ArticleCytotechnology2025
CBX3 contributes to pancreatic adenocarcinoma progression via promoting KIF20A expression.
Article in Cytotechnology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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6 authors.
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Abstract
Pancreatic adenocarcinoma (PAAD) is one of the malignant tumors with poor prognosis. This study aims to inquiry the effects of Chromobox homologue 3 (CBX3) on PAAD progression. Pan-cancer analysis of CBX3 and its correlation with PAAD progression were investigated by informatics analysis. The role of CBX3 in PAAD was explored in vitro and in vivo. Cell viability, proliferation, migration and invasion were inspected by CCK-8 assay, EdU staining, scratch test and transwell assay, respectively. The morphology of tumors was observed by hematoxylin-eosin staining. Immunohistochemistry (Ki67) was performed to inspect the proliferation of tumor tissue. The protein levels were measured by western blot. Moreover, the downstream genes of CBX3 were screened, and the effects of target gene on PAAD was investigated in vitro. CBX3 was overexpressed in multi cancers, and high CBX3 expression indicated poor prognosis in PAAD. Through the in vitro assays, knockdown of CBX3 suppressed the viability, migration and invasion of PAAD cells, and restrained tumor growth in vivo. Subsequently, kinesin family member 20A (KIF20A) was screened as the downstream gene of CBX3, which was up-regulated in PAAD and related to low overall survival. Mechanistically, we discovered that CBX3 could regulate KIF20A expression. Knockdown of CBX3 promoted the oncogenic effects of KIF20A silencing on PAAD cells, and attenuated the pro-oncogenic effects of KIF20A overexpression on PPAD. Collectively, silencing CBX3 suppressed PAAD progression through regulating KIF20A expression, providing an underlying target for PAAD treatment.
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