Nutrients

Our medical research library holds 5 studies published in Nutrients (2016–2026). Each entry links to the study's record on PubMed and, where there is one, to the publisher's page and a free full text. 5 have an abstract, the authors' own summary as PubMed records it: open "Abstract" to read it.

About the journal

• Publisher: MDPI Publishing
• Published: 2009 to the present, Switzerland
• Language: English
• ISSN: 2072-6643 (electronic)
• Its record in the NLM Catalog

2020s

• Hexokinase II as a Potential Target of Apigenin Through the Induction of Apoptosis and Necroptosis in Malignant Mesothelioma. M.K. Cho, S.H. Lee, H.S. Nam, et al. 2026;18(19). PubMed · Publisher · Free full text

  Abstract

  Background: Lactate-acclimated MSTO-211HAcT and H2452AcT malignant mesothelioma (MM) cells were previously found to tolerate gemcitabine more readily than their parental cells while remaining sensitive to apigenin. We examined whether changes in glucose metabolism and HKII contribute to the apigenin response. Methods: Apigenin was evaluated in monolayer and spheroid cultures and in a xenograft model; HKII was also silenced in the acclimated cells. Results: Apigenin reduced cell viability, p-AKT (Ser473), glycolysis-associated proteins including HKII, and mitochondrial electron transport chain proteins, while increasing p53 and markers of cell death. Tumor growth and selected metabolic proteins were reduced in the xenograft model. HKII silencing reduced cell viability and glucose utilization, lowered cellular ATP, altered mitochondrial membrane potential, and increased markers of apoptosis and necroptosis. Conclusions: HKII-associated metabolism contributes to survival of lactate-acclimated MM cells, and apigenin affects this metabolic phenotype. Direct targeting of HKII by apigenin and the complete mitochondrial apoptotic pathway require further study.

• Capsaicin Exerts Antitumor Activity in Mesothelioma Cells. E. Andretta, A. Costa, E. Ventura, et al. 2024;16(21). PubMed · Publisher · Free full text

  Abstract

  Background/Objectives: Mesothelioma is an aggressive cancer with limited treatment options. Mesothelioma therapy often involves a multimodal approach including surgery, radiotherapy and chemotherapy. However, the prognosis for patients remains poor. Difficult diagnosis, late symptoms when the tumor is in an advanced stage and the onset of chemotherapy resistance make mesothelioma difficult to treat. For this reason, it is essential to discover new pharmacological approaches. Capsaicin (CAPS) is the active compound of chili peppers. Based on CAPS's anticancer properties on various tumor lines and its chemo-sensitizing action on resistant cells, in this study, we evaluated the effects of CAPS on mesothelioma cells to assess its potential use in mesothelioma therapy.

  Methods: To evaluate antiproliferative effects of CAPS, we performed MTS assays on various mesothelioma cells, representative of all major mesothelioma subtypes. Transwell migration and wound-healing assays were used to examine the effect of CAPS on mesothelioma cell migration. We also determined the effects of CAPS on oncogenic signaling pathways by assessing the levels of AKT and MAPK activation.

  Results: In this study, we show that CAPS significantly reduces proliferation of both parental and cisplatin-resistant mesothelioma cells. CAPS promotes S-phase cell cycle arrest and inhibits lateral motility and migration of mesothelioma cells. Accordingly, CAPS suppresses AKT and ERK1/2 activation in MSTO-211H and NCI-H2052 cells. Our results support an antitumor effect of CAPS on cisplatin-resistant mesothelioma cells, suggesting that it may reduce resistance to cisplatin.

  Conclusions: Our results could pave the way for further studies to evaluate the use of CAPS for mesothelioma treatment.

