Results 71 to 80 of about 2,675,337 (312)

Exploiting metabolic adaptations to overcome dabrafenib treatment resistance in melanoma cells

Molecular Oncology, EarlyView.
We show that dabrafenib‐resistant melanoma cells undergo mitochondrial remodeling, leading to elevated respiration and ROS production balanced by stronger antioxidant defenses. This altered redox state promotes survival despite mitochondrial damage but renders resistant cells highly vulnerable to ROS‐inducing compounds such as PEITC, highlighting redox
Silvia Eller, Susanne Ebner, Carmen Haselrieder, Julia K. Günther, Astrid Drasche, Sophie Strich, Chiara Volani, Andrea Medici, Aleksandar Nikolajevic, Alex Deltedesco, Johannes E. Sigmund, Michael J. Blumer, Martin Hermann, Johanna Vanacker, Gerald Brandacher, Eduard Stefan, Omar Torres‐Quesada, Jakob Troppmair   +17 more
wiley   +1 more source

Cell surface interactome analysis identifies TSPAN4 as a negative regulator of PD‐L1 in melanoma

Molecular Oncology, EarlyView.
Using cell surface proximity biotinylation, we identified tetraspanin TSPAN4 within the PD‐L1 interactome of melanoma cells. TSPAN4 negatively regulates PD‐L1 expression and lateral mobility by limiting its interaction with CMTM6 and promoting PD‐L1 degradation.
Guus A. Franken, Andrea Abel Gutierrez, Imke van Rossum, Cornelia G. Spruijt, Michiel Vermeulen, Guido van Mierlo, Blanca Scheijen, Annemiek B. van Spriel   +7 more
wiley   +1 more source

Therapeutic strategies for MMAE‐resistant bladder cancer through DPP4 inhibition

Molecular Oncology, EarlyView.
We established monomethyl auristatin E (MMAE)‐resistant bladder cancer (BC) cell lines by exposure to progressively increasing concentrations of MMAE in vitro. RNA sequencing showed DPP4 expression was increased in MMAE‐resistant BC cells. Both si‐DPP4 and the DPP4 inhibitor sitagliptin suppressed the viability of MMAE‐resistant BC cells.
Gang Li, Shuichi Tatarano, Hirofumi Yoshino, Saeki Saito, Mitsuhiko Tominaga, Junya Arima, Ikumi Fukuda, Takashi Sakaguchi, Ryosuke Matsushita, Yasutoshi Yamada, Hideki Enokida   +10 more
wiley   +1 more source

Recurrent cancer‐associated ERBB4 mutations are transforming and confer resistance to targeted therapies

Molecular Oncology, EarlyView.
We show that the majority of the 18 analyzed recurrent cancer‐associated ERBB4 mutations are transforming. The most potent mutations are activating, co‐operate with other ERBB receptors, and are sensitive to pan‐ERBB inhibitors. Activating ERBB4 mutations also promote therapy resistance in EGFR‐mutant lung cancer.
Veera K. Ojala, Sini Ahonen, Sara Peltola, Aura Tuohisto‐Kokko, Olaya Esparta, Peppi Suominen, Anne Jokilammi, Iman Farahani, Deepankar Chakroborty, Nikol Dibus, Steffen Boettcher, Tomi T. Airenne, Mark S. Johnson, Lisa D. Eli, Klaus Elenius, Kari J. Kurppa   +15 more
wiley   +1 more source

Peroxidasin enables melanoma immune escape by inhibiting natural killer cell cytotoxicity

Molecular Oncology, EarlyView.
Peroxidasin (PXDN) is secreted by melanoma cells and binds the NK cell receptor NKG2D, thereby suppressing NK cell activation and cytotoxicity. PXDN depletion restores NKG2D signaling and enables effective NK cell–mediated melanoma killing. These findings identify PXDN as a previously unrecognized immune evasion factor and a potential target to improve
Hsu‐Min Sung, David Bickel, Lena C. M. Krause, Daria Ezeriņa, Christian Ickes, Julian Wojtachnia, Christine S. Gibhardt, Magdalena Shumanska, Khadija Wahni, Andrea Paluschkiwitz, Julia Malo Pueyo, Ekaterina Baranova, Wim Vranken, Hedwig Stanisz, Ioana Stejerean‐Todoran, Michael P. Schön, Joris Messens, Ivan Bogeski   +17 more
wiley   +1 more source

