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Oncotarget

Oncotarget published this trending research paper on May 19, 2023 in Volume 14, entitled, “Role of creatine shuttle in colorectal cancer cells" by researchers from the Department of Molecular Pathology, Nara Medical University, Kashihara, Nara 634-8521, Japan; Department of Pharmacology, Saveetha Dental College, Saveetha Institute of Medical and Technical Sciences, Chennai 600077, India; Jiangsu Key Laboratory of Neuroregeneration, Nantong University, Nantong, Jiangsu 226001, China.

DOI - https://doi.org/10.18632/oncotarget.28436

Correspondence to - Hiroki Kuniyasu -  cooninh@zb4.so-net.ne.jp, and Rina Fujiwara-Tani - rina_fuji@naramed-u.ac.jp

Abstract

The creatine shuttle translocates the energy generated by oxidative phosphorylation to the cytoplasm via mitochondrial creatine kinase (MTCK) and creatine kinase B (CKB) in the cytoplasm. It is not apparent how the creatine shuttle is related to cancer. Here, we analyzed the expression and function of CKB and MTCK in colorectal cancer (CRC) and investigated the role of the creatine shuttle in CRC. Compared with normal mucosa, 184 CRC tissues had higher levels of CKB and MTCK, and these levels were associated with histological grade, tumor invasion, and distant metastasis. CK inhibitor dinitrofluorobenzene (DNFB) on CRC cell lines HT29 and CT26 inhibited cell proliferation and stemness to less than 2/3 and 1/20 of their control levels, respectively. In this treatment, the production of reactive oxygen species increased, mitochondrial respiration decreased, and mitochondrial volume and membrane potential decreased. In a syngeneic BALB/c mouse model using CT26 cells pretreated with DNFB, peritoneal metastasis was suppressed to 70%. Phosphorylation of EGFR, AKT, and ERK1/2 was inhibited in DNFB-treated tumors. High ATP concentrations prevented EGFR phosphorylation in HT29 cells following DNFB treatment, CKB or MTCK knockdown, and cyclocreatine administration. Despite not being immunoprecipitated, CKB and EGFR were brought closer together by EGF stimulation. These findings imply that blocking the creatine shuttle decreases the energy supply, suppresses oxidative phosphorylation, and blocks ATP delivery to phosphorylation signals, preventing signal transduction. These findings highlight the critical role of the creatine shuttle in cancer cells and suggest a potential new cancer treatment target.

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Keywords - creatine kinase B, mitochondrial creatine kinase, ATP metabolism, phosphorylation signal, stemness

About Oncotarget

Oncotarget is a primarily oncology-focused, peer-reviewed, open access journal. Papers are published continuously within yearly volumes in their final and complete form, and then quickly released to Pubmed. On September 15, 2022, Oncotarget was accepted again for indexing by MEDLINE. Oncotarget is now indexed by Medline/PubMed and PMC/PubMed.

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Role of Creatine Shuttle in Colorectal Cancer Cells

Teach Me in 10

Scientists use human iPSC-derived cells to model human disease in the lab without relying on hard to source patient-derived cells or inaccurate animal models. Watch this expert interview with Dr Will Bernard to get a primer on the latest innovations in in vitro human cell technology, and learn how scientists are adopting these new tools to simplify and standardize experiments in human disease research, and drug discovery.

Revolutionising in vitro Disease Models with iPSC Reprogramming Technology

Aging (Aging-US)

Aging-US published this research paper on May 13, 2023, in Volume 15, Issue 9, entitled, “Highly multiplexed immune profiling throughout adulthood reveals kinetics of lymphocyte infiltration in the aging mouse prostate" by researchers from Department of Molecular, Cell, and Developmental Biology, University of California, Los Angeles, CA; Molecular Biology Interdepartmental Program, University of California, Los Angeles, CA; Division of Hematology-Oncology, Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, CA; Department of Urology, David Geffen School of Medicine, University of California, Los Angeles, CA; Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research, University of California, Los Angeles, CA; Jonsson Comprehensive Cancer Center, University of California, Los Angeles, CA; Molecular Biology Institute, University of California, Los Angeles, CA; Current Address: Division of Biology and Biological Engineering, California Institute of Technology, Pasadena, CA; Current Address: Keck School of Medicine, University of Southern California, Los Angeles, CA; Current Address: Division of Cardiac Surgery, Department of Surgery, Johns Hopkins University School of Medicine, Baltimore, MD.

DOI - https://doi.org/10.18632/aging.204708

Corresponding author - Andrew S. Goldstein - AGoldstein@mednet.ucla.edu

Abstract

Aging is a significant risk factor for disease in several tissues, including the prostate. Defining the kinetics of age-related changes in these tissues is critical for identifying regulators of aging and evaluating interventions to slow the aging process and reduce disease risk. An altered immune microenvironment is characteristic of prostatic aging in mice, but whether features of aging in the prostate emerge predominantly in old age or earlier in adulthood has not previously been established. Using highly multiplexed immune profiling and time-course analysis, we tracked the abundance of 29 immune cell clusters in the aging mouse prostate. Early in adulthood, myeloid cells comprise the vast majority of immune cells in the 3-month-old mouse prostate. Between 6 and 12 months of age, there is a profound shift towards a T and B lymphocyte-dominant mouse prostate immune microenvironment. Comparing the prostate to other urogenital tissues, we found similar features of age-related inflammation in the mouse bladder but not the kidney. In summary, our study offers new insight into the kinetics of prostatic inflammaging and the window when interventions to slow down age-related changes may be most effective.

