Results 131 to 140 of about 855,861 (301)

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

KDM7A and KDM1A inhibition suppresses tumour promoting pathways in prostate cancer

open access: yesMolecular Oncology, EarlyView.
Treatment resistance is a major challenge for patients with advanced prostate cancer. This study examined an alternative approach to target the major prostate cancer‐promoting pathway by targeting epigenetic factors, whose levels are higher in tumours.
Jennie N Jeyapalan   +16 more
wiley   +1 more source

Insights into orphan nuclear receptors as prognostic markers and novel therapeutic targets for breast cancer

open access: yesFrontiers in Endocrinology, 2015
The roles of orphan nuclear receptors in breast cancer development and progression are not well understood. In this review, we correlate orphan nuclear receptor expression in breast cancer tumour subtypes with patient outcomes and provide an overview of ...
Reidun eAesoy   +6 more
doaj   +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

Transcriptional Regulation by Nuclear Corepressors and PGC-1α: Implications for Mitochondrial Quality Control and Insulin Sensitivity

open access: yesPPAR Research, 2012
The peroxisome proliferator-activated receptors (PPARs) and estrogen-related receptor (ERRα) are ligand-activated nuclear receptors that coordinately regulate gene expression.
Zhengtang Qi, Shuzhe Ding
doaj   +1 more source

Exploiting vulnerabilities of cancer by targeting nuclear receptors of stromal cells in tumor microenvironment

open access: yesMolecular Cancer, 2019
The tumor microenvironment is a complex and dynamic cellular community comprising the tumor epithelium and various tumor-supporting cells such as immune cells, fibroblasts, immunosuppressive cells, adipose cells, endothelial cells, and pericytes.
Hong Sheng Cheng   +3 more
doaj   +1 more source

Nuclear Receptors

open access: yesBritish Journal of Pharmacology, 2004
Guide to Receptors and ChannelsSPH Alexander, A Mathie, JA PetersBritish Journal of Pharmacology (2004) 141, S97–S101.
openaire   +2 more sources

Hijacking emergency granulopoiesis: Neutrophil ontogeny and reprogramming in cancer

open access: yesMolecular Oncology, EarlyView.
Neutrophils are highly plastic innate immune cells; their functions in cancer extend beyond the tumour microenvironment. This Review summarises current understanding of neutrophil maturation and heterogeneity and highlights tumour‐induced granulopoiesis as a systemic programme that expands immature, immunosuppressive neutrophils via tumour‐derived ...
Gabriela Marinescu, Yi Feng
wiley   +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

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

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