Cell Culture

Aging (Aging-US)

Aging-US published this trending editorial on March 1, 2023 in Volume 15, Issue 5 entitled, “Senescence and extracellular vesicles: novel partners in vascular amyloidosis" by researchers from the British Heart Foundation Centre of Research Excellence, School of Cardiovascular and Metabolic Medicine and Sciences, King’s College London, London, UK.

DOI - https://doi.org/10.18632/aging.204571 (PDF)

Corresponding author - Catherine M. Shanahan -  cathy.shanahan@kcl.ac.uk

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Keywords - aging, amyloid, smooth muscle cells, senescence, extracellular vesicles, medin

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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Senescence and Extracellular Vesicles: Novel Partners in Vascular Amyloidosis

Oncotarget

Oncotarget published this research paper on March 24, 2023 in Volume 14, entitled, “Polyisoprenylated cysteinyl amide inhibitors deplete singly polyisoprenylated monomeric G-proteins in lung and breast cancer cell lines" by researchers from the Florida A&M University College of Pharmacy Pharmaceutical Sciences, Institute of Public Health, Tallahassee, FL; Department of Pharmaceutical Chemistry, College of Clinical Pharmacy, Imam Abdulrahman bin Faisal University, Dammam, Eastern Province, Kingdom of Saudi Arabia.

DOI - https://doi.org/10.18632/oncotarget.28390

Correspondence to - Nazarius S. Lamango - nazarius.lamango@famu.edu

Abstract

Finding effective therapies against cancers driven by mutant and/or overexpressed hyperactive G-proteins remains an area of active research. Polyisoprenylated cysteinyl amide inhibitors (PCAIs) are agents that mimic the essential posttranslational modifications of G-proteins. It is hypothesized that PCAIs work as anticancer agents by disrupting polyisoprenylation-dependent functional interactions of the G-Proteins. This study tested this hypothesis by determining the effect of the PCAIs on the levels of RAS and related monomeric G-proteins. Following 48 h exposure, we found significant decreases in the levels of KRAS, RHOA, RAC1, and CDC42 ranging within 20–66% after NSL-YHJ-2-27 (5 μM) treatment in all four cell lines tested, A549, NCI-H1299, MDA-MB-231, and MDA-MB-468. However, no significant difference was observed on the G-protein, RAB5A. Interestingly, 38 and 44% decreases in the levels of the farnesylated and acylated NRAS were observed in the two breast cancer cell lines, MDA-MB-231, and MDA-MB-468, respectively, while HRAS levels showed a 36% decrease only in MDA-MB-468 cells. Moreover, after PCAIs treatment, migration, and invasion of A549 cells were inhibited by 72 and 70%, respectively while the levels of vinculin and fascin dropped by 33 and 43%, respectively. These findings implicate the potential role of PCAIs as anticancer agents through their direct interaction with monomeric G-proteins.

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Keywords - PCAIs, G-proteins, KRAS, RHOA, RAC1

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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Polyisoprenylated Cysteinyl Amide Inhibitors Deplete G-Proteins in Cancer Cell Lines

Oncotarget published this trending research paper on March 21, 2023 in Volume 14, entitled, “Attenuation of cancer proliferation by suppression of glypican-1 and its pleiotropic effects in neoplastic behavior" by researchers from the Department of Experimental Medical Science, Glycobiology Group, Lund University, Biomedical Center A13, Lund, Sweden; Genevia Technologies Oy, Tampere 33100, Finland.

