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Objective: The purpose of this paper was to investigate the role and mechanism of EEF1D in various diseases, especially in tumorigenesis and development, and explore the possibility of EEF1D as a biological target., Background: EEF1D is a part of the EEF1 protein complex, which can produce four protein isoforms, of which three short isoforms are used as translation elongation factors. The three short isoforms play a role in anti-aging, regulating the cell cycle, and promoting the occurrence and development of malignant tumors, and the only long-form isoform plays a role in the development of the nervous system., Methods: We searched the PubMed and Web of Science databases for literature up to January 2021 using relevant keywords, including "EEF1D", "eukaryotic translation elongation factor 1 delta", "translation elongation factor", "translation elongation factor and cancer", and "translation elongation factor and nervous system disease". We then created an overview of the literature and summarized the results of the paper., Conclusions: Through the review of relevant articles, we found that EEF1D is obviously overexpressed in a variety of tumors, and can regulate the proliferation of tumor cells and tumor growth, as well as play a role in tumor invasion. EEF1D is likely to become a new biological target for tumor therapy and diagnosis., Competing Interests: Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://dx.doi.org/10.21037/atm-21-5025). The authors have no conflicts of interest to declare., (2021 Annals of Translational Medicine. All rights reserved.)

Background: Esophageal cancer (EC) is a malignant tumor with high mortality. Correlations have been found between the expression level of tropomyosin 3 (TPM3) and the depth of tumor invasion, lymph node metastasis, and the 5-year survival rate. However, the specific mechanisms underlying EC remain unclear., Methods: Stably transfected TPM3-overexpresing and TPM3-knockdown esophageal squamous cell carcinoma (ESCC) cell lines (ECa109 and EC9706) were constructed, and the association between TPM3 and the proliferation, invasion, and migration of ESCC was investigated using molecular biology methods. The associations between TPM3 and matrix metalloproteinase (MMP)2/9 or epithelial-mesenchymal transition (EMT)-related proteins were verified, and the potential tumor-promoting mechanism was explored by Gelatin Zymography Experiment., Results: TPM3 was found to promote the proliferation, migration, and metastatic potential of ESCC in vivo and in vitro, and stimulate the expression of MMP2/9 and certain EMT markers other than E-cadherin. The replenishment of MMP2/9 restored the malignant behavior of ESCC caused by TPM3. A gelatinase assay showed that the expression of TPM3 was related to the activity of MMP9., Conclusions: TPM3 promoted proliferation, migration, and metastatic potential in EC cells. Additionally, TPM3 promoted the EMT process. This function may be achieved via the regulation the expression of MMP2/9., Competing Interests: Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://dx.doi.org/10.21037/atm-21-4043). The authors have no conflicts of interest to declare., (2021 Annals of Translational Medicine. All rights reserved.)