ACT001 inhibited CD133 transcription by targeting and inducing Olig2 ubiquitination degradation.
Ontology highlight
ABSTRACT: Lung cancer is the most lethal malignancies with high aggressive and poor prognosis. Until now, the five-year survival rate has not been improved which brings serious challenge to human health. Lung cancer stem cells (LCSCs) serve as the root of cancer occurrence, progression, recurrence, and drug resistance. Therefore, effective anti-cancer agents and molecular mechanisms which could specifically eliminate LCSCs are urgently needed for drug design. In this article, we discovered Olig2 was overexpressed in clinical lung cancer tissues and acted as a transcription factor to regulate cancer stemness by regulating CD133 gene transcription. The results suggested Olig2 could be a promising target in anti-LCSCs therapy and new drugs targeted Olig2 may exhibit excellent clinical results. Furtherm
SUBMITTER: Deng H
PROVIDER: S-EPMC10060425 | biostudies-literature | 2023 Mar
REPOSITORIES: biostudies-literature
ACCESS DATA