<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Pan J</submitter><funding>Suzhou municipal key clinical disciplines cultivate program</funding><funding>Suzhou Medical Innovation Applied Research Project</funding><funding>National Natural Science Foundation of China</funding><funding>Innovative and Entrepreneurial Talent Program of Jiangsu for Guohua Shi team, the China Postdoctoral Science Foundation</funding><funding>Projects of International Cooperation of Jiangsu Province</funding><pagination>10</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9890863</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>24(1)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Glioblastoma (GBM) is the most common malignant intracranial tumor with a low survival rate. However, only few drugs responsible for GBM therpies, hence new drug development for it is highly required. The natural product Cudraflavone B (CUB) has been reported to potentially kill a variety of tumor cells. Currently, its anit-cancer effect on GBM still remains unknown. Herein, we investigated whether CUB could affect the proliferation and apoptosis of GBM cells to show anti-GBM potential.&lt;h4>Results&lt;/h4>CUB selectively inhibited cell viability and induced cell apoptosis by activating the endoplasmic reticulum stress (ER stress) related pathway, as well as harnessing the autophagy-related PI3K/mTOR/LC3B signaling pathway. Typical morphological changes of autophagy were also</pubmed_abstract><journal>BMC neuroscience</journal><pubmed_title>Cudraflavone B induces human glioblastoma cells apoptosis via ER stress-induced autophagy.</pubmed_title><pmcid>PMC9890863</pmcid><funding_grant_id>81903028</funding_grant_id><funding_grant_id>SZFCXK202142</funding_grant_id><funding_grant_id>BZ2020004</funding_grant_id><funding_grant_id>SKYD2022090</funding_grant_id><funding_grant_id>2020M671599</funding_grant_id><pubmed_authors>Sun M</pubmed_authors><pubmed_authors>Liu Y</pubmed_authors><pubmed_authors>Pan J</pubmed_authors><pubmed_authors>Yang J</pubmed_authors><pubmed_authors>Zhao R</pubmed_authors><pubmed_authors>Zhou Y</pubmed_authors><pubmed_authors>Zhang R</pubmed_authors><pubmed_authors>Ahmad N</pubmed_authors><pubmed_authors>Dong C</pubmed_authors></additional><is_claimable>false</is_claimable><name>Cudraflavone B induces human glioblastoma cells apoptosis via ER stress-induced autophagy.</name><description>&lt;h4>Background&lt;/h4>Glioblastoma (GBM) is the most common malignant intracranial tumor with a low survival rate. However, only few drugs responsible for GBM therpies, hence new drug development for it is highly required. The natural product Cudraflavone B (CUB) has been reported to potentially kill a variety of tumor cells. Currently, its anit-cancer effect on GBM still remains unknown. Herein, we investigated whether CUB could affect the proliferation and apoptosis of GBM cells to show anti-GBM potential.&lt;h4>Results&lt;/h4>CUB selectively inhibited cell viability and induced cell apoptosis by activating the endoplasmic reticulum stress (ER stress) related pathway, as well as harnessing the autophagy-related PI3K/mTOR/LC3B signaling pathway. Typical morphological changes of autophagy were also</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Jan</publication><modification>2025-04-21T22:50:33.239Z</modification><creation>2025-04-05T18:52:59.039Z</creation></dates><accession>S-EPMC9890863</accession><cross_references><pubmed>36721107</pubmed><doi>10.1186/s12868-023-00778-4</doi></cross_references></HashMap>