KHDRBS3 facilitates self-renewal and temozolomide resistance of glioblastoma cell lines
Issued Date
2024-12-01
Resource Type
ISSN
00243205
eISSN
18790631
Scopus ID
2-s2.0-85206306199
Journal Title
Life Sciences
Volume
358
Rights Holder(s)
SCOPUS
Bibliographic Citation
Life Sciences Vol.358 (2024)
Suggested Citation
Somrit K., Krobthong S., Yingchutrakul Y., Phueakphud N., Wongtrakoongate P., Komyod W. KHDRBS3 facilitates self-renewal and temozolomide resistance of glioblastoma cell lines. Life Sciences Vol.358 (2024). doi:10.1016/j.lfs.2024.123132 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/101687
Title
KHDRBS3 facilitates self-renewal and temozolomide resistance of glioblastoma cell lines
Corresponding Author(s)
Other Contributor(s)
Abstract
Glioblastoma is a deadly tumor which possesses glioblastoma stem cell populations involved in temozolomide (TMZ) resistance. To gain insight into the mechanisms of self-renewing and therapy-resistant cancer stem cells, subcellular proteomics was utilized to identify proteins whose expression is enriched in U251-derived glioblastoma stem-like cells. The KH RNA Binding Domain Containing, Signal Transduction Associated 3, KHDRBS3, was successfully identified as a gene up-regulated in the cancer stem cell population compared with its differentiated derivatives. Depletion of KHDRBS3 by RNA silencing led to a decrease in cell proliferation, neurosphere formation, migration, and expression of genes involved in glioblastoma stemness. Importantly, TMZ sensitivity can be induced by the gene knockdown. Collectively, our results highlight KHDRBS3 as a novel factor associated with self-renewal of glioblastoma stem-like cells and TMZ resistance. As a consequence, targeting KHDRBS3 may help eradicate glioblastoma stem-like cells.