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How Does Obesity Cause Cancer?
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How Does Obesity Cause Cancer?

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Oncology".

Deadline for manuscript submissions: closed (31 August 2023) | Viewed by 6464

Special Issue Editor

Dr. Daniel W. Nixon

E-Mail Website
Guest Editor
Morehouse School of Medicine, Atlanta, GA 30310, USA
Interests: adipokines and cancer; cancer and Alzheimer’s disease; cancer; obesity and diet
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Obesity is clearly related to many types of cancer, but the precise molecular mechanisms remain largely unknown. Does excess body fat/energy intake somehow trigger a normal cell to become malignant, or do fat-produced substances promote growth of malignant cells induced by other carcinogens? Conversely, perhaps some adipokine induces malignant change, and chronic caloric excess is a promoter? What is the exact role of the many molecular processes induced by obesity, including alterations in signaling pathways (p53, Notch, Wnt, and others)? What are the major adipokines driving cancer, and can these be altered by lifestyle chances or drugs?

This Special Issue will explore these and other questions. Appropriate topics include the role of excess calories in cancer as well as the specific activities of various adipokines in the malignant process. Novel hypotheses in these and other areas are needed and welcome. Precise information on the fat–cancer connection should stimulate important cancer prevention and treatment clinical research.

Dr. Daniel W. Nixon
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • obesity
  • body fat
  • cancer
  • adipokines
  • leptin
  • adiponectin
  • angiogenesis
  • molecular activity
  • signaling pathways

Published Papers (3 papers)

