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GLUT1 promotes cell proliferation via binds and stabilizes phosphorylated EGFR in lung adenocarcinoma

dc.contributor.authorZhiqing Zhou
dc.contributor.authorYu Li
dc.contributor.authorSijie Chen
dc.contributor.authorZhangrong Xie
dc.contributor.authorYuhui Du
dc.contributor.authorYue Liu
dc.contributor.authorYuxuan Shi
dc.contributor.authorXiangyi Lin
dc.contributor.authorXiaofei Zeng
dc.contributor.authorHuijie Zhao
dc.contributor.authorGuoan Chen
dc.contributor.otherDepartment of Human Cell Biology and Genetics, Joint Laboratory of Guangdong-Hong Kong Universities for Vascular Homeostasis and Diseases, School of Medicine, Southern University of Science and Technology
dc.contributor.otherDepartment of Human Cell Biology and Genetics, Joint Laboratory of Guangdong-Hong Kong Universities for Vascular Homeostasis and Diseases, School of Medicine, Southern University of Science and Technology
dc.contributor.otherDepartment of Human Cell Biology and Genetics, Joint Laboratory of Guangdong-Hong Kong Universities for Vascular Homeostasis and Diseases, School of Medicine, Southern University of Science and Technology
dc.contributor.otherDepartment of Human Cell Biology and Genetics, Joint Laboratory of Guangdong-Hong Kong Universities for Vascular Homeostasis and Diseases, School of Medicine, Southern University of Science and Technology
dc.contributor.otherDepartment of Human Cell Biology and Genetics, Joint Laboratory of Guangdong-Hong Kong Universities for Vascular Homeostasis and Diseases, School of Medicine, Southern University of Science and Technology
dc.contributor.otherDepartment of Human Cell Biology and Genetics, Joint Laboratory of Guangdong-Hong Kong Universities for Vascular Homeostasis and Diseases, School of Medicine, Southern University of Science and Technology
dc.contributor.otherDepartment of Human Cell Biology and Genetics, Joint Laboratory of Guangdong-Hong Kong Universities for Vascular Homeostasis and Diseases, School of Medicine, Southern University of Science and Technology
dc.contributor.otherDepartment of Human Cell Biology and Genetics, Joint Laboratory of Guangdong-Hong Kong Universities for Vascular Homeostasis and Diseases, School of Medicine, Southern University of Science and Technology
dc.contributor.otherDepartment of Human Cell Biology and Genetics, Joint Laboratory of Guangdong-Hong Kong Universities for Vascular Homeostasis and Diseases, School of Medicine, Southern University of Science and Technology
dc.contributor.otherDepartment of Human Cell Biology and Genetics, Joint Laboratory of Guangdong-Hong Kong Universities for Vascular Homeostasis and Diseases, School of Medicine, Southern University of Science and Technology
dc.contributor.otherDepartment of Human Cell Biology and Genetics, Joint Laboratory of Guangdong-Hong Kong Universities for Vascular Homeostasis and Diseases, School of Medicine, Southern University of Science and Technology
dc.date.accessioned2024-06-09T11:27:19Z
dc.date.accessioned2025-10-08T08:07:02Z
dc.date.available2025-10-08T08:07:02Z
dc.date.issued2024-06
dc.identifier.urihttp://digilib.fisipol.ugm.ac.id/repo/handle/15717717/35614
dc.description.abstractAbstract Background While previous studies have primarily focused on Glucose transporter type 1 (GLUT1) related glucose metabolism signaling, we aim to discover if GLUT1 promotes tumor progression through a non-metabolic pathway. Methods The RNA-seq and microarray data were comprehensively analyzed to evaluate the significance of GLUT1 expression in lung adenocarcinoma (LUAD). The cell proliferation, colony formation, invasion, and migration were used to test GLUT1 ‘s oncogenic function. Co-immunoprecipitation and mass spectrum (MS) were used to uncover potential GLUT1 interacting proteins. RNA-seq, DIA-MS, western blot, and qRT-PCR to probe the change of gene and cell signaling pathways. Results We found that GLUT1 is highly expressed in LUAD, and higher expression is related to poor patient survival. GLUT1 knockdown caused a decrease in cell proliferation, colony formation, migration, invasion, and induced apoptosis in LUAD cells. Mechanistically, GLUT1 directly interacted with phosphor-epidermal growth factor receptor (p-EGFR) and prevented EGFR protein degradation via ubiquitin-mediated proteolysis. The GLUT1 inhibitor WZB117 can increase the sensitivity of LUAD cells to EGFR-tyrosine kinase inhibitors (TKIs) Gefitinib. Conclusions GLUT1 expression is higher in LUAD and plays an oncogenic role in lung cancer progression. Combining GLUT1 inhibitors and EGFR-TKIs could be a potential therapeutic option for LUAD treatment.
dc.language.isoEN
dc.publisherBMC
dc.subject.lccMedicine
dc.titleGLUT1 promotes cell proliferation via binds and stabilizes phosphorylated EGFR in lung adenocarcinoma
dc.typeArticle
dc.description.keywordsLUAD
dc.description.keywordsGLUT1
dc.description.keywordsEGFR
dc.description.keywordsGefitinib
dc.description.keywordsWZB117
dc.description.pages1-16
dc.description.doi10.1186/s12964-024-01678-8
dc.title.journalCell Communication and Signaling
dc.identifier.e-issn1478-811X
dc.identifier.oaid46beaf3778d4fe7928e3c9eb3bbea34
dc.journal.infoVolume 22, Issue 1


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