BackgroundTheCDH1gene codes for the epithelial-cadherin (E-cad) protein, which is embedded in the plasma membrane of epithelial cells to form adherens junctions. E-cad is known to be essential for maintaining the integrity of epithelial tissues, and the loss of E-cad has been widely considered a hallmark of metastatic cancers enabling carcinoma cells to acquire the ability to migrate and invade nearby tissues. However, this conclusion has come under scrutiny.MethodsTo assess howCDH1and E-cad expression changes during cancer progression, we analyzed multiple large transcriptomics, proteomics, and immunohistochemistry datasets on clinical cancer samples and cancer cell lines to determine theCDH1mRNA and E-cad protein expression profiles in tumor and normal cells.ResultsIn contrast to the textbook knowledge of the loss of E-cad during tumor progression and metastasis, the levels ofCDH1mRNA and E-cad protein are either upregulated or remain unchanged in most carcinoma cells compared to normal cells. In addition, theCDH1mRNA upregulation occurs in the early stages of tumor development and the levels remain elevated as tumors progress to later stages across most carcinoma types. Furthermore, E-cad protein levels are not downregulated in most metastatic tumor cells compared to primary tumor cells. TheCDH1mRNA and E-cad protein levels are positively correlated, and theCDH1mRNA levels are positively correlated to cancer patient’s survival. We have discussed potential mechanisms underlying the observed expression changes inCDH1and E-cad during tumor progression.ConclusionsCDH1mRNA and E-cadherin protein are not downregulated in most tumor tissues and cell lines derived from commonly occurring carcinomas. The role of E-cad in tumor progression and metastasis may have previously been oversimplified.CDH1mRNA levels may serve as a reliable biomarker for the diagnosis of some tumors (such as colon and endometrial carcinomas) due to the marked upregulation ofCDH1mRNA in the early stages of tumor development of these carcinomas.Supplementary InformationThe online version contains supplementary material available at 10.1186/s12885-023-10916-0.