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Keywords - aging, prostate, immune microenvironment, mass cytometry, inflammation, lymphocyte

About Aging-US

Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.

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The Aging Mouse Prostate: Kinetics of Lymphocyte Infiltration

CD Genomics

To support the increasing research interest in small RNA, CD Genomics is offering the qualified small RNA sequencing service that covers novel small RNA discovery, mutation characterization, and expression profiling of small RNAs by leveraging of advanced NGS technologies and data analysis pipeline.	https://www.cd-genomics.com/Small-RNA.html

Small RNA Sequencing: Challengs and Workflow

CD Genomics has been providing the accurate and affordable whole genome sequencing service for couple of years. We combine both Illumina (short reads) and PacBio (long reads) platforms to achieve whole genome de novo assemblies and re-sequencing for viruses, microbes, plants, animals and humans.	https://www.cd-genomics.com/Whole-Genome-Sequencing.html

Methods and Workflow of Whole Genome Sequencing

16S/18S/ITS Amplicon Sequencing has now been a well-established method for microbial identification and phylogeny studies of samples from complicated microbiomes or environments. In addition to next-generation sequencing platforms, CD Genomics also provides full-length 16S/18S/ITS amplicon sequencing by using PacBio SMRT sequencing technology.	 https://www.cd-genomics.com/16S-18S-ITS-Amplicon-Sequencing.html

Bioinformatics analysis of 16S rRNA sequencing data: Amplicon Sequencing

Sequencing-based Approaches for Profiling DNA Methylation at CD Genomics. Learn more at https://www.cd-genomics.com/

Sequencing-based Approaches for Profiling DNA Methylation at CD Genomics

Oncotarget published this research paper on May 19, 2023 in Volume 14, entitled, “G-protein-coupled receptor 141 mediates breast cancer proliferation and metastasis by regulating oncogenic mediators and the p-mTOR/p53 axis" by researchers from the Cancer Biology Lab, Gene Function and Regulation Group, Institute of Life Sciences, Chandrasekharpur, Bhubaneswar 751023, Odisha, India; Regional Centre for Biotechnology, NCR Biotech Science Cluster, Faridabad 121001, Haryana (NCR Delhi), India; Department of Pathology, All India Institute of Medical Sciences, Bhubaneswar 751019, Odisha, India.

DOI - https://doi.org/10.18632/oncotarget.28433

Correspondence to - Sandip K. Mishra - sandipkmishra@ils.res.in

Abstract

Breast cancer morbidity is surging towards the peak in females across the globe. An inherent property of cancer cells is enhanced cell proliferation rate and migration capability, leading to deregulated cell signaling cascades. G-protein-coupled receptors (GPCRs) have recently emerged as a hot-spot target in cancer research. We identify aberrant expression of G-protein-coupled receptor 141 (GPR141) in different breast cancer subtypes that correlate with poor prognosis. However, the molecular mechanism via which GPR141 advances breast cancer remains elusive. Increased GPR141 expression enhances the migratory behavior of breast cancer, driving oncogenic pathways both in vitro and in vivo through activation of epithelial to mesenchymal transition (EMT), oncogenic mediators and regulation of p-mTOR/p53 signaling. Our study unveils a molecular mechanism for p53 downregulation and activation of p-mTOR1 and its substrates in GPR141 overexpressed cells, accelerating breast tumorigenesis. We find that an E3 ubiquitin ligase, Cullin1, partly mediates p53 degradation via proteasomal pathway. Co-immunoprecipitation result shows that the phosphorylated form of 40S ribosome protein S6 (ps6., a p-mTOR1 substrate) forms a complex with Cullin1. These findings suggest an interplay between Cullin1 and p-mTOR1 in GPR141 overexpressed cells that downregulates p53 expression, thus inducing tumor growth. GPR141 silencing restores p53 expression and attenuates p-mTOR1 signaling events, thereby impeding proliferation and migration in breast cancer cells. Our findings describe the role of GPR141 in breast cancer proliferation, and metastasis, as well as in influencing the tumor microenvironment. Modulating GPR141 expression could pave the way for a better therapeutic approach to regulating breast cancer progression and metastasis.

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Keywords - G-protein-coupled receptor 141, cell migration, metastasis, p-mTOR, p53

About Oncotarget

Oncotarget is a primarily oncology-focused, peer-reviewed, open access journal. Papers are published continuously within yearly volumes in their final and complete form, and then quickly released to Pubmed. On September 15, 2022, Oncotarget was accepted again for indexing by MEDLINE. Oncotarget is now indexed by Medline/PubMed and PMC/PubMed.

To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us:

SoundCloud - https://soundcloud.com/oncotarget
Facebook - https://www.facebook.com/Oncotarget/
Twitter - https://twitter.com/oncotarget
Instagram - https://www.instagram.com/oncotargetjrnl/
YouTube - https://www.youtube.com/@OncotargetJournal
LinkedIn - https://www.linkedin.com/company/oncotarget
Pinterest - https://www.pinterest.com/oncotarget/
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Media Contact
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18009220957

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