Nutrition and Cancer-An International Journal最新文献

Ferroptosis plays an important role in the pathogenesis of neuronal damage, generally mediated by iron and lipid peroxidation. In the present study, we measured the protective effects of puerarin against corticosterone-induced neuronal injury via PI3K/AKT-mediated activation of nuclear factor erythroid 2-related factor 2 (Nrf2). After exposing corticosterone-treated PC12 cells to indicated compounds, we measured the key regulators of ferroptosis (ferritin, SLC7A11, and Ptgs2), ferroptosis events (levels of iron, ROS, MDA, and GSH), and the PI3K/AKT/Nrf2 axis. Corticosterone induced ferroptosis in PC12 cells, evidenced by reduced levels of ferritin, SLC7A11, and GSH and increased levels of iron, ROS, and MDA. These effects were reversed by inhibiting ferroptosis with ferrostatin-1. Puerarin-mediated activation of Nrf2 repressed ferroptosis in corticosterone-treated PC12 cells by upregulating ferritin and SLC7A11 expression. Moreover, the protective effects of puerarin on ferroptosis in corticosterone-treated cells relied on the activation of the PI3K/AKT pathway though the upregulation of nuclear Nrf2. These findings indicate that ferroptosis plays an essential role in corticosterone-induced neuronal damage, and puerarin protects against ferroptosis in corticosterone-treated cells via PI3K/AKT-mediated activation of Nrf2.

This study investigates the impact of neoadjuvant therapy (NT) on body composition and its correlation with long-term survival and other clinical outcomes in patients with advanced gastric cancer. We utilized Computed Tomography (CT) scans to measure body composition before and after NT, including Subcutaneous Adipose Tissue Index (SATI), Visceral Adipose Tissue Index (VATI), Skeletal Muscle Index (SMI), and Muscle Density (MA). We then analyzed the decrease in body composition in relation to tumor regression, inflammatory markers, nutritional scores, and long-term survival. Our findings reveal a negative correlation between the decrease in SATI and VATI after NT, and both tumor regression and nutritional score. Notably, patients who experienced a significant loss in SATI or VATI post-NT had shorter Recurrence-Free Survival (RFS) and Overall Survival (OS). Additionally, significant loss in SATI and VATI emerged as an independent risk factor for both RFS and OS. In conclusion, our study convincingly demonstrates that in patients with advanced gastric cancer, SATI and VATI decreases after NT and is negatively associated with tumor regression and nutritional score. A significant loss in SATI and VATI is a risk factor for shorter RFS and OS, thereby underscoring the importance of maintaining body composition during NT.

Previous cohort studies have shown conflicting findings on the associations between obesity and the risk of thyroid cancer. This meta-analysis aimed to investigate the associations between them by using a meta-analysis of cohort studies. PubMed and EMBASE were searched using keywords from inception until November 2023 to identify relevant studies on this topic. Two authors independently reviewed and selected relevant studies according to the predefined criteria. Out of 475 studies searched from the databases, a total of 22 cohort studies were included in the final analysis. In a random-effects meta-analysis, obesity was significantly associated with an increased risk of thyroid cancer [odds ratio (OR), relative risk (RR), or hazard ratio (HR) = 1.33; 95% confidence interval (CI) 1.24 - 1.43]. Obesity was consistently associated with the increased risk of thyroid cancer in the subgroup meta-analyses by various factors such as study type (prospective or retrospective cohort study), gender (male or female), continent (America, Europe, or Asia), and study quality (high or low). This meta-analysis of cohort studies suggests that obesity increases the risk of thyroid cancer.

Individual observational studies examining the association between polyphenols and the risk of lung cancer have reported mixed findings. Therefore, we performed a systematic review and meta-analysis to determine the pooled effects between polyphenol intake and lung cancer risk. A systematic search was performed on PubMed, Scopus, and Web of Science databases in April 2023. Random-effect models were used to estimate odd ratios (OR) and 95% confidence intervals (95% CI). In total, 20 studies were included in the systematic review. The pooled analyses indicated that a higher intake of flavonoids (OR = 0.81; 95% CI: 0.67,0.98; p = 0.03) and isoflavone (OR = 0.82; 95% CI: 0.74,0.92; p < 0.001) were associated with lower odds of lung cancer. In addition, the ingestion of anthocyanidin (OR = 0.80; 95% CI: 0.65,0.98; p = 0.04), kaempferol (OR = 0.78; 95% CI: 0.64,0.96; p = 0.02), quercetin (OR = 0.66; 95% CI: 0.48,0.91; p = 0.01) and flavanones (OR = 0.71; 95% CI: 0.59,0.85; p < 0.001) reduced the likelihood of developing lung cancer. Overall, our findings suggest that flavonoids, isoflavones, anthocyanidin, kaempferol, quercetin, and flavanones may protect against lung cancer.

