The activities of MYC, MNT and the MAX-interactome in lymphocyte proliferation and oncogenesis.

Biochim Biophys Acta

Shriners Hospitals for Children Portland, 3101 SW Sam Jackson Park Road, Portland, OR 97239, USA; Department of Cell and Developmental Biology, Oregon Health & Science University, 3181 SW Sam Jackson Park Road, Portland, OR 97239, USA; Knight Cancer Institute, Oregon Health & Science University, 3181 SW Sam Jackson Park Road, Portland, OR 97239, USA. Electronic address:

Published: May 2015

The MYC family of proteins plays essential roles in embryonic development and in oncogenesis. Efforts over the past 30 years to define the transcriptional activities of MYC and how MYC functions to promote proliferation have produced evolving models of MYC function. One picture that has emerged of MYC and its partner protein MAX is of a transcription factor complex with a seemingly unique ability to stimulate the transcription of genes that are epigenetically poised for transcription and to amplify the transcription of actively transcribed genes. During lymphocyte activation, MYC is upregulated and stimulates a pro-proliferative program in part through the upregulation of a wide variety of metabolic effector genes that facilitate cell growth and cell cycle progression. MYC upregulation simultaneously sensitizes cells to apoptosis and activated lymphocytes and lymphoma cells have pro-survival attributes that allow MYC-driven proliferation to prevail. For example, the MAX-interacting protein MNT is upregulated in activated lymphocytes and was found to protect lymphocytes from MYC-dependent apoptosis. Here we review the activities of MYC, MNT and other MAX interacting proteins in the setting of T and B cell activation and oncogenesis. This article is part of a Special Issue entitled: Myc proteins in cell biology and pathology.

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.bbagrm.2014.04.004DOI Listing

Publication Analysis

Top Keywords

activities myc
12
myc
9
myc mnt
8
activated lymphocytes
8
mnt max-interactome
4
max-interactome lymphocyte
4
lymphocyte proliferation
4
proliferation oncogenesis
4
oncogenesis myc
4
myc family
4

Similar Publications

Background: Targeting glutamine metabolism has emerged as a promising strategy in cancer therapy. However, several barriers, such as anti-tumor efficacy, drug toxicity, and safety, remain to be overcome to achieve clinical utility. Prior preclinical studies had generated encouraging data showing promises of cancer metabolism targeting drugs, although most were performed on immune-deficient murine models.

View Article and Find Full Text PDF

Myc hyperactivation coordinately regulates numerous metabolic processes to drive lymphomagenesis. Here, we elucidate the temporal and functional relationships between the medley of pathways, factors, and mechanisms that cooperate to control redox homeostasis in Myc-overexpressing B cell lymphomas. We find that Myc overexpression rapidly stimulates the oxidative pentose phosphate pathway (oxPPP), nucleotide synthesis, and mitochondrial respiration, which collectively steers cellular equilibrium to a more oxidative state.

View Article and Find Full Text PDF

CASC8 activates the pentose phosphate pathway to inhibit disulfidptosis in pancreatic ductal adenocarcinoma though the c-Myc-GLUT1 axis.

J Exp Clin Cancer Res

January 2025

Department of Hepato-Biliary-Pancreatic Surgery, General Surgery, Huadong Hospital, Fudan University, Shanghai, 200040, PR China.

Purpose: Glucose starvation induces the accumulation of disulfides and F-actin collapse in cells with high expression of SLC7A11, a phenomenon termed disulfidptosis. This study aimed to confirm the existence of disulfidptosis in pancreatic ductal adenocarcinoma (PDAC) and elucidate the role of Cancer Susceptibility 8 (CASC8) in this process.

Methods: The existence of disulfidptosis in PDAC was assessed using flow cytometry and F-actin staining.

View Article and Find Full Text PDF

Mina53 catalyzes arginine demethylation of p53 to promote tumor growth.

Cell Rep

January 2025

Ministry of Education Key Laboratory of Biosystems Homeostasis & Protection, College of Life Sciences, Zhejiang University, Hangzhou, China; Department of Hepatobiliary and Pancreatic Surgery, The First Affiliated Hospital, Zhejiang Provincial Key Laboratory of Pancreatic Disease, School of Medicine, Zhejiang University, Hangzhou, China; Cancer Center, Zhejiang University, Hangzhou, China. Electronic address:

Arginine methylation is a common post-translational modification that plays critical roles in many biological processes. However, the existence of arginine demethylases that remove the modification has not been fully established. Here, we report that Myc-induced nuclear antigen 53 (Mina53), a member of the jumonji C (JmjC) protein family, is an arginine demethylase.

View Article and Find Full Text PDF

A single-cell sequencing-based analysis of a 13-year-old with maxillary sinus NUT carcinoma.

Oral Oncol

January 2025

Clinical Research Center (CRC), Medical Pathology Center (MPC), Cancer Early Detection and Treatment Center (CEDTC) and Translational Medicine Research Center (TMRC), Chongqing University Three Gorges Hospital, Chongqing University, Wanzhou District, Chongqing 404100, China; Chongqing Technical Innovation Center for Quality Evaluation and Identification of Authentic Medicinal Herbs, Wanzhou District, Chongqing 404100, China; School of Medicine Chongqing University, Chongqing University, Shapingba District, Chongqing 400030, China. Electronic address:

NUT carcinoma is a rare and highly aggressive malignancy, predominantly affecting adolescents and young adults. This tumor demonstrates rapid progression, resistance to conventional anti-cancer treatments, and an extremely poor prognosis. Currently, research on NUT carcinoma is limited, and effective treatment options remain scarce.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!