Relationship between hemoglobin and lung cancer: evidence from Mendelian randomization and National Health and Nutrition Examination Survey

Background Lung cancer is the primary cause of cancer-related mortality worldwide. Hemoglobin (Hb) represents the most widely utilized test parameter in clinical settings. However, few articles have examined the causal relationship between Hb concentration and lung cancer incidence. Methods Mendelian randomization (MR) was first conducted to investigate the potential causality between Hb and lung cancer. Sensitivity analyses were applied to validate the reliability of MR results. Then, the National Health and Nutrition Examination Survey (NHANES) database was used to verify the effect of Hb on the prognosis of lung cancer. Results The MR analysis demonstrated that Hb was casually associated with the decreased risk of lung cancer in the European population (ORIVW 0.84, 95% CI 0.75–0.95, p = 0.006; ORWeighted-median 0.78, 95% CI 0.65–0.94, p = 0.008; ORMR-Egger 0.82, 95% CI 0.64–1.04, p = 0.11). The results from the NHANES database showed that a high value of Hb was associated with better outcomes for patients with lung cancer (HR 0.45, 95% CI 0.26–0.79, p = 1.6E−03). Conclusions Our study provides further evidence for the relationship between Hb levels and lung cancer, highlighting the potential significance of Hb as a biomarker for predicting the risk and prognosis of lung cancer (AU)

FHL2 promotes the aggressiveness of lung adenocarcinoma by inhibiting autophagy via activation of the PI3K/AKT/mTOR pathway.

BACKGROUND: Increasing evidence indicates that four and a half LIM domains 2 (FHL2) plays a crucial role in the progression of various cancers. However, the biological functions and molecular mechanism of FHL2 in lung adenocarcinoma (LUAD) remain unclear. METHODS: We evaluated the prognostic value of FHL2 in LUAD using public datasets and further confirmed its prognostic value with our clinical data. The biological functions of FHL2 in LUAD were evaluated by in vitro and in vivo experiments. Pathway analysis and rescue experiments were subsequently performed to explore the molecular mechanism by which FHL2 promoted the progression of LUAD. RESULTS: FHL2 was upregulated in LUAD tissues compared to adjacent normal lung tissues, and FHL2 overexpression was correlated with unfavorable outcomes in patients with LUAD. FHL2 knockdown significantly suppressed the proliferation, migration and invasion of LUAD cells, while FHL2 overexpression had the opposite effect. Mechanistically, FHL2 upregulated the PI3K/AKT/mTOR pathway and subsequently inhibited autophagy in LUAD cells. The effects FHL2 on the proliferation, migration and invasion of LUAD cells are dependent on the inhibition of autophagy, as of induction autophagy attenuated the aggressive phenotype induced by FHL2 overexpression. CONCLUSIONS: FHL2 promotes the progression of LUAD by activating the PI3K/AKT/mTOR pathway and subsequently inhibiting autophagy, which can be exploited as a potential therapeutic target for LUAD.

Relationship between hemoglobin and lung cancer: evidence from Mendelian randomization and National Health and Nutrition Examination Survey.

BACKGROUND: Lung cancer is the primary cause of cancer-related mortality worldwide. Hemoglobin (Hb) represents the most widely utilized test parameter in clinical settings. However, few articles have examined the causal relationship between Hb concentration and lung cancer incidence. METHODS: Mendelian randomization (MR) was first conducted to investigate the potential causality between Hb and lung cancer. Sensitivity analyses were applied to validate the reliability of MR results. Then, the National Health and Nutrition Examination Survey (NHANES) database was used to verify the effect of Hb on the prognosis of lung cancer. RESULTS: The MR analysis demonstrated that Hb was casually associated with the decreased risk of lung cancer in the European population (ORIVW 0.84, 95% CI 0.75-0.95, p = 0.006; ORWeighted-median 0.78, 95% CI 0.65-0.94, p = 0.008; ORMR-Egger 0.82, 95% CI 0.64-1.04, p = 0.11). The results from the NHANES database showed that a high value of Hb was associated with better outcomes for patients with lung cancer (HR 0.45, 95% CI 0.26-0.79, p = 1.6E-03). CONCLUSIONS: Our study provides further evidence for the relationship between Hb levels and lung cancer, highlighting the potential significance of Hb as a biomarker for predicting the risk and prognosis of lung cancer.

Different Roles of the Insulin-like Growth Factor (IGF) Axis in Non-small Cell Lung Cancer.

Non-small cell lung cancer (NSCLC) remains one of the deadliest malignant diseases, with high incidence and mortality worldwide. The insulin-like growth factor (IGF) axis, consisting of IGF-1, IGF-2, related receptors (IGF-1R, -2R), and high-affinity binding proteins (IGFBP 1-6), is associated with promoting fetal development, tissue growth, and metabolism. Emerging studies have also identified the role of the IGF axis in NSCLC, including cancer growth, invasion, and metastasis. Upregulation of IGE-1 and IGF-2, overexpression of IGF-1R, and dysregulation of downstream signaling molecules involved in the PI-3K/Akt and MAPK pathways jointly increase the risk of cancer growth and migration in NSCLC. At the genetic level, some noncoding RNAs could influence the proliferation and differentiation of tumor cells through the IGF signaling pathway. The resistance to some promising drugs might be partially attributed to the IGF axis. Therapeutic strategies targeting the IGF axis have been evaluated, and some have shown promising efficacy. In this review, we summarize the biological roles of the IGF axis in NSCLC, including the expression and prognostic significance of the related components, noncoding RNA regulation, involvement in drug resistance, and therapeutic application. This review offers a comprehensive understanding of NSCLC and provides insightful ideas for future research.

Effects of different obesity-related adipokines on the occurrence of obstructive sleep apnea.

Obstructive sleep apnea (OSA), characterized by recurrent episodes of apnea during sleep and daytime sleepiness, seriously affects human health and may lead to systemic organ dysfunction. The pathogenesis of OSA is complex and still uncertain, but multiple surveys have shown that obesity is an important factor, and the incidence of OSA in people with obesity is as high as 30%. Adipokines are a group of proteins secreted from adipocytes, which are dysregulated in obesity and may contribute to OSA. Here, we review the most important and representative research results regarding the correlation between obesity-related adipokines including leptin, adiponectin, omentin-1, chemerin, and resistin and OSA in the past 5 years, provide an overview of these key adipokines, and analyze possible intrinsic mechanisms and influencing factors. The existing research shows that OSA is associated with an increase in the serum levels of leptin, chemerin, and resistin and a decrease in the levels of adiponectin and omentin-1; the findings presented here can be used to monitor the development of OSA and obesity, prevent future comorbidities, and identify risk factors for cardiovascular and other diseases, while different adipokines can be linked to OSA through different pathways such as insulin resistance, intermittent hypoxia, and inflammation, among others. We hope our review leads to a deeper and more comprehensive understanding of OSA based on the relevant literature, which will also provide directions for future clinical research.