• Role of Beta-Carotene in Lung Cancer Primary Chemoprevention: A Systematic Review with Meta-Analysis and Meta-Regression. J. Kordiak, F. Bielec, S. Jabłoński, et al. 2022;14(7). Meta-analysis · Systematic review PubMed · Publisher · Free full text

  Abstract

  Lung cancer is one of the most common neoplasms globally, with about 2.2 million new cases and 1.8 million deaths annually. Although the most important factor in reducing lung cancer risk is lifestyle change, most patients favour the use of supplements, for example, rather than quitting smoking or following a healthy diet. To better understand the efficacy of such interventions, a systematic review was performed of data from randomized controlled trials concerning the influence of beta-carotene supplementation on lung cancer risk in subjects with no lung cancer before the intervention. The search corpus comprised a number of databases and eight studies involving 167,141 participants, published by November 2021. The findings indicate that beta-carotene supplementation was associated with an increased risk of lung cancer (RR = 1.16, 95% CI = 1.06-1.26). This effect was even more noticeable among smokers and asbestos workers (RR = 1.21, 95% CI = 1.08-1.35) and non-medics (RR = 1.18, 95% CI = 1.07-1.29). A meta-regression found no relationship between the beta-carotene supplementation dose and the size of the negative effect associated with lung cancer risk. Our findings indicate that beta-carotene supplementation has no effect on lung cancer risk. Moreover, when used as the primary chemoprevention, beta-carotene may, in fact, increase the risk of lung cancer.

  In plain English

  This systematic review and meta-analysis pooled randomized controlled trials of beta-carotene supplements for preventing lung cancer. It included eight trials with 167,141 participants in the USA, Finland, the UK and China, published by November 2021. One trial group (CARET) was 4,060 male asbestos workers in the USA, randomly assigned to placebo or to 30 mg beta-carotene daily plus retinol. Every trial also tested other substances, though some participants in some trials took beta-carotene without them. Overall, people given beta-carotene had a higher relative risk (RR) of lung cancer than those given placebo: 1.16 (95% CI 1.06–1.26). For smokers and asbestos workers combined, the RR was 1.21 (95% CI 1.08–1.35). The asbestos-worker group on its own had an RR of 1.40 (95% CI 0.95–2.07), a range that includes no difference. No statistically significant link was found between dose and risk. The authors concluded that beta-carotene has a negative effect on lung cancer risk in smokers and asbestos workers. They noted that because other antioxidants were also given, the effect may not come from beta-carotene alone.

  We wrote this plain-English summary from the full article with the help of AI, and a second AI model checked each sentence against the article. It is not the authors' wording; the abstract and the article are their own account.

2010s

• Malignant Mesothelioma and Delivery of Polyphenols. K.S. Bishop, A.J. Braakhuis, L.R. Ferguson. 2016;8(6). PubMed · Publisher · Free full text

  Abstract

  Malignant Mesothelioma (MM) is a rare form of cancer that affects the thin cell wall lining of the body's internal organs and structures.[...].

• The Potential Protective Effects of Polyphenols in Asbestos-Mediated Inflammation and Carcinogenesis of Mesothelium. M. Benvenuto, R. Mattera, G. Taffera, et al. 2016;8(5). Review PubMed · Publisher · Free full text

  Abstract

  Malignant Mesothelioma (MM) is a tumor of the serous membranes linked to exposure to asbestos. A chronic inflammatory response orchestrated by mesothelial cells contributes to the development and progression of MM. The evidence that: (a) multiple signaling pathways are aberrantly activated in MM cells; (b) asbestos mediated-chronic inflammation has a key role in MM carcinogenesis; (c) the deregulation of the immune system might favor the development of MM; and (d) a drug might have a better efficacy when injected into a serous cavity thus bypassing biotransformation and reaching an effective dose has prompted investigations to evaluate the effects of polyphenols for the therapy and prevention of MM. Dietary polyphenols are able to inhibit cancer cell growth by targeting multiple signaling pathways, reducing inflammation, and modulating immune response. The ability of polyphenols to modulate the production of pro-inflammatory molecules by targeting signaling pathways or ROS might represent a key mechanism to prevent and/or to contrast the development of MM. In this review, we will report the current knowledge on the ability of polyphenols to modulate the immune system and production of mediators of inflammation, thus revealing an important tool in preventing and/or counteracting the growth of MM.

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