Glucose is an important energy source for tumors, however the molecular mechanisms by which tumor cells regulate glucose uptake remain unclear. In this study, we aimed to investigate the regulation mechanism of the WNT7B/β-catenin pathway for glucose transporter 1 (GLUT1)-mediated glucose metabolism in colorectal cancer. Here, we found that WNT7B expression levels were significantly increased in colorectal cancer tissues and closely associated with the clinical stage and lymph node metastasis in patients with colorectal cancer. Next, we confirmed that WNT7B significantly increased the glucose consumption and lactic acid levels in SW480 cells by overexpressing WNT7B. Additionally, gene and protein levels of GLUT1 were increased in WNT7B-overexpressing SW480 cells. However, WNT7B knockdown reversed these effects. WNT7B also enhanced GLUT1-mediated cell proliferation, invasion, and migration. WNT7B overexpression inhibited the effect of glucose deprivation on apoptosis. The WNT/β-catenin signaling pathway inhibitor, LGK974, inhibited WNT7B secretion, leading to GLUT1 levels downregulation and promotion of cell apoptosis. Ectopic tumor xenograft model experiments revealed that WNT7B promoted tumor progression in mice. Overall, our results suggest that WNT7B promotes β-catenin entry into the nucleus to initiates GLUT1 transcription, increases glucose transport and consumption, and enhances aerobic glycolysis, thus promoting tumor progression in colorectal cancer cells.

Isoquercitrin possesses anti-tumor activity in several types of cancers, however, its effects and underlying mechanisms on lung cancer have not been reported. Human lung cancer cell lines as well as normal lung epithelial BEAS-2B cells were treated with isoquercitrin. The influences of isoquercitrin in vitro were evaluated by determining cell viability, apoptosis, pyroptosis, and ferroptosis. Additionally, A549 tumor-bearing mice were generated to explore the anti-cancer effect of isoquercitrin in vivo. We found that isoquercitrin dose-dependently reduced lung cancer cells' viability, with no toxicity against BEAS-2B cells. Isoquercitrin at 40 μM and 80 μM was used in vitro. Isoquercitrin increased apoptosis, elevated NLRP3 inflammasome activation-mediated pyroptosis, and promoted ferroptosis in lung cancer cells. NLRP3 knockdown and caspase-1 selective inhibitor VX-765 attenuated isoquercitrin-induced pyroptosis and ferroptosis, but not apoptosis. Furthermore, isoquercitrin accelerated ROS generation, while ROS inhibitor N-acetylcysteine abrogated isoquercitrin-induced apoptosis, NLRP3 related-pyroptosis and ferroptosis. In vivo, isoquercitrin (1 mg/kg and 5 mg/kg) inhibited tumor growth, increased apoptosis, NLRP3-related pyroptosis, ferroptosis and ROS generation in tumors. Taken together, isoquercitrin inhibits lung cancer growth by triggering ROS/NLRP3-mediated pyroptosis and ferroptosis, with ROS also directly inducing apoptosis. This suggests that isoquercitrin might be a potential therapeutic agent for lung cancer.

Purpose: To develop a simple and convenient inflammation-nutrition-adiposity biomarker to complement the TNM staging system, further assess the prognosis of patients with colorectal cancer cachexia.

Methods: This study was a multi-centre cohort study. The triceps skinfold thickness-albumin index (TA) was calculated by combining the triceps skinfold thickness (TSF) and serum albumin levels. Kaplan-Meier analysis and Cox proportional risk regression models were used to assess the relationship between the TA and all-cause mortality. Internal validation was carried out.

Results: We included 1025 patients with colorectal cancer cachexia, 61.2% of whom were male, with a mean age of 58.91 (12.45) years. As the TA increased, overall mortality decreased in female patients (hazard ratio [HR], 0.95) but not in male patients (HR, 0.99). Multivariate Cox analysis showed that patients in the normal TA group had a significantly lower risk of death than those in the low TA group (HR, 0.53, 95% CI, 0.40-0.72). Patients with a normal TA had a lower risk of malnutrition, poor quality of life, and poor short-term prognosis than those with a low TA.

