway. NCAPG expression correlates with EC prognosis, revealing its significance as a therapeutic target for advanced cases, illuminating EC progression mechanisms.

Non-SMC Condensin I Complex Subunit G Promotes the Proliferation, Invasion and Homologous Recombination Repair of Endometrial Cancer Through PI3K/AKT Signaling Pathway

Ren,

Zheng,

Xiao

et al. 2023

Identification of Biomarkers for Endometrial Cancer Based on Natural Killer Cell-Related Genes

Wang,

Zheng,

et al. 2024

Endometrial cancer (EC) is a malignant tumor. Natural killer (NK) cells play a crucial role in various cancers, but their role in EC is unclear. To this purpose, in this paper, differential expression analysis was performed on transcriptome data from the TCGA database, and the obtained DEGs and the collected NRGs were intersected, and single-factor Cox regression analysis and Lasso-Cox regression analysis were performed on the intersected genes to obtain prognosis-related genes and risk model, respectively. These genes and models were validated by Kaplan-Meier (KM) survival curve analysis and ROC analysis on the internal and external test sets. In addition, nomogram models were constructed based on prognosis-associated genes, sample risk scores, and clinical factors. Finally, we explored the immune landscape of high- and low-risk groups of EC. The results showed that the risk models constructed in this paper exhibited excellent predictive effects, which will facilitate research on the precision treatment of EC. There were significant differences in prognosis, immune cell infiltration abundance, immune checkpoint-associated genes, and HLA gene expression between high- and low-risk groups of EC. The risk model in this paper can provide a reference for the personalized treatment of EC. In addition, we performed RT-qPCR to validate the levels of genes significantly associated with prognosis.

The Role of miR-132-3p in Inhibiting the Proliferation, Invasion and Metastasis of Colon Cancer by Targeted Regulation of PDGF

Li,

Lu,

Lang

et al. 2024

This study investigated the impact of miR-132-3p on colon cancer cell behavior by targeting PDGF, offering insights into potential approaches for understanding colon cancer development and gene-targeted therapy. The study involved qRT-PCR analysis to assess miR-132-3p expression in colon cancer and adjacent tissues. Overexpression of miR-132-3p in HCT-116 cells was examined through CCK-8 assays for proliferation, flow cytometry for apoptosis, and Transwell/scratch assays for invasion/metastasis. Pearson correlation analysis evaluated miR-132-3p-PDGF relationship, validated via luciferase assays. qRT-PCR/Western blot assessed PDGF mRNA/protein levels. In vivo tumorigenesis assays in nude mice confirmed miR-132-3p’s inhibitory effect on HCT-116 cells. Results showed reduced miR-132-3p expression in colon cancer tissues (vs. adjacent tissues), correlating with decreased cell proliferation and invasion upon miR-132-3p overexpression. Luciferase activity confirmed PDGF as a miR-132-3p target. Additionally, miR-132-3p inhibited tumor growth, while miR-132-3p+PDGF reversed these effects. In conclusion, miR-132-3p regulates PDGF, suppressing colon cancer cell proliferation, invasion, and metastasis, thereby promoting apoptosis. This highlights the potential of miR-132-3p as a therapeutic target for colon cancer treatment.