ArticleCell death & disease2021
TMED3 promotes the progression and development of lung squamous cell carcinoma by regulating EZR.
Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
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Who cites it
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.
- TMED family genes and their roles in human diseases.International journal of medical sciences · 2023Pooled it
- Role of microRNAs in cisplatin response of cancer stem cells.Stem cell research & therapy · 2026Review
- Bidirectional mendelian randomization identifies plasma proteins associated with cervical cancer risk.Journal of the Egyptian National Cancer Institute · 2026Article
- Downregulation ofJournal of thoracic disease · 2026Article
- A TMED3-governed disulfidptosis-related diagnostic signature reveals tumor microenvironment remodeling in intrahepatic cholangiocarcinoma.Frontiers in immunology · 2026Article
- Vesicle-mediated transport-related gene SEC23A promotes cell proliferation by regulating cell cycle leading to gastric cancer progression.Acta biochimica et biophysica Sinica · 2025Article
- KCNK1 promotes proliferation and metastasis of breast cancer cells by activating lactate dehydrogenase A (LDHA) and up-regulating H3K18 lactylation.PLoS biology · 2024Article
- Article
- Analysis and Validation of TMED3 correlates with poor prognosis and tumor immune infiltration of glioma.Journal of cancer research and clinical oncology · 2023Article
- Comprehensive analyses of a CD8BMC bioinformatics · 2023Article
- Trafficking protein TMED3 promotes esophageal squamous cell carcinoma.Biomedical journal · 2023Article
- When it doesn't run in the blood(vessels) - events involved in vascular disorders.Biomedical journal · 2023Article
- Comprehensive analysis of 33 human cancers reveals clinical implications and immunotherapeutic value of the solute carrier family 35 member A2.Frontiers in immunology · 2023Article
- Screening of the novel immune-suppressive biomarkers of TMED family and whether knockdown of TMED2/3/4/9 inhibits cell migration and invasion in breast cancer.Annals of translational medicine · 2022Article
- Vesicle-mediated transport-related genes are prognostic predictors and are associated with tumor immunity in lung adenocarcinoma.Frontiers in immunology · 2022Article
- TMED2/9/10 Serve as Biomarkers for Poor Prognosis in Head and Neck Squamous Carcinoma.Frontiers in genetics · 2022Article
- TMED3/RPS15A Axis promotes the development and progression of osteosarcoma.Cancer cell international · 2021Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lung squamous cell carcinoma (LUSC) has a poor clinical prognosis and lacks effective targeted therapy. The transmembrane emp24 trafficking protein 3 (TMED3) belongs to the TMED family, which is responsible for the transport of intracellular proteins. This study was to explore the clinicopathological significance and biological effects of TMED3 in LUSC. Expression of TMED3 in LUSC was detected by immunohistochemical (IHC). The loss-of-function assays were used to investigate the effects of TMED3 on proliferation, apoptosis, cell cycle, and migration of LUSC cells. The influence of TMED3 knockdown on tumor growth in vivo was evaluated by mice xenograft models. In addition, the downstream target of TMED3 was recognized by RNA sequencing and Ingenuity Pathway Analysis (IPA). Moreover, TMED3 was upregulated in LUSC tissue, which was positively correlated with pathological grade. TMED3 knockdown was involved in the regulation of LUSC cell function, such as inhibition of proliferation, reduction of colony formation, induction of apoptosis, and reduction of migration. TMED3 knockdown induced abnormalities in apoptosis-related proteins in LUSC cells. In addition, the inhibition of cell migration by TMED3 knockdown was achieved by regulating EMT. Mechanically, EZR was considered as a potential target for TMED3 to regulate the progress of LUSC. Inhibition of EZR can inhibit the progression of LUSC, and even reduce the promoting effects of TMED3 overexpression on LUSC. In conclusion, TMED3 promoted the progression and development of LUSC by EZR, which may be a novel therapeutic target for LUSC.
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