Results 131 to 140 of about 2,431,497 (250)

Somatostatin receptor 4 (SSTR4) is a tumor suppressor in cutaneous and head & neck squamous cell carcinomas

open access: yesMolecular Oncology, EarlyView.
This study identifies somatostatin receptor 4 (Sstr4) as a critical tumor suppressor against skin and head/neck cancers (HNSCC, cSCC, and BCC). The loss of Sstr4 removes a check on cell growth, causing hyperactivation of the MAPK‐ERK signaling pathway (↑).
Ali Taqvi   +6 more
wiley   +1 more source

ADP‐ribosylation: An emerging regulator of the epigenome

open access: yesMolecular Oncology, EarlyView.
ADP‐ribosylation has emerged as a dynamic epigenetic signaling mechanism that modifies histones and chromatin‐associated proteins. Through coordinated PARylation and MARylation, it integrates with other histone modifications to regulate chromatin structure, transcription factor activity, and gene expression, influencing genome function and disease ...
Cristel V. Camacho   +2 more
wiley   +1 more source

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

open access: yesMolecular 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   +3 more
wiley   +1 more source

Synthesis of β-Amino and β-Methoxy Ketones by Lewis Acids Promoted β-Substitution Reactions of β,γ-Unsaturated Ketones

open access: yes, 2009
A reaction mixture of β,γ-unsaturated ketone and BF3·OEt2 in CH3OH was stirred at room temperature and β-methoxy ketone was produced in high yield. The β-amino ketone was obtained as the major product from a reaction mixture of β,γ-unsaturated ketone ...
Lee, Adam Shih-yuan; Wang, Shu-huei; Chang, Yu-ting; Chu, Shu-fang
core  

Unraveling the epigenetic code in cancer cell–tumor microenvironment crosstalk

open access: yesMolecular Oncology, EarlyView.
Epigenetic regulation is a key driver of cancer development and progression. Diverse epigenetic alterations in cancer cells and components of the tumor microenvironment (TME) orchestrate their communication through multiple mechanisms. We discuss how the epigenetic code coordinates bidirectional cancer cell–TME crosstalk to promote cancer progression ...
Ji Hoon Park, Mi‐Young Kim
wiley   +1 more source

Arginine methylation as a regulatory ratchet in cancer: From substrate selection to malignant‐state stabilization

open access: yesMolecular Oncology, EarlyView.
Arginine methylation can be viewed as a persistence‐prone post‐translational modification regulated by a network of PRMTs. Competitive and compensatory interactions among PRMTs can redistribute methylation across substrate pools shaped by sequence, structural, spatial, and environmental layers, reinforcing RNA‐processing, chromatin, and signaling ...
So Hyun Kwon, Ji Min Lee
wiley   +1 more source

Mechanisms and therapeutic opportunities of the ribotoxic stress response in cancer

open access: yesMolecular 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   +7 more
wiley   +1 more source

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

open access: yesMolecular 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   +2 more
wiley   +1 more source

NAPRT loss promotes lung tumor initiation and growth through AKT signaling independently of NAD+ biosynthesis

open access: yesMolecular Oncology, EarlyView.
Loss of NAPRT promotes lung tumor initiation and growth through a noncanonical mechanism, independent of its role in NAD+ biosynthesis. Mechanistically, NAPRT depletion activates the mTORC2‐driven AKT/β‐catenin signaling axis to enhance clonogenic and invasive phenotypes. Furthermore, lung‐specific Naprt deletion significantly increases tumor burden in
Myung Joon Oh   +11 more
wiley   +1 more source

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