Results 271 to 280 of about 5,348,766 (308)

Inhibitor of DNA binding‐1 is a key regulator of cancer cell vasculogenic mimicry

Molecular Oncology, EarlyView.
Elevated expression of transcriptional regulator inhibitor of DNA binding 1 (ID1) promoted cancer cell‐mediated vasculogenic mimicry (VM) through regulation of pro‐angiogenic and pro‐cancerous genes (e.g. VE‐cadherin (CDH5), TIE2, MMP9, DKK1). Higher ID1 expression also increased metastases to the lung and the liver.
Emma J. Thompson, Emma L. Dorward, Kristyn Jurrius, Nathalie Nataren, Markus Tondl, Kay K. Myo Min, Michaelia P. Cockshell, Anahita Fouladzadeh, John Toubia, Mark DeNichilo, Delphine Merino, Claudine S. Bonder   +11 more
wiley   +1 more source

Inhibition of colorectal cancer cell growth by downregulation of M2-PK and reduction of aerobic glycolysis by clove active ingredients. [PDF]

Front Pharmacol
Liu L, Xing G, Guo X, Chen H, Li J, Wang J, Li Y, Liang G, Liu M.   +8 more
europepmc   +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

Dual Roles of Canagliflozin on Cholangiocarcinoma Cell Growth and Enhanced Growth Suppression in Combination with FK866. [PDF]

Int J Mol Sci
Taguchi D, Shirakami Y, Sakai H, Minowa D, Miwa T, Maeda T, Kubota M, Imai K, Ibuka T, Shimizu M.   +9 more
europepmc   +1 more source

Ubiquitination of transcription factors in cancer: unveiling therapeutic potential

Molecular Oncology, EarlyView.
In cancer, dysregulated ubiquitination of transcription factors contributes to the uncontrolled growth and survival characteristics of tumors. Tumor suppressors are degraded by aberrant ubiquitination, or oncogenic transcription factors gain stability through ubiquitination, thereby promoting tumorigenesis.
Dongha Kim, Hye Jin Nam, Sung Hee Baek
wiley   +1 more source

A synthetic methylotroph achieves accelerated cell growth by alleviating transcription-replication conflicts. [PDF]

Nat Commun
Meng X, Hu G, Li X, Gao C, Song W, Wei W, Wu J, Liu L.   +7 more
europepmc   +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

ATM-dependent DNA damage response constrains cell growth and drives clonal hematopoiesis in telomere biology disorders. [PDF]

J Clin Invest
Sande CM, Chen S, Mitchell DV, Lin P, Abraham DM, Cheng JM, Gebhard T, Deolikar RJ, Freeman C, Zhou M, Kumar S, Bowman M, Bowman RL, Zheng S, Munkhbileg B, Chen Q, Stanley NL, Guo K, Lapite A, Hausler R, Taylor DM, Corines J, Morrissette JJ, Lieberman DB, Yang G, Shestova O, Gill S, Zheng J, Smith-Simmer K, Banaszak LG, Shoger KN, Reinig EF, Peterson M, Nicholas P, Walne AJ, Dokal I, Rosenheck JP, Oetjen KA, Link DC, Gelman AE, Reilly CR, Dutta R, Lindsley RC, Brundige KJ, Agarwal S, Bertuch AA, Churpek JE, Tague LK, Johnson FB, Olson TS, Babushok DV.   +50 more
europepmc   +1 more source

Changes in the cell constitution of baker's yeast in changing growth conditions

, 1963
Heikki Suomalainen
openalex   +2 more sources

Aberrant expression of nuclear prothymosin α contributes to epithelial‐mesenchymal transition in lung cancer

Molecular Oncology, EarlyView.
Nuclear prothymosin α inhibits epithelial‐mesenchymal transition (EMT) in lung cancer by increasing Smad7 acetylation and competing with Smad2 for binding to SNAI1, TWIST1, and ZEB1 promoters. In early‐stage cancer, ProT suppresses TGF‐β‐induced EMT, while its loss in the nucleus in late‐stage cancer leads to enhanced EMT and poor prognosis.
Liyun Chen, Chung‐Teng Wang, Jia‐Ming Chang, Ai‐Li Shiau, Gia‐Shing Shieh, Yau‐Lin Tseng, Yi‐Ting Yen, Tang‐Hsiu Huang, Li‐Hsin Cheng, Yu‐Chih Wu, Chao‐Liang Wu, Bing‐Hua Su, Pensee Wu   +12 more
wiley   +1 more source