NAT COMMUN: Cytoskeleton-regulating proteins drive the occurrence of glioblastomas
-
Last Update: 2020-07-16
-
Source: Internet
-
Author: User
Search more information of high quality chemicals, good prices and reliable suppliers, visit
www.echemi.com
glioblastoma is a deadly cancer !---- and there is no effective treatment to datewe urgently need to better understand and identify selective targetsrecently, researchers found that advillin (AVIL) was over-expressed in all glioblastomas tested, including glioblastoma stem cells/start cells, but the protein was almost undetectable in non-tumor astrocytes, neural stem cells, or normal brainsThe prognosis was poor in patients with an increased expression of avilsilent AVIL almost eradicated glioblastoma cells in cultures and significantly inhibited heterotransplantation in mice, but had no effect on normal control cells, overexpression promotes cell proliferation and migration, frees fibroblasts from contact inhibition, and transforms immortal astrocytes, which support savil proteins as a true cancer gene, the experimental evidence suggests that a tumor-inducing part of AVIL is mediated by FOXM1, and that the expression of FOXM1 regulation LIN28B and LIN28B is also associated with clinical prognosisAVIL regulates the cytoskeleton by regulating F-actin, while the mutantthat that destroys the F-actin binding is defective in its ability to cause tumors
This article is an English version of an article which is originally in the Chinese language on echemi.com and is provided for information purposes only.
This website makes no representation or warranty of any kind, either expressed or implied, as to the accuracy, completeness ownership or reliability of
the article or any translations thereof. If you have any concerns or complaints relating to the article, please send an email, providing a detailed
description of the concern or complaint, to
service@echemi.com. A staff member will contact you within 5 working days. Once verified, infringing content
will be removed immediately.
