Cancer Research

Oncotarget

Oncotarget published this research paper on December 1, 2023 in Volume 14, entitled, “Osteopontin induces mitochondrial biogenesis in deadherent cancer cells” by Gulimirerouzi Fnu and Georg F. Weber from the University of Cincinnati Academic Health Center, James L. Winkle College of Pharmacy, Cincinnati, OH.

DOI - https://doi.org/10.18632/oncotarget.28540

Correspondence to - Georg F. Weber - georg.weber@uc.edu

Abstract

Metastasizing cells display a unique metabolism, which is very different from the Warburg effect that arises in primary tumors. Over short time frames, oxidative phosphorylation and ATP generation are prominent. Over longer time frames, mitochondrial biogenesis becomes a pronounced feature and aids metastatic success. It has not been known whether or how these two phenomena are connected. We hypothesized that Osteopontin splice variants, which synergize to increase ATP levels in deadherent cells, also increase the mitochondrial mass via the same signaling mechanisms. Here, we report that autocrine Osteopontin does indeed stimulate an increase in mitochondrial size, with the splice variant -c being more effective than the full-length form -a. Osteopontin-c achieves this via its receptor CD44v, jointly with the upregulation and co-ligation of the chloride-dependent cystine-glutamate transporter SLC7A11. The signaling proceeds through activation of the known mitochondrial biogenesis inducer PGC-1 (which acts as a transcription coactivator). Peroxide is an important intermediate in this cascade, but surprisingly acts upstream of PGC-1 and is likely produced as a consequence of SLC7A11 recruitment and activation. In vivo, suppression of the biogenesis-inducing mechanisms leads to a reduction in disseminated tumor mass. This study confirms a functional connection between the short-term oxidative metabolism and the longer-term mitochondrial biogenesis in cancer metastasis – both are induced by Osteopontin-c. The results imply possible mechanisms and targets for treating cancer metastasis.

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Keywords - cancer, metastasis, metabolism, anchorage independence, mitochondrial mass, peroxide

About Oncotarget

Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science.

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Osteopontin Induces Mitochondrial Biogenesis in Deadherent Cancer Cells | Oncotarget

Oncotarget published this editorial on November 27, 2023 in Volume 14, entitled, “The double-edge sword of CRISPR application for in vivo studies” by Martin K. Thomsen from the Department of Biomedicine, Aarhus University, Aarhus C 8000, Denmark.

DOI - https://doi.org/10.18632/oncotarget.28459

Correspondence to - Martin K. Thomsen - mkt@biomed.au.dk

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Keywords - cancer, CRISPR, in vivo, mouse models, Adenoassociated virus

About Oncotarget

Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science.

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The Double-Edge Sword of CRISPR Application for In Vivo Studies | Oncotarget

Oncotarget published this trending editorial on April 24, 2023 in Volume 14, entitled, “The critical immune basis for differential responses to immunotherapy in primary versus metastatic pancreatic cancer" by researchers from the Department of Surgery, Trinity Health of New England, Waterbury, CT.

DOI - https://doi.org/10.18632/oncotarget.28373

Correspondence to - George Miller -  gedalyamil@gmail.com

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Keywords - cancer, pancreatic cancer, liver metastasis, immunnotherapy

About Oncotarget 

Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science.

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Immune Responses in Pancreatic Cancer: Primary vs. Metastatic | Oncotarget

Oncotarget published this trending editorial on July 1, 2023 in Volume 14, entitled, “Obesity paradox and lung cancer, metformin-based therapeutic opportunity?" by researchers from the Thoracic Oncology Functional Unit (UFOT), Laboratorio de Medicina Personalizada, Instituto Nacional de Cancerología, S.S.A., Mexico City.

DOI - https://doi.org/10.18632/oncotarget.28432

Correspondence to - Oscar Arrieta -  ogarrieta@gmail.com

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Keywords - cancer, obesity, lung cancer, metformin, tyrosine-kinase inhibitors, BMI, EGFR, obesity paradox

About Oncotarget 

Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science.

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Obesity Paradox and Lung Cancer, Metformin-based Therapeutic Opportunity? | Oncotarget

Oncotarget published this editorial perspective on March 11, 2023 in Volume 14, entitled, “C/EBPβ cooperates with MYB to maintain the oncogenic program of AML cells” by Karl-Heinz Klempnauer from the Institute for Biochemistry, Westfälische-Wilhelms-Universität, Muenster D-48149, Germany.

DOI - https://doi.org/10.18632/oncotarget.28377

Correspondence to - Karl-Heinz Klempnauer -  klempna@uni-muenster.de

Abstract

Studies on the role of transcription factor MYB in acute myeloid leukemia (AML) have identified MYB as a key regulator of a transcriptional program for self-renewal of AML cells. Recent work summarized here has now highlighted the CCAAT-box/ enhancer binding protein beta (C/EBPβ) as an essential factor and potential therapeutic target that cooperates with MYB and coactivator p300 in the maintenance of the leukemic cells.

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Keywords - cancer, MYB, C/EBPbeta, p300, GFI1, AML

About Oncotarget

Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science.

