ArticleCell communication and signaling : CCS2022
Cell adhesion molecule BVES functions as a suppressor of tumor cells extrusion in hepatocellular carcinoma metastasis.
Article in Cell communication and signaling : CCS, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 8 citations in OpenAlex.
- CTSZ-dependent anoikis resistance enhances malignant characters of glioblastoma via NF-κB signaling.iScience · 2026Article
- DNA hypermethylation drives BVES-mediated autophagy to promote cisplatin resistance in lung adenocarcinoma.Journal of bioenergetics and biomembranes · 2026Article
- Effect and mechanism of auranofin on extrusion and migration of breast cancer cells.Translational cancer research · 2025Article
- The role of lnc‑MAPKAPK5‑AS1 in immune cell infiltration in hepatocellular carcinoma: Bioinformatics analysis and validation.Oncology letters · 2025Article
- Prognostic model development using novel genetic signature associated with adenosine metabolism and immune status for patients with hepatocellular carcinoma.Journal of physiology and biochemistry · 2025Article
- CYB561 a potential prognostic biomarker for liver hepatocellular carcinoma.Clinical and experimental medicine · 2024Article
- Multiomics characterization of fatty acid metabolism for the clinical management of hepatocellular carcinoma.Scientific reports · 2023Article
- Identification and experimental verification of an anoikis and immune related signature in prognosis for lung adenocarcinoma.Translational cancer research · 2023Article
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7 authors at 2 institutions in 1 country.
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Abstract
backgroundTumor cells detachment from primary lesions is an early event for hepatocellular carcinoma (HCC) metastasis, in which cell adhesion molecules play an important role. The role of mechanical crowding has attracted increasing attention. Previous studies have found that overcrowding can induce live cells extrusion to maintain epithelial cell homeostasis, and normally, live extruded cells eventually die through a process termed anoikis, suggesting the potential of tumor cells resistant to anoikis might initiate metastasis from primary tumors by cell extrusion. We have demonstrated transmembrane adhesion molecule blood vessel epicardial substance (BVES) suppression as an early event in HCC metastasis. However, whether its suppression is involved in HCC cell extrusion, especially in HCC metastasis, remains unknown. This study aims to investigate the role of BVES in tumor cells extrusion in HCC metastasis, as well as the underlying mechanisms.
methodsCells extrusion was observed by silicone chamber, petri dish inversion, and three-dimensional cell culture model. Polymerase chain reaction, western blotting, immunohistochemistry, immunofluorescence, co-immunoprecipitation, and RhoA activity assays were used to explore the underlying mechanisms of cell extrusion regulated by BVES. An orthotopic xenograft model was established to investigate the effects of BVES and cell extrusion in HCC metastasis in vivo.
resultsTumor cell extrusion was observed in HCC cells and tissues. BVES expression was decreased both in HCC and extruded tumor cells. BVES overexpression led to the decrease in HCC cells extrusion in vitro and in vivo. Moreover, our data showed that BVES co-localized with ZO-1 and GEFT, regulating ZO-1 expression and localization, and GEFT distribution, thus modulating RhoA activity.
conclusionThe present study revealed that BVES downregulation in HCC enhanced tumor cells extrusion, thus promoting HCC metastasis, which contributed to a more comprehensive understanding of tumor metastasis, and provided clues for developing novel HCC therapy strategies. Video abstract.
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