Combining antibody conjugates with cytotoxic and immune‐stimulating payloads maximizes anti‐cancer activity

Molecular Oncology, EarlyView.
Methods to improve antibody–drug conjugate (ADC) treatment durability in cancer therapy are needed. We utilized ADCs and immune‐stimulating antibody conjugates (ISACs), which are made from two non‐competitive antibodies, to enhance the entry of toxic payloads into cancer cells and deliver immunostimulatory agents into immune cells.
Tiexin Wang, Dong Jun Koo, Peter M. Tessier, Greg M. Thurber   +3 more
wiley   +1 more source

TRAIL‐PEG‐Apt‐PLGA nanosystem as an aptamer‐targeted drug delivery system potential for triple‐negative breast cancer therapy using in vivo mouse model

Molecular Oncology, EarlyView.
Aptamers are used both therapeutically and as targeting agents in cancer treatment. We developed an aptamer‐targeted PLGA–TRAIL nanosystem that exhibited superior therapeutic efficacy in NOD/SCID breast cancer models. This nanosystem represents a novel biotechnological drug candidate for suppressing resistance development in breast cancer.
Gulen Melike Demirbolat, Aslihan Kucuk, Omer Erdogan, Samed Ozer, Bensu Kozan, Tugba Cuceli, Erkan Gumus, Evrim Cevik, Ozge Cevik   +8 more
wiley   +1 more source

Dimethyl fumarate combined with cisplatin at subcytotoxic doses sensitizes cervical cancer toward ferroptosis and apoptosis through GSH restriction and p53 (re)activation

Molecular Oncology, EarlyView.
Dimethyl fumarate (DMF) reduces growth of HPV‐positive cervical cancer spheroids and induces ferroptosis in cervical cancer cells via blocking SLC7A11/Glutathione (GSH) axis. Combination of subcytotoxic doses of DMF and cisplatin (CDDP) further suppresses spheroid growth and drives cell death in 2D culture models.
Carolina Punziano, Giuseppina Minopoli, Simona Romano, Laura Marrone, Katia Aquilano, Maria Lina Tornesello, Raffaella Faraonio   +6 more
wiley   +1 more source

RIPK4 function interferes with melanoma cell adhesion and metastasis

Molecular Oncology, EarlyView.
RIPK4 promotes melanoma growth and spread. RIPK4 levels increase as skin lesions progress to melanoma. CRISPR/Cas9‐mediated deletion of RIPK4 causes melanoma cells to form less compact spheroids, reduces their migratory and invasive abilities and limits tumour growth and dissemination in mouse models.
Norbert Wronski, Sławomir Lasota, Ewelina Madej, Anna A. Brożyna, Małgorzata Szczygieł, Agnieszka Harazin‐Lechowska, Jan Czerbniak, Janusz Rys, Jaroslaw Czyz, Agnieszka Wolnicka‐Glubisz   +9 more
wiley   +1 more source

COMP–PMEPA1 axis promotes epithelial‐to‐mesenchymal transition in breast cancer cells

Molecular Oncology, EarlyView.
This study reveals that cartilage oligomeric matrix protein (COMP) promotes epithelial‐to‐mesenchymal transition (EMT) in breast cancer. We identify PMEPA1 (protein TMEPAI) as a novel COMP‐binding partner that mediates EMT via binding to the TSP domains of COMP, establishing the COMP–PMEPA1 axis as a key EMT driver in breast cancer.
Konstantinos S. Papadakos, Gilar Gorji‐bahri, Lejla Gradjan, Julia Zajac, Kacper Gil, Yvonne Thokozile Nduku, Anna M. Blom   +6 more
wiley   +1 more source