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Depleting TMED3 alleviates the development of endometrial carcinoma
1Department of Obstetrics and Gynecology, Shengjing Hospital of China Medical University, No.36 Sanhao Street, Shenyang, Liaoning, China.
Background:
As one of gynecologic tumors, endometrial carcinoma (EC) has been characterized by high incidence rate, but its molecular pathogenesis has remained unclear. TMED3 is a membrane protein and has been indicated to implicate several tumor-related diseases. In the current study, we aimed to explore the physiological function of TMED3 in EC progression.
Methods:
Through bioinformatic analysis using The Cancer Genome Atlas database and immunohistochemistry assay on tissue microarray, we examined whether TMED3 was upregulated in EC tissues. After constructing TMED3-knockdown cell models via lentiviral transfection, qPCR and western blot were employed to determine the expression levels of TMED3 mRNA and protein. Then, Celigo cell counting assay, CCK8 assay, flow cytometry, wound-healing assay and Transwell assay were used to detect cell proliferation, cell cycle, cell apoptosis and cell migration, respectively.
Results:
As a result, it was found that TMED3 was upregulated in EC cells, which was also verified in clinical samples. We then found that downregulation of TMED3 considerably restrained cell cycle, cell growth and migration but promoted apoptosis of EC cells. The following in-vivo experiments also verified that tumor growth was inhibited after TMED3 knockdown. The exploration in molecular mechanisms showed that TMED3 deletion may weaken cellular viability through upregulating pro-apoptotic proteins and targeting PI3K/AKT signaling pathways.
Conclusions:
This study suggested that knocking down TMED3 affected the malignant phenotype of EC cells and thus limited tumor progression, which provided insights to the development of targeted drugs for EC treatment.
Insights
Downregulating TMED3 protein inhibits endometrial carcinoma (EC) cell growth, migration, and tumor progression by promoting apoptosis and targeting PI3K/AKT pathways, offering potential therapeutic strategies for EC.
Area of Science:
- Oncology
- Molecular Biology
- Gynecologic Oncology
Background:
- Endometrial carcinoma (EC) is a prevalent gynecologic tumor with unclear molecular pathogenesis.
- TMED3, a membrane protein, is implicated in various tumor-related diseases.
- Understanding TMED3's role in EC is crucial for developing targeted therapies.
Purpose of the Study:
- To investigate the physiological function of TMED3 in endometrial carcinoma (EC) progression.
- To determine if TMED3 is upregulated in EC tissues and cells.
- To explore the impact of TMED3 modulation on EC cell behavior.
Main Methods:
- Bioinformatic analysis of The Cancer Genome Atlas (TCGA) database and immunohistochemistry on tissue microarrays.
- Construction of TMED3-knockdown EC cell models using lentiviral transfection.
- Assessment of cell proliferation, cell cycle, apoptosis, and migration using assays like CCK8, flow cytometry, wound-healing, and Transwell.
Main Results:
- TMED3 expression was found to be upregulated in EC cells and clinical samples.
- Downregulation of TMED3 significantly inhibited EC cell proliferation, cell cycle progression, and migration.
- TMED3 knockdown promoted EC cell apoptosis and suppressed tumor growth in vivo, potentially via PI3K/AKT signaling pathway modulation.
Conclusions:
- TMED3 knockdown negatively impacts the malignant phenotype of EC cells, thereby limiting tumor progression.
- Targeting TMED3 presents a promising therapeutic strategy for endometrial carcinoma treatment.
- This research provides valuable insights into the molecular mechanisms underlying EC development.
