Results 131 to 140 of about 473,147 (302)

CCDC80 suppresses high‐grade serous ovarian cancer migration via negative regulation of B7‐H3

open access: yesMolecular Oncology, EarlyView.
PAX8 is a lineage‐specific master regulator of transcription in high‐grade serous ovarian cancer (HGSC) progression. We show for the first time that PAX8 facilitates proliferation and metastasis by repressing the cell autonomous tumor suppressor CCDC80 and inducing B7‐H3 expression.
Aya Saleh   +12 more
wiley   +1 more source

E2A selectively regulates TGF‐β–induced apoptosis in KRAS‐mutant non‐small cell lung cancer

open access: yesMolecular Oncology, EarlyView.
Ability to induce apoptosis by TGF‐β is frequently lost in advanced lung adenocarcinoma despite intact TGF‐β signaling. We identify E2A as a mutant KRAS–dependent mediator of resistance to TGF‐β–induced apoptosis. TGF‐β induces E2A via SMAD3 in mutant KRAS cells, and E2A silencing restores apoptosis and enhances radiation response in cell lines ...
Sergei Chuikov   +3 more
wiley   +1 more source

CD47 promotes mitogen‐activated protein kinase and epithelial‐to‐mesenchymal transition molecular programs to drive prometastatic phenotypes in non‐small cell lung cancer

open access: yesMolecular Oncology, EarlyView.
Beyond its role in immune evasion, this study identified that CD47 drives tumor‐intrinsic signaling in non‐small cell lung cancer (NSCLC). Transcriptomic profiling and functional studies revealed that CD47 regulates cell adhesion, migration, and metastasis through an ERK–EMT signaling axis.
Asa P.Y. Lau   +8 more
wiley   +1 more source

Cell‐cycle‐specific lesion evolution rather than inhibition of double‐strand‐break repair underpins cisplatin radiosensitization

open access: yesMolecular Oncology, EarlyView.
We analyze cisplatin–DNA adducts (CDAs) and double‐strand breaks (DSBs) in a cell‐cycle‐dependent manner. We find that CDAs form similarly across all cell cycle phases. DSBs arise only in S‐phase. CDAs might not directly impair DSB repair, but S‐phase DSB lesions evolve in the presence of CDAs and disrupt repair in G2, also causing radiosensitization ...
Ye Qiu   +10 more
wiley   +1 more source

Dual-locked fluorescent probes for precise diagnosis and targeted treatment of tumors

open access: yesHeliyon
Cancer continues to pose a significant threat to global health, with its high mortality rates largely attributable to delayed diagnosis and non-specific treatments. Early and accurate diagnosis is crucial, yet it remains challenging due to the subtle and
Tang Gao   +3 more
doaj   +1 more source

NKCC1: A key regulator of glioblastoma progression

open access: yesMolecular Oncology, EarlyView.
Glioblastoma (GBM) progression is driven by disrupted chloride cotransporter homeostasis. NKCC1 is highly expressed in stem‐like, astrocytic, and progenitor cells, correlating with earlier recurrence, while overall survival remains unaffected. NKCC1 serves as a prognostic marker and potential therapeutic target, linking chloride transporter imbalance ...
Anja Thomsen   +5 more
wiley   +1 more source

Interaction of HS1BP3 with cortactin modulates TKS5 localisation, cell secretion and cancer malignancy

open access: yesMolecular Oncology, EarlyView.
Here, we demonstrate that HS1BP3 interacts with Cortactin through a proline‐rich region (PRR3.1) and show that this interaction, and HS1BP3 itself, promote cancer cell proliferation and invasion. Inhibition of this interaction leads to build‐up of TKS5 in multivesicular endosomes and altered secretion of CD63 and CD9, providing an explanation for the ...
Arja Arnesen Løchen   +9 more
wiley   +1 more source

Proteasome inhibitor, ixazomib prevents topoisomerase‐I degradation and reverses irinotecan resistance in colorectal cancer

open access: yesMolecular Oncology, EarlyView.
Ixazomib inhibits proteasome‐mediated degradation of topoisomerase I induced by irinotecan, thereby restoring drug sensitivity and promoting tumor cell death in colorectal cancer. Irinotecan, a topoisomerase I (topoI) inhibitor, is widely used for colorectal cancer, but resistance remains a major clinical challenge.
Yuho Ebata   +10 more
wiley   +1 more source

Loss of IGF‐1R impairs DNA‐PKcs recruitment to chromatin leading to defective end‐joining

open access: yesMolecular Oncology, EarlyView.
IGF‐1R promotes radioresistance by facilitating DNA‐PKcs recruitment to chromatin, enabling non‐homologous end‐joining (NHEJ) repair of double‐strand breaks. Inhibition or loss of IGF‐1R disrupts this recruitment to damage sites, driving compensatory reliance on microhomology‐mediated end‐joining (MMEJ) repair.
Matthew O. Ellis   +3 more
wiley   +1 more source

Unlocking the Multifaceted Role of CB1R in the Endocannabinoid System with Labeled Chemical Probes

open access: yesCHIMIA
The endocannabinoid system is a key homeostatic regulator that influences multiple physiological processes across nervous, immune, and metabolic systems in humans.
Leonard Mach, Marc Nazare
doaj   +1 more source

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