Results 11 to 20 of about 179,166 (149)

Escape from TGF‐β‐induced senescence promotes aggressive hallmarks in epithelial hepatocellular carcinoma cells

Molecular Oncology, EarlyView.
Chronic TGF‐β exposure drives epithelial HCC cells from a senescent state to a TGF‐β resistant mesenchymal phenotype. This transition is characterized by the loss of Smad3‐mediated signaling, escape from senescence, enhanced invasiveness and metastatic potential, and upregulation of key resistance modulators such as MARK1 and GRM8, ultimately promoting
Minenur Kalyoncu, Dilara Demirci, Sude Eris, Bengisu Dayanc, Ece Cakiroglu, Merve Basol, Merve Uysal, Gulcin Cakan‐Akdogan, Fang Liu, Mehmet Ozturk, Gökhan Karakülah, Serif Senturk   +11 more
wiley   +1 more source

Breakthrough Solution for Antimicrobial Resistance Detection: Surface‐Enhanced Raman Spectroscopy‐based on Artificial Intelligence

Advanced Materials Interfaces, EarlyView., 2023
This review discusses the use of Surface‐Enhanced Raman Spectroscopy (SERS) combined with Artificial Intelligence (AI) for detecting antimicrobial resistance (AMR). Various SERS studies used with AI techniques, including machine learning and deep learning, are analyzed for their advantages and limitations.
Zakarya Al‐Shaebi, Munevver Akdeniz, Awel Olsido Ahmed, Mine Altunbek, Omer Aydin   +4 more
wiley   +1 more source

MET and NF2 alterations confer primary and early resistance to first‐line alectinib treatment in ALK‐positive non‐small‐cell lung cancer

Molecular Oncology, EarlyView.
Alectinib resistance in ALK+ NSCLC depends on treatment sequence and EML4‐ALK variants. Variant 1 exhibited off‐target resistance after first‐line treatment, while variant 3 and later lines favored on‐target mutations. Early resistance involved off‐target alterations, like MET and NF2, while on‐target mutations emerged with prolonged therapy.
Jie Hu, Ning Ding, Xiaobo Xu, Yedan Chen, Yong Zhang, Jingwen Liu, Jiebai Zhou, Hairong Bao, Donghui Zhang, Yijun Song, Yang Shao, Yuanlin Song   +11 more
wiley   +1 more source

Targeted protein degradation in oncology: novel therapeutic opportunity for solid tumours?

Molecular Oncology, EarlyView.
Current anticancer therapies are limited by the occurrence of resistance and undruggability of most proteins. Targeted protein degraders are novel, promising agents that trigger the selective degradation of previously undruggable proteins through the recruitment of the ubiquitin–proteasome machinery. Their mechanism of action raises exciting challenges,
Noé Herbel, Sophie Postel‐Vinay
wiley   +1 more source

Determination of ADP/ATP translocase isoform ratios in malignancy and cellular senescence

Molecular Oncology, EarlyView.
The individual functions of three isoforms exchanging ADP and ATP (ADP/ATP translocases; ANTs) on the mitochondrial membrane remain unclear. We developed a method for quantitatively differentiating highly similar human ANT1, ANT2, and ANT3 using parallel reaction monitoring. This method allowed us to assess changes in translocase levels during cellular
Zuzana Liblova, Dominika Maurencova, Barbora Salovska, Marek Kratky, Tomas Mracek, Zuzana Korandova, Alena Pecinova, Pavla Vasicova, David Rysanek, Ladislav Andera, Ivo Fabrik, Rudolf Kupcik, Pavel Kashmel, Pinky Sultana, Vojtech Tambor, Jiri Bartek, Josef Novak, Marie Vajrychova, Zdenek Hodny   +18 more
wiley   +1 more source

The subcellular distribution of phosphorylated Y‐box‐binding protein‐1 at S102 in colorectal cancer patients, stratified by KRAS mutational status and clinicopathological features

Molecular Oncology, EarlyView.
This study identifies nuclear YB‐1 S102 phosphorylation as a marker associated with KRAS and FBXW7 mutations in colorectal cancer. Mutated KRAS correlates specifically with nuclear, not cytoplasmic, S102 YB‐1. These findings provide the first ex vivo evidence of this link in CRC and suggest future studies should assess the prognostic and therapeutic ...
Konstanze Lettau, Stephan Forchhammer, Birgit Fehrenbacher, Lejla Mahmutovic, Marcus Scharpf, Gunnar Blumenstock, Martin Schaller, Irina Bonzheim, Shayan Khozooei, Mahmoud Toulany   +9 more
wiley   +1 more source

BMP antagonist CHRDL2 enhances the cancer stem‐cell phenotype and increases chemotherapy resistance in colorectal cancer

Molecular Oncology, EarlyView.
Overexpression of CHRDL2 in colon cancer cells makes them more stem‐like and resistant to chemo‐ and radiotherapy. CHRDL2‐high cells have upregulation of the WNT pathway, genes involved in the DNA damage response (DDR) pathway and epithelial‐to‐mesenchymal transition (EMT). This leads to quicker repair of damaged DNA and more cell migration.
Eloise Clarkson, Annabelle Lewis
wiley   +1 more source

METTL3 knockout accelerates hepatocarcinogenesis via inhibiting endoplasmic reticulum stress response

FEBS Open Bio, EarlyView.
Liver‐specific knockout of N6‐methyladenosine (m6A) methyltransferase METTL3 significantly accelerated hepatic tumor initiation under various oncogenic challenges, contrary to the previously reported oncogenic role of METTL3 in liver cancer cell lines or xenograft models. Mechanistically, METTL3 deficiency reduced m6A deposition on Manf transcripts and
Bo Cui, Silin Tu, Haibo Li, Zhancheng Zeng, Ruiqi Xiao, Jing Guo, Xiaoqi Liang, Chang Liu, Lijie Pan, Wenjie Chen, Mian Ge, Xiaofen Zhong, Linsen Ye, Huaxin Chen, Qi Zhang, Yan Xu   +15 more
wiley   +1 more source

Long non‐coding RNAs as therapeutic targets in head and neck squamous cell carcinoma and clinical application

FEBS Open Bio, EarlyView.
Long non‐coding RNAs (lncRNAs) occupy an abundant fraction of the eukaryotic transcriptome and an emerging area in cancer research. Regulation by lncRNAs is based on their subcellular localization in HNSCC. This cartoon shows the various functions of lncRNAs in HNSCC discussed in this review.
Ellen T. Tran, Ruchi A. Patel, Amogh Chariyamane, Ratna B. Ray   +3 more
wiley   +1 more source

Knockout of the mitoribosome rescue factors Ict1 or Mtrfr is viable in zebrafish but not mice: compensatory mechanisms underlying each factor's loss

FEBS Open Bio, EarlyView.
Mitochondria contain two mitoribosome rescue factors, ICT1 and MTRFR (C12orf65). ICT1 also functions as a mitoribosomal protein in mice and humans, and its loss is lethal. Although Mtrfr knockout mice could not be generated, knockout zebrafish lines for ict1 and mtrfr were established.
Nobukazu Nameki, Chika Tomisawa, Soichiro Hoshino, Hidehiko Shimizu, Masashi Abe, Sho Arai, Kanako Kuwasako, Naoki Asakawa, Yusuke Inoue, Takuro Horii, Izuho Hatada, Masakatsu Watanabe   +11 more
wiley   +1 more source