Results 161 to 170 of about 17,756,051 (243)

Castration‐resistant prostate cancer cells are addicted to the high activity of cyclin‐dependent kinase 2

Molecular Oncology, EarlyView.
We show that emergence of castration‐resistant prostate (CRPC) is associated with significant upregulation of cyclins that positively regulate cyclin‐dependent kinase 2 (CDK2) and concomitant downregulation of CDK4 cyclins. This renders CRPC cells dependent on the high activity of CDK2, and CDK2 inhibitors synergistically sensitize CRPC cells to both ...
Joyeeta Chatterjee, Alessia Marin, Shivani Yalala, Harri M. Itkonen   +3 more
wiley   +1 more source

Partial FAK suppression promotes tumor growth, an effect reversed by macrophage p110δ PI3K inactivation

Molecular Oncology, EarlyView.
Partial inhibition of focal adhesion kinase (FAK) can paradoxically promote tumor growth, rather than simply producing a weaker antitumor effect than that observed with strong FAK suppression. In breast cancer and melanoma models, targeting p110δ PI3K, particularly in macrophages, counteracted these tumor‐promoting effects, highlighting the importance ...
Lydia Xenou, Niki Tzenaki, Anna Tsapara, Maria Tzardi, Evangelia A. Papakonstanti   +4 more
wiley   +1 more source

Mechanisms and therapeutic opportunities of the ribotoxic stress response in cancer

Molecular Oncology, EarlyView.
Cancer cells' high translational demand creates opportunities to therapeutically target ribosome function. Ribosome stalling and collisions activate ZAKα and the ribotoxic stress response (RSR), which can trigger rapid, p53‐independent apoptosis in cancer.
Anastassiya Kim, Maryam Aslam, Elouise Torruella, Alphons Sony, Asif Rahman, Simira Smith, Columba de la Parra, Moira Sauane   +7 more
wiley   +1 more source

Profiling neoadjuvant therapy response in rectal cancer using meta‐analysis of publicly available transcriptomic RNA‐seq datasets

Molecular Oncology, EarlyView.
This study integrates publicly available transcriptomic datasets to identify molecular signatures associated with response to neoadjuvant chemoradiotherapy in locally advanced rectal cancer. By analyzing a combination of multiple cohorts with bioinformatics approaches, we reveal biological pathways and immune‐related features that may improve ...
Aleksandra Stanojevic, Rafael Stroggilos, Mladen Marinkovic, Ana Djuric, Suzana Stojanovic‐Rundic, Radmila Jankovic, Sergi Castellvi‐Bel, Remond J.A. Fijneman, Antonia Vlahou, Jerome Zoidakis, Milena Cavic   +10 more
wiley   +1 more source

The VHL tumor suppressor at the crossroad of protein folding, aggregation, and cancer

Molecular Oncology, EarlyView.
Mutations, environmental stress, and chaperone dysfunction can destabilize pVHL, promoting its conversion from the native folded state into amyloid‐like assemblies. This transition may contribute to protein storage, cell dormancy, survival, and drug resistance.
Lara Abad, Silvio Carlo Ermanno Tosatto, Emanuela Leonardi   +2 more
wiley   +1 more source

Regulation of the lncRNA NEAT1 by p53‐ΔNp63 crosstalk modulates the DNA damage response and therapeutic efficacy in HNSCC

Molecular Oncology, EarlyView.
In head and neck squamous cell carcinoma (HNSCC) p53 and p63 exert opposite roles on the transcription regulation of the lncRNA NEAT1. Under basal conditions, p53 levels are low and p63 represses NEAT1 expression. Upon genotoxic stress, p53 is rapidly induced, displacing p63 from the NEAT1 promoter leading to NEAT1 transcriptional activation and ...
Sara De Domenico, Veronica La Banca, Silvia D'Amico, Stefano Scalera, Sara Nicolai, Angelo Peschiaroli   +5 more
wiley   +1 more source

p190A/ARHGAP35 and p190B/ARHGAP5 proteins in endometrial cancer: a novel cancer‐relevant paralog interplay

Molecular Oncology, EarlyView.
This study identifies ARHGAP5, in addition to the frequently mutated ARHGAP35, as significantly mutated in endometrial cancer. Mutations in both genes co‐occur and are associated with their correlated downregulation. Functional CRISPR studies show that both paralogs regulate similar pathways, including actin cytoskeleton organization.
Mathilde Pinault, Capucine Heraud, Mélissa Correia de Oliveira, Véronique Neaud, Valérie Valesco, Valérie Prouzet‐Mauleon, Béatrice Turcq, Jean‐William Dupuy, Anne‐Aurélie Raymond, Sabrina Croce, Frédéric Saltel, Valérie Lagrée, Violaine Moreau   +12 more
wiley   +1 more source

Unique circulating miRNAome signatures captured with distinct molecular states in Lynch syndrome and sporadic colorectal cancer

Molecular Oncology, EarlyView.
Circulating microRNA profiles distinguish nonmalignant Lynch syndrome from cancer‐associated Lynch syndrome, sporadic colorectal cancer, and healthy controls. Age‐stratified analysis reveals disease‐specific regulatory states, and a six‐miRNA panel shows concordant separation in an independent colorectal tissue cohort.
Ramadhani Salum Chambuso, Md Shohel Ul Islam, Rosa M Xicola, Raj Ramesar, Xavier Llor, Sinclair Steele   +5 more
wiley   +1 more source

Mutant p53R273H disrupts PDPK1 homodimerization and contributes to PDPK1 activation

Molecular Oncology, EarlyView.
How mutant p53R273H drives AKT signaling is unclear. We show that p53R273H, but not wild‐type, directly binds PDPK1 via a mutation‐dependent conformational change. This interaction disrupts inhibitory PDPK1 homodimerization and enhances AKT phosphorylation.
Mei Chee Lim, Alvin Kunyao Guo, Yoko Itahana, Srinivasaraghavan Kannan, Valerie Goh, Mingmin Ong, Terina Yan Wen Tay, Weiying Ye, Sabhashina Radha Krishnan, Jun Nishiyama, Chandra S Verma, Koji Itahana   +11 more
wiley   +1 more source

Targeting the EpCAM‐AXL axis to overcome drug resistance in lung cancer

Molecular Oncology, EarlyView.
Lung cancer cells often evade therapy by hijacking signaling pathways. We reveal that cleaved EpCAM (sEpCAM) stabilizes the oncogenic protein AXL, driving NF‐κB and STAT3‐mediated chemoresistance. This EpCAM‐AXL axis identifies a high‐risk patient subset with poor prognosis.
Alexa Guerrero‐Alba, Mark Shacker, Timothy P. Fleming, Michael A. Smith, Ross M. Bremner, Narendra V. Sankpal   +5 more
wiley   +1 more source