DOI - https://doi.org/10.18632/oncotarget.28388

Correspondence to - Katrin Mani - katrin.mani@med.lu.se

Abstract

Glypicans (GPC1-6) are associated with tumorigenic processes and their involvement in neoplastic behavior has been discussed in different cancer types. Here, a cancer-wide GPC expression study, using clinical cancer patient data in The Cancer Genome Atlas, reveals net upregulation of GPC1 and GPC2 in primary solid tumors, whereas GPC3, GPC5 and GPC6 display lowered expression pattern compared to normal tissues. Focusing on GPC1, survival analyses of the clinical cancer patient data reveal statistically significant correlation between high expression of GPC1 and poor prognosis in 10 particular cancer types i.e., bladder urothelial carcinoma, brain lower grade glioma, liver hepatocellular carcinoma, colon adenocarcinoma, kidney renal clear cell carcinoma, lung adenocarcinoma, mesothelioma, ovarian serous cystadenocarcinoma, uterine corpus endometrial carcinoma and uveal melanoma. In vitro studies targeting GPC1 expression by CRISPR/Cas9 or siRNA or treatment with an anti-GPC1 antibody resulted in attenuation of proliferation of cancer cells from bladder carcinoma, glioma and hepatocellular carcinoma patients (T24, U87 and HepG2 cells). Further, overexpression of GPC1 exhibited a significant and negative correlation between GPC1 expression and proliferation of T24 cells. Attempt to reveal the mechanism through which downregulation of GPC1 leads to attenuation of tumor growth using systematic Ingenuity Pathway Analysis indicate that suppression of GPC1 results in ECM-mediated inhibition of specific pro-cancer signaling pathways involving TGF-β and p38 MAPK. Identified differential expression and pleiotropic effects of GPCs in specific cancer types emphasize their potential as novel diagnostic tools and prognostic factors and open doors for future GPC targeted therapy.

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Keywords - Glypican-1, TCGA, bladder carcinoma, hepatocellular carcinoma, glioma

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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Attenuation of Cancer Proliferation by Suppression of Glypican-1 and Pleiotropic Effects

Aging-US published this trending research paper in Volume 15, Issue 5, entitled, "Senescence-associated exosomes transfer miRNA-induced fibrosis to neighboring cells" by researchers from the School of Engineering, Center for Biomedical Engineering, Brown University, Providence, RI; Molecular Biology, Cell Biology, and Biochemistry, Brown University, Providence, RI.

DOI - https://doi.org/10.18632/aging.204539

Corresponding authors - Michelle R. Dawson - michelle_dawson@brown.edu
Abstract

Radiation-induced fibrosis is a common side effect of radiotherapy, which is the most common treatment for cancer. However, radiation also causes p53-mediated cell cycle arrest, prolonged expression of p21, and the development of senescence in normal cells that reside in irradiated tissues. Bone marrow-derived mesenchymal stem cells (MSCs) accumulate in primary tumor sites because of their natural tropism for inflammatory and fibrotic tissues. MSCs are extremely sensitive to low doses of ionizing radiation and acquire senescence as a result of bystander radiation effects. Senescent cells remain metabolically active but develop a potent senescence-associated secretory phenotype (SASP) that correlates to hyperactive secretion of cytokines, pro-fibrotic growth factors, and exosomes (EXOs). Integrative pathway analysis highlighted that radiation-induced senescence significantly enriched cell-cycle, extracellular matrix, transforming growth factor-β (TGF-β) signaling, and vesicle-mediated transport genes in MSCs. EXOs are cell-secreted nanovesicles (a subclass of small extracellular vesicles) that contain biomaterials—proteins, RNAs, microRNAs (miRNAs)—that are critical in cell-cell communication. miRNA content analysis of secreted EXOs further revealed that radiation-induced senescence uniquely altered miRNA profiles. In fact, several of the standout miRNAs directly targeted TGF-β or downstream genes. To examine bystander effects of radiation-induced senescence, we further treated normal MSCs with senescence-associated EXOs (SA-EXOs). These modulated genes related to TGF-β pathway and elevated both alpha smooth muscle actin (protein increased in senescent, activated cells) and Ki-67 (proliferative marker) expression in SA-EXO treated MSCs compared to untreated MSCs. We revealed SA-EXOs possess unique miRNA content that influence myofibroblast phenotypes via TGF-β pathway activation. This highlights that SA-EXOs are potent SASP factors that play a large role in cancer-related fibrosis.

