Abstract
BackgroundNowadays, colorectal cancer (CRC) is one of the most commonly diagnosed malignant tumors worldwide, the incidence rate of which is still increasing year by year. Herein, the objective of this study is to investigate whether CDC42EP3 has regulatory effects in CRC.MethodsFirst, CDC42EP3 knockdown cell model based on HCT116 and RKO cell lines was successfully constructed, which was further used for constructing mouse xenotransplantation models. Importantly, effects of CDC42EP3 knockdown on proliferation, colony formation, apoptosis, and migration of CRC were accessed by MTT assay, EdU staining assay, colony formation assay, Flow cytometry, and Transwell assay.ResultsAs the results, we showed that CDC42EP3 was significantly upregulated in CRC, and its high expression was associated with tumor progression. Furthermore, knockdown of CDC42EP3 could inhibit proliferation, colony formation and migration, and promote apoptosis of CRC cells in vitro. In vivo results further confirmed knockdown of CDC42EP3 attenuated tumor growth in CRC. Interestingly, the regulation of CRC by CDC42EP3 involved not only the change of a variety of apoptosis-related proteins, but also the regulation of downstream signaling pathway.ConclusionIn conclusion, the role of CDC42EP3 in CRC was clarified and showed its potential as a target of innovative therapeutic approaches for CRC.
Highlights
Nowadays, colorectal cancer (CRC) is one of the most commonly diagnosed malignant tumors worldwide, the incidence rate of which is still increasing year by year
CDC42EP3 is upregulated in Colorectal Cancer In order to better understand the relationship of CDC42EP3 in the development of colorectal cancer, IHC analysis was undertaken on 97 colorectal cancer tissues and 75 normal tissues as a means to identify observable CDC42EP3 expressions
CDC42EP3 was identified in both normal tissues and colorectal cancer tissues, showing obviously higher expression in colorectal cancer tissues
Summary
Colorectal cancer (CRC) is one of the most commonly diagnosed malignant tumors worldwide, the incidence rate of which is still increasing year by year. Colorectal cancer (CRC) is a prevalent cancer type with a high incidence and mortality rate in the colon or rectum, and is the fourth leading cause of cancer-related death worldwide [1, 2]. Yang et al reported that Cdc exhibited relatively high expression in pancreatic cancer, could facilitate the fast growth of tumor, and showed significant correlation with prognosis of patients [10]. CDC42EP3 is a member of Cdc effector protein family, whose biological functions in human diseases were rarely reported. Some studies showed that CDC42EP3 plays a role in the function of cancer-associated fibroblasts and DNA damage repair, both of which could be adjusted Cdc42 [13,14,15]. The overexpression of Cdc in colorectal cancer and its clinical relevance have been studied to some extent [16], the role of CDC42EP3 in colorectal cancer has not been reported, which attracted our attention
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