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Research

11 pages, 925 KiB  
Article
Low Muscle and High Fat Percentages Are Associated with Low Natural Killer Cell Activity: A Cross-Sectional Study
by A-Ra Cho, Eunkyung Suh, Hyoju Oh, Baek Hwan Cho, Minchan Gil and Yun-Kyong Lee
Int. J. Mol. Sci. 2023, 24(15), 12505; https://doi.org/10.3390/ijms241512505 - 6 Aug 2023
Viewed by 1338
Abstract
This study aimed to investigate whether body fat and muscle percentages are associated with natural killer cell activity (NKA). This was a cross-sectional study, conducted on 8058 subjects in a medical center in Korea. The association between the muscle and fat percentage tertiles [...] Read more.
This study aimed to investigate whether body fat and muscle percentages are associated with natural killer cell activity (NKA). This was a cross-sectional study, conducted on 8058 subjects in a medical center in Korea. The association between the muscle and fat percentage tertiles and a low NKA, defined as an interferon-gamma level lower than 500 pg/mL, was assessed. In both men and women, the muscle mass and muscle percentage were significantly low in participants with a low NKA, whereas the fat percentage, white blood cell count, and C-reactive protein (CRP) level were significantly high in those with a low NKA. Compared with the lowest muscle percentage tertile as a reference, the fully adjusted odd ratios (ORs) (95% confidence intervals (CIs)) for a low NKA were significantly lower in T2 (OR: 0.69; 95% CI: 0.55–0.86) and T3 (OR: 0.74; 95% CI: 0.57–0.95) of men, and T3 (OR: 0.76; 95% CI: 0.59–0.99) of women. Compared with the lowest fat percentage tertile as a reference, the fully adjusted OR was significantly higher in T3 of men (OR: 1.31; 95% CI: 1.01–1.69). A high muscle percentage was significantly inversely associated with a low NKA in men and women, whereas a high fat percentage was significantly associated with a low NKA in men. Full article
(This article belongs to the Special Issue How Does Obesity Cause Cancer?)
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15 pages, 5039 KiB  
Article
Obesity Associated with Prediabetes Increases the Risk of Breast Cancer Development and Progression—A Study on an Obese Rat Model with Impaired Glucose Tolerance
by Prathap Reddy Kallamadi, Deepshika Esari, Utkarsh Reddy Addi, Rushendhiran Kesavan, Uday Kumar Putcha, Siddavaram Nagini and Geereddy Bhanuprakash Reddy
Int. J. Mol. Sci. 2023, 24(14), 11441; https://doi.org/10.3390/ijms241411441 - 14 Jul 2023
Cited by 2 | Viewed by 2332
Abstract
Patients with comorbidities of obesity and diabetes are recognized to be at high risk of breast cancer development and face worse breast cancer outcomes. Though several reports showed the reinforced link between obesity, diabetes, and prediabetes with breast cancer, the underlying molecular mechanisms [...] Read more.
Patients with comorbidities of obesity and diabetes are recognized to be at high risk of breast cancer development and face worse breast cancer outcomes. Though several reports showed the reinforced link between obesity, diabetes, and prediabetes with breast cancer, the underlying molecular mechanisms are still unknown. The present study aimed to investigate the underlying molecular link between increased risks of breast cancer due to coincident diabetes or obesity using a spontaneous obese rat model with impaired glucose tolerance (WNIN/GR-Ob rat). A single dose of solubilized DMBA suspension (40 mg/kg body weight) was orally administered to the animals at the age of 60 days to induce breast tumors. The tumor incidence, latency period, tumor frequency, and tumor volume were measured. Histology, immunohistochemistry, and immunoblotting were performed to evaluate the tumor morphology and expression levels of signal molecules. The development of mammary tumors in GR-Ob rats was characterized by early onset and shorter latency periods compared to control lean rats. While 62% of obese rats developed breast tumors, tumor development in lean rats was only 21%. Overexpression of ER, PR, Ki67, and p53 markers was observed in tumor tissues of obese rats in comparison with lean rats. The levels of the hallmarks of cell proliferation and angiogenesis involved in IGF-1/PI3K/Akt/GSK3β/β-catenin signaling pathway molecules were upregulated in obese rat breast tumors compared to lean rats. Furthermore, obesity with prediabetes is associated with changes in IGF-1 signaling and acts on PI3K/Akt/GSK3β/β-catenin signaling, which results in rapid cell proliferation and development of breast tumors in obese rats than the lean rats. These results indicate that tumor onset and development were faster in spontaneous obese rat models with impaired glucose tolerance than in their lean counterparts. Full article
(This article belongs to the Special Issue How Does Obesity Cause Cancer?)
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17 pages, 4069 KiB  
Article
Metformin Mitigated Obesity-Driven Cancer Aggressiveness in Tumor-Bearing Mice
by Chun-Jung Chen, Chih-Cheng Wu, Cheng-Yi Chang, Jian-Ri Li, Yen-Chuan Ou, Wen-Ying Chen, Su-Lan Liao and Jiaan-Der Wang
Int. J. Mol. Sci. 2022, 23(16), 9134; https://doi.org/10.3390/ijms23169134 - 15 Aug 2022
Cited by 8 | Viewed by 2337
Abstract
Metformin may offer benefits to certain cancer populations experiencing metabolic abnormalities. To extend the anticancer studies of metformin, a tumor model was established through the implantation of murine Lewis Lung Carcinoma (LLC) cells to Normal Diet (ND)-fed and High-Fat Diet (HFD)-fed C57BL/6 mice. [...] Read more.
Metformin may offer benefits to certain cancer populations experiencing metabolic abnormalities. To extend the anticancer studies of metformin, a tumor model was established through the implantation of murine Lewis Lung Carcinoma (LLC) cells to Normal Diet (ND)-fed and High-Fat Diet (HFD)-fed C57BL/6 mice. The HFD-fed mice displayed metabolic and pro-inflammatory alterations together with accompanying aggressive tumor growth. Metformin mitigated tumor growth in HFD-fed mice, paralleled by reductions in circulating glucose, insulin, soluble P-selectin, TGF-β1 and High Mobility Group Box-1 (HMGB1), as well as tumor expression of cell proliferation, aerobic glycolysis, glutaminolysis, platelets and neutrophils molecules. The suppressive effects of metformin on cell proliferation, migration and oncogenic signaling molecules were confirmed in cell study. Moreover, tumor-bearing HFD-fed mice had higher contents of circulating and tumor immunopositivity of Neutrophil Extracellular Traps (NETs)-associated molecules, with a suppressive effect from metformin. Data taken from neutrophil studies confirmed the inhibitory effect that metformin has on NET formation induced by HMGB1. Furthermore, HMGB1 was identified as a promoting molecule to boost the transition process towards NETs. The current study shows that metabolic, pro-inflammatory and NET alterations appear to play roles in the obesity-driven aggressiveness of cancer, while also representing candidate targets for anticancer potential of metformin. Full article
(This article belongs to the Special Issue How Does Obesity Cause Cancer?)
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