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Keywords - aging, radiation-induced senescence, exosomes (EXOs), microRNA (miRNA), transforming growth factor-β (TGF-β), mesenchymal stem cells (MSCs)

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.

Please visit our website at https://www.Aging-US.com​​ and connect with us:

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Facebook - https://www.facebook.com/AgingUS/
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LinkedIn - https://www.linkedin.com/company/aging/
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Senescence-Associated Exosomes Transfer miRNA-Induced Fibrosis to Neighboring Cells

Oncotarget published this research paper on March 11, 2023 in Volume 14, entitled, “Genomic landscape of metastatic breast cancer (MBC) patients with methylthioadenosine phosphorylase (MTAP) loss" by researchers from the Department of Internal Medicine, SUNY Upstate Medical University, Syracuse, NY; Department of Internal Medicine, Division of Hematology Oncology, SUNY Upstate Medical University, Syracuse, NY; SUNY Upstate Medical University, Syracuse, NY; Foundation Medicine, Inc., Morrisville, NC; Departments of Pathology and Urology, SUNY Upstate Medical University, Syracuse, NY.

DOI - https://doi.org/10.18632/oncotarget.28376

Correspondence to - Abirami Sivapiragasam - sivapira@upstate.edu

Abstract

Introduction: Homozygous deletion of MTAP upregulates de novo synthesis of purine (DNSP) and increases the proliferation of neoplastic cells. This increases the sensitivity of breast cancer cells to DNSP inhibitors such as methotrexate, L-alanosine and pemetrexed.

Materials and Methods: 7,301 cases of MBC underwent hybrid-capture based comprehensive genomic profiling (CGP). Tumor mutational burden (TMB) was determined on up to 1.1 Mb of sequenced DNA and microsatellite instability (MSI) was determined on 114 loci. Tumor cell PD-L1 expression was determined by IHC (Dako 22C3).

Results: 208 (2.84%) of MBC featured MTAP loss. MTAP loss patients were younger (p = 0.002) and were more frequently ER− (30% vs. 50%; p < 0.0001), triple negative (TNBC) (47% vs. 27%; p < 0.0001) and less frequently HER2+ (2% vs. 8%; p = 0.0001) than MTAP intact MBC. Lobular histology and CDH1 mutations were more frequent in MTAP intact (14%) than MTAP loss MBC (p < 0.0001). CDKN2A (100%) and CDKN2B (97%) loss (9p21 co-deletion) were significantly associated with MTAP loss (p < 0.0001). Likely associated with the increased TNBC cases, BRCA1 mutation was also more frequent in MTAP loss MBC (10% vs. 4%; p < 0.0001). As for immune checkpoint inhibitors biomarkers, higher TMB >20 mut/Mb levels in the MTAP intact MBC (p < 0.0001) and higher PD-L1 low expression (1–49% TPS) in the MTAP loss MTAP (p = 0.002) were observed.

Conclusions: MTAP loss in MBC has distinct clinical features with genomic alterations (GA) affecting both targeted and immunotherapies. Further efforts are necessary to identify alternative means of targeting PRMT5 and MTA2 in MTAP-ve cancers to benefit from the high-MTA environment of MTAP-deficient cancers.
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Press release - https://www.oncotarget.com/news/pr/oncotarget-mtap-loss-in-metastatic-breast-cancer-patients-genomic-landscape/

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Keywords - breast cancer, metastatic, MTAP loss

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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MTAP Loss in Metastatic Breast Cancer Patients: Genomic Landscape

Oncotarget published this review in Volume 14, entitled, “What is hemoglobin, albumin, lymphocyte, platelet (HALP) score? A comprehensive literature review of HALP’s prognostic ability in different cancer types" by researchers from the Department of Urology, George Washington University School of Medicine, Washington, DC; Department of Surgery, George Washington University School of Medicine, Washington, DC.