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 C/EBPβ Cooperates with MYB to Maintain Oncogenic Program of AML Cells | Oncotarget

Aging (Aging-US)

Aging-US published this trending research paper on September 27, 2023, in Volume 15, Issue 20, entitled, “WNT enhancing signals in pancreatic cancer are transmitted by LGR6" by researchers from the Department of General, Visceral and Transplantation Surgery, Hospital of the University of Munich, Ludwig-Maximilians-University (LMU), Munich, Bavaria, Germany; Department of General Surgery, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui, P.R. China; Department of Surgery, School of Medicine, Klinikum Rechts der Isar, Technical University of Munich, Munich, Bavaria, Germany; German Cancer Consortium (DKTK), Partner Site Munich, Munich, Bavaria, Germany; Bavarian Cancer Research Center (BZKF), LMU Munich, Munich, Bavaria, Germany.

DOI - https://doi.org/10.18632/aging.205101

Corresponding author - Matthias Ilmer - mailmer@med.lmu.de

Abstract

The G-protein-coupled receptor LGR6 associates with ligands of the R-Spondin (RSPO) family to potentiate preexisting signals of the canonical WNT pathway. However, its importance in pancreatic ductal adenocarcinoma (PDAC) remains unclear. Here, we show that LGR6 is differentially expressed in various PDAC cell lines of mesenchymal and epithelial phenotype, respectively, siding with the latter subsets. LGR6 expression is altered based upon the cells’ WNT activation status. Furthermore, extrinsic enhancement of WNT pathway signaling increased LGR6 expression suggestive of a reinforcing self-regulatory loop in highly WNT susceptible cells. Downregulation of LGR6 on the other hand, seemed to tamper those effects. Last, downregulation of LGR6 reduced cancer stemness as determined by functional in vitro assays. These findings shed new insights into regulatory mechanisms for the canonical WNT pathway in pancreatic cancer cells. It may also have potential value for treatment stratification of PDAC.

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Keywords - aging, pancreatic ductal adenocarcinoma, WNT signaling, epithelial-mesenchymal transition, LGR6, cancer stem cells

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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WNT Enhancing Signals in Pancreatic Cancer are Transmitted by LGR6 | Aging-US

Oncotarget published this trending editorial on March 31, 2023 in Volume 14, entitled, “Impact of SHP2 tyrosine phosphorylation on the development of acquired resistance to allosteric SHP2 inhibitors" by Giulia Franciosa and Jesper V. Olsen from the Proteomics Program, Novo Nordisk Foundation Center for Protein Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.

DOI - https://doi.org/10.18632/oncotarget.28392

Correspondence to - Giulia Franciosa - giulia.franciosa@cpr.ku.dk

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Keywords - cancer, SHP2, PTPN11, tyrosine, phosphorylation

About Oncotarget 

Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science.

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SHP2 Tyrosine Phosphorylation and Allosteric Inhibitor Resistance | Oncotarget

Oncotarget published this editorial on October 31, 2023 in Volume 14, entitled, “The uncharted role of HER2 mutant alleles in breast cancer” by researchers from the Lester and Sue Smith Breast Center, Baylor College of Medicine, Houston, TX; Department of Medicine, Baylor College of Medicine, Houston, TX.

DOI - https://doi.org/10.18632/oncotarget.28489

Correspondence to - Shyam M. Kavuri - meghashyam.kavuri@bcm.edu

Abstract

Somatic HER2 mutations are a novel class of therapeutic targets across different cancer types. Treatment with the tyrosine kinase inhibitor (TKI) neratinib as a single agent continues to be evaluated in HER2-mutant metastatic disease. However, responses are heterogeneous, with frequent early progression. Herein, we discuss the under-explored effects of individual HER2 mutant alleles on therapeutic response, a role for HER2 mutation in metastatic propensity, and differences in patient outcomes in ER+ invasive lobular carcinoma (ILC) versus invasive ductal carcinoma (IDC). The preclinical efficacy of additional agents is also discussed, particularly the pan-HER inhibitor poziotinib.

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Keywords - cancer, metastasis, poziotinib, HER2, neratinib, invasive lobular breast carcinoma

About Oncotarget

Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science.

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The Uncharted Role of HER2 Mutant Alleles in Breast Cancer | Oncotarget

Oncotarget published this trending editorial on March 31, 2023 in Volume 14, entitled, “Trending: p53 protects against formation of extrahepatic biliary precancerous lesions in the context of oncogenic Kras" by researchers from the Department of Gastroenterology and Hepatology, Kyoto University Graduate School of Medicine, Sakyo-ku, Kyoto 606-8507, Japan.

DOI - https://doi.org/10.18632/oncotarget.28380

Correspondence to - Akihisa Fukuda - fukuda26@kuhp.kyoto-u.ac.jp

Abstract

KRAS and TP53 mutations are frequently observed in extrahepatic biliary cancer. Mutations of KRAS and TP53 are independent risk factors for poor prognosis in biliary cancer. However, the exact role of p53 in the development of extrahepatic biliary cancer remains elusive. In this study, we found that simultaneous activation of Kras and inactivation of p53 induces biliary neoplasms that resemble human biliary intraepithelial neoplasia in the extrahepatic bile duct and intracholecystic papillarytubular neoplasm in the gall bladder in mice. However, inactivation of p53 was not sufficient for the progression of biliary precancerous lesions into invasive cancer in the context of oncogenic Kras within the observation period. This was also the case in the context of additional activation of the Wnt signaling pathway. Thus, p53 protects against formation of extrahepatic biliary precancerous lesions in the context of oncogenic Kras.

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Keywords - cancer, BilIN, ICPN, biliary cancer, Kras, p53

About Oncotarget 

Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science.

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