ArticleAmerican journal of translational research2022
Gab1 regulates invadopodia and autocrine VEGF through SHP2/ERK1/2 in hilar cholangiocarcinoma cells.
Article in American journal of translational research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 5 citations in OpenAlex.
- Tyrosine phosphatase SHP2 accelerated ovarian cancer via modulating integrin/ E-Cadherin/ ZEB1 induced EMT.Scientific reports · 2025Article
- The Role of GAB1 in Cancer.Cancers · 2023Review
- An overview of extrahepatic cholangiocarcinoma: from here to where?Frontiers in oncology · 2023Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesHilar cholangiocarcinoma is the most common malignant tumors of the biliary tract and it has high invasiveness. Invadopodia and autocrine vascular endothelial growth factor (VEGF) are closely related to tumor invasiveness. We investigated the role of Grb2-associated binder 1 (Gab1) in invadopodia and autocrine VEGF in hilar cholangiocarcinoma cells.
methodsThe expression of Gab1 and vascular endothelial growth factor receptor 2 (VEGFR-2) in tumor cells was detected by real-time PCR. MTT, flow cytometry and transwell assays were used to determine the effect of Gab1 on the biological behavior of tumor cells. In situ gelatin zymogram, western blotting, ELISA and immunofluorescence were used to study Gab1- and apatinib-regulated invadopodia, epithelial-mesenchymal transition (EMT), and VEGF autocrine signaling through the SHP2/ERK1/2 pathway.
resultsGab1 controlled invadopodia maturation via the regulation of cortactin and EMT. Additionally, Gab1-regulated autocrine VEGF was observed in tumor cells expressing VEGFR-2, and endogenous and exogenous VEGF regulated VEGF expression through p-VEGFR-2 nuclear aggregation. Furthermore, the Gab1/SHP2/ERK1/2 axis regulated invadopodia and VEGF autocrine function in tumor cells. Finally, apatinib inhibited the malignant behavior of tumor cells and the nuclear aggregation of p-VEGFR-2 by inhibiting the phosphorylation of VEGFR-2 (direct) and the expression of Gab1 (indirect) in tumor cells.
conclusionsThis study demonstrates that Gab1 and apatinib affect tumor cell invadopodia and autocrine VEGF expression through the Gab1/SHP2/ERK1/2 axis in hilar cholangiocarcinoma cells.
Indexed as
Identifiers
36628230PMC9827304W4315619105What OpenQuestion holds
Registered trials
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