DOI - https://doi.org/10.18632/oncotarget.28367

Correspondence to - Christian Mark Farag - cmfarag@gwu.edu

Abstract

Since its inception, the Hemoglobin, Albumin, Lymphocyte, Platelet Score (HALP) has gained attention as a new prognostic biomarker to predict several clinical outcomes in a multitude of cancers. In our review, we searched PubMed for articles between the first paper on HALP in 2015 through September 2022, yielding 32 studies in total that evaluated HALP's association with various cancers, including Gastric, Colorectal, Bladder, Prostate, Kidney, Esophageal, Pharyngeal, Lung, Breast, and Cervical cancers, among others. This review highlights the collective association HALP has with demographic factors such as age and sex in addition to TNM staging, grade, and tumor size. Furthermore, this review summarizes HALP's prognostic ability to predict overall survival, progression-free survival, recurrence-free survival, among other outcomes. In some studies, HALP has also been able to predict response to immunotherapy and chemotherapy.

This review article also aims to serve as a comprehensive and encyclopedic report on the literature that has evaluated HALP as a biomarker in various cancers, highlighting the heterogeneity surrounding HALP's utilization. Because HALP requires only a complete blood count and albumin - already routinely collected for cancer patients - HALP shows potential as a cost-effective biomarker to aid clinicians in improving outcomes for immuno-nutritionally deficient patients.

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Keywords - HALP score, biomarker, prognosis, cancer, survival

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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What is Hemoglobin, Albumin, Lymphocyte, Platelet (HALP) Score?

Creative Bioarray

Creative Bioarray provides high-quality cell cycle assays and professional results analysis services relying on our advanced technique platform and experienced scientific team.

https://cell.creative-bioarray.com/cell-cycle-assays.html

Cell Cycle Assays

Oncotarget published this editorial in Volume 14, entitled, “Unveiling the non-canonical functions of EZH2 in prostate cancer" by researchers from the Department of Urology, Feinberg School of Medicine, Northwestern University, Chicago, IL; Robert H. Lurie Comprehensive Cancer Center, Northwestern University Feinberg School of Medicine, Chicago, IL.

DOI - https://doi.org/10.18632/oncotarget.28357 (PDF Download)

Correspondence to - Qi Cao - qi.cao@northwestern.edu

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Keywords - EZH2, prostate cancer, FBL, CDCA8, E2F1

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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Unveiling the Non-Canonical Functions of EZH2 in Prostate Cancer

Aging (Aging-US) published this trending review in Volume 15, Issue 14, entitled, “Cellular senescence: when growth stimulation meets cell cycle arrest” by Dr. Mikhail V. Blagosklonny from Roswell Park Comprehensive Cancer Center, Buffalo, NY.

DOI - https://doi.org/10.18632/aging.204543

Corresponding author - Mikhail V. Blagosklonny - Blagosklonny@oncotarget.com, Blagosklonny@rapalogs.com

ABSTRACT

At the very moment of cell-cycle arrest, the cell is not senescent yet. For several days in cell culture, the arrested cell is acquiring a senescent phenotype. What is happening during this geroconversion? Cellular enlargement (hypertrophy) and hyperfunctions (lysosomal and hyper-secretory) are hallmarks of geroconversion. 

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Keywords - aging, rapamycin, mTOR, hyperfunction theory of aging, cell volume and enlargement, gerogenic conversion

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.

Please visit our website at https://www.Aging-US.com​​ and connect with us:

SoundCloud - https://soundcloud.com/Aging-Us
Facebook - https://www.facebook.com/AgingUS/
Twitter - https://twitter.com/AgingJrnl
Instagram - https://www.instagram.com/agingjrnl/
YouTube - https://www.youtube.com/@AgingJournal
LinkedIn - https://www.linkedin.com/company/aging/
Pinterest - https://www.pinterest.com/AgingUS/

Aging-US is published by Impact Journals, LLC: http://www.ImpactJournals.com​​

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