Conclusions: TA index enables clinicians to assess the prognosis of patients as early as possible to improve the survival of patients with colorectal cancer cachexia.

Currently, the combination of atezolizumab and bevacizumab (Atez/Bev) is recommended as the first-line therapy for patients with advanced hepatocellular carcinoma (HCC). However, there is a lack of research on the levels of nutrient elements in advanced HCC patients receiving Atez/Bev treatment. In this study, data from 35 patients with advanced HCC and 37 healthy individuals of similar age and sex were included. The levels of alanine aminotransferase, aspartate aminotransferase, and alkaline phosphatase were significantly increased in patients with HCC. These levels returned to the reference range after three rounds of Atez/Bev treatment. Additionally, the levels of blood urea nitrogen and creatinine (Cr) increased after Atez/Bev treatment. In HCC patients, the levels of calcium (Ca), iron (Fe), and copper (Cu) were significantly higher, while the levels of sodium (Na), magnesium (Mg), and zinc (Zn) were significantly lower compared to healthy individuals. These changes were reversed after Atez/Bev treatment. In conclusion, our findings indicate that treatment with Atez/Bev influences the levels of Ca, Fe, Cu, Na, Mg, and Zn in patients with HCC. The alterations in these elements caused by Atez/Bev treatment require mechanistic research in the future.

Objective: The primary objective of this investigation was to assess the impact of acupuncture intervention and explore the intricacies of acupoint selection as a therapeutic strategy for chemotherapy-induced Anorexia (CIA).

Method: Eight electronic databases were searched to identify relevant studies on the use of acupuncture for the treatment of CIA to conduct a comprehensive meta-analysis. Following this, the Apriori algorithm, correlation analysis, and cluster analysis were performed to identify correlations between the selection of acupoints.

Results: Acupuncture significantly reduced the incidence of anorexia (RR = 0.76, 95%CI: 0.65, 0.90; I²=63%; p = 0.001; n = 503) and anorexia score (SMD=-0.33, 95%CI: -0.53, -0.14; I²=22%; p = 0.0008; n = 419), as well as preserved body mass (MD = 2.70, 95%CI: 1.08, 4.32; I²=0%; p = 0.001; n = 187) and enhanced physical strength (MD = 4.23, 95%CI: 1.90, 6.55; I²=58%; p = 0.0004; n = 377). Moreover, subgroup analysis highlighted its efficacy in managing anorexia associated with non-gastrointestinal tumors and mitigating the severity of cisplatin-induced anorexia. Meanwhile, Zusanli (ST36), Neiguan (PC6), Tianshu (ST25), Zhongwan (RN12), and Qihai (RN6) were identified as crucial acupoints in CIA management.

Conclusion: Acupuncture holds promise as a potential non-pharmacological approach for managing anorexia during cancer chemotherapy. To provide robust evidence of its effectiveness, well-designed Randomized Controlled Trials (RCTs) with larger participant cohorts, and consistent core outcome measures are essential.

There is inconclusive evidence on the role of dietary intake of vitamin B₁₂ in cancer. We evaluated the association between vitamin B₁₂ intake and cancer risk in a hospital-based case-control study, comprising 3,758 cancer cases and 2,995 controls in Vietnam. Vitamin B₁₂ intake was derived from the validated food frequency questionnaire. Unconditional logistic regression model was used to calculate the odds ratios (ORs), and respective 95% confidence intervals (CIs) for the association between vitamin B₁₂ and cancer risk. There was a U-shaped association between vitamin B₁₂ intake and overall risk of cancer. Individuals with intakes lower than the median intake had a 6% (OR = 1.06, 95% CI: 0.86-1.31)-107% (OR = 2.07, 95% CI: 1.58-2.71), increased risk of cancer (P_trend<0.001), whereas those with higher intakes than the median intake had a 20% (OR = 1.20, 95% CI: 0.97-1.48)-52% (OR = 1.52, 95% CI: 1.22-1.89) increased risk of cancer (P_trend<0.04). The excess risk of cancer associated with low intakes of vitamin B₁₂ was observed among esophageal, lung, and breast cancer patients, whereas with high intakes of vitamin B₁₂ among gastric cancer patients. In summary, a U-shaped association between vitamin B₁₂ intake and increased cancer risk was observed in the Vietnamese population.