Results 51 to 60 of about 10,965 (175)
ABSTRACT Patient‐derived organoids (PDOs) have emerged as an effective experimental platform for bridging the long‐standing gap between traditional in vitro cancer models and the biological complexity of actual tumors. These three‐dimensional cultures (3D), derived directly from patient tissues, preserve essential architectural, genomic, and phenotypic
Abdullah Jabri +10 more
wiley +1 more source
MiR-194 functions as a tumor suppressor in laryngeal squamous cell carcinoma by targeting Wee1
The emerging roles of microRNAs (miRs) have been deeply investigated in cancer. However, the role of miR-194 in human laryngeal squamous cell carcinoma (LSCC) is still unclear.
Pei Li +16 more
doaj +1 more source
The tomato mars1/rough mutant displays enhanced root regeneration and rough fruits due to ectopic cell proliferation. The causal gene encodes a lysine‐specific histone demethylase that normally maintains gene silencing. Its loss alters histone methylation, upregulating several genes, including those B‐type cyclins involved in tissue‐specific cellular ...
Eduardo Larriba +14 more
wiley +1 more source
This study introduces a biomimetic “nanofusion” platform that integrates the biostability of threose nucleic acids (TNA) with homotypic cell‐membrane cloaking to combat drug‐resistant TNBC. By leveraging a non‐canonical membrane‐fusion pathway for direct cytosolic delivery, the platform bypasses endosomal sequestration. To achieve potent AKT2 silencing
Wei Zheng +7 more
wiley +1 more source
Cytokinetic effects of Wee1 disruption in pancreatic cancer [PDF]
The Wee1 kinase, which is activated in response to DNA damage, regulates exit from G2 through inhibitory phosphorylation of Cdk1/Cdc2, and is an attractive drug target. However, recent work has highlighted effects of Cdk2 phosphorylation by Wee1 on movement through S-phase, suggesting the potential to sensitize to S-phase specific agents by Wee1 ...
Qing, Chang +5 more
openaire +2 more sources
A WEE1 family business: regulation of mitosis, cancer progression, and therapeutic target
The inhibition of the DNA damage response (DDR) pathway in the treatment of cancer has recently gained interest, and different DDR inhibitors have been developed. Among them, the most promising ones target the WEE1 kinase family, which has a crucial role
Andrea Ghelli Luserna di Rorà +3 more
doaj +1 more source
This study unveils a pathogenic axis in oral cancer where NUDT21 suppresses a tumor suppressor network, prominently PTEN, via 3'UTR lengthening. To exploit this transcriptomic vulnerability, we developed a biomimetic Nano‐APA‐editor. By delivering CRISPR/Cas9, we reprogrammed the global 3'UTR landscape, restoring multi‐target tumor suppression and ...
Yiran Ao +5 more
wiley +1 more source
Substrate Competition as a Source of Ultrasensitivity in the Inactivation of Wee1 [PDF]
The mitotic regulators Wee1 and Cdk1 can inactivate each other through inhibitory phosphorylations. This double-negative feedback loop is part of a bistable trigger that makes the transition into mitosis abrupt and decisive. To generate a bistable response, some component of a double-negative feedback loop must exhibit an ultrasensitive response to its
Kim, Sun Young, Ferrell, James E.
openaire +2 more sources
Ultrasound‐responsive nanoplatforms reprogram the tumor immune microenvironment by targeting tumor cells, immune cells, and non‐immune stromal cells to enhance the efficacy of cancer immunotherapy. Abstract Cancer immunotherapy represents a significant advancement in cancer treatment by enhancing the specific recognition and elimination of cancer cells.
Shilong Zhao +4 more
wiley +1 more source
Cdk1-Dependent Regulation of the Mitotic Inhibitor Wee1 [PDF]
The Wee1 kinase phosphorylates and inhibits cyclin-dependent kinase 1 (Cdk1), thereby delaying entry into mitosis until appropriate conditions have been met. An understanding of the mechanisms that regulate Wee1 should provide new insight into how cells make the decision to enter mitosis.
Harvey, Stacy L. +4 more
openaire +2 more sources

