Results 161 to 170 of about 3,596,843 (342)

PYCR1 inhibition in bone marrow stromal cells enhances bortezomib sensitivity in multiple myeloma cells by altering their metabolism

open access: yesMolecular Oncology, EarlyView.
This study investigated how PYCR1 inhibition in bone marrow stromal cells (BMSCs) indirectly affects multiple myeloma (MM) cell metabolism and viability. Culturing MM cells in conditioned medium from PYCR1‐silenced BMSCs impaired oxidative phosphorylation and increased sensitivity to bortezomib.
Inge Oudaert   +13 more
wiley   +1 more source

In vitro properties of patient serum predict clinical outcome after high dose rate brachytherapy of hepatocellular carcinoma

open access: yesMolecular Oncology, EarlyView.
Following high dose rate brachytherapy (HDR‐BT) for hepatocellular carcinoma (HCC), patients were classified as responders and nonresponders. Post‐therapy serum induced increased BrdU incorporation and Cyclin E expression of Huh7 and HepG2 cells in nonresponders, but decreased levels in responders.
Lukas Salvermoser   +14 more
wiley   +1 more source

Advancing the scale of synthetic biology via cross-species transfer of cellular functions enabled by iModulon engraftment [PDF]

open access: gold
Donghui Choe   +6 more
openalex   +1 more source

Inhibition of CDK9 enhances AML cell death induced by combined venetoclax and azacitidine

open access: yesMolecular Oncology, EarlyView.
The CDK9 inhibitor AZD4573 downregulates c‐MYC and MCL‐1 to induce death of cytarabine (AraC)‐resistant AML cells. This enhances VEN + AZA‐induced cell death significantly more than any combination of two of the three drugs in AraC‐resistant AML cells.
Shuangshuang Wu   +18 more
wiley   +1 more source

A synthetic benzoxazine dimer derivative targets c‐Myc to inhibit colorectal cancer progression

open access: yesMolecular Oncology, EarlyView.
Benzoxazine dimer derivatives bind to the bHLH‐LZ region of c‐Myc, disrupting c‐Myc/MAX complexes, which are evaluated from SAR analysis. This increases ubiquitination and reduces cellular c‐Myc. Impairing DNA repair mechanisms is shown through proteomic analysis.
Nicharat Sriratanasak   +8 more
wiley   +1 more source

Author Correction: Loss of mRNA surveillance pathways results in widespread protein aggregation

open access: yesScientific Reports, 2021
Nur Hidayah Jamar   +2 more
doaj   +1 more source

Adaptaquin is selectively toxic to glioma stem cells through disruption of iron and cholesterol metabolism

open access: yesMolecular Oncology, EarlyView.
Adaptaquin selectively kills glioma stem cells while sparing differentiated brain cells. Transcriptomic and proteomic analyses show Adaptaquin disrupts iron and cholesterol homeostasis, with iron chelation amplifying cytotoxicity via cholesterol depletion, mitochondrial dysfunction, and elevated reactive oxygen species.
Adrien M. Vaquié   +16 more
wiley   +1 more source

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