Opportunities and Challenges of Kava in Lung Cancer Prevention

Freeman, Breanne; Mamallapalli, Jessica; Bian, Tengfei; Ballas, Konstantinos; Lynch, Allison M.; Scala, Alexander; Huo, Zhiguang; Fredenburg, Kristianna M.; Bruijnzeel, Adrie W.; Baglole, Carolyn J.; Lü, Junxuan; Salloum, Ramzi G.; Malaty, John; Xing, Chengguo

doi:10.3390/ijms24119539

Cited by 5 publications

(3 citation statements)

References 152 publications

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“…Lung cancer is a highly prevalent malignancy and remains a primary contributor to cancer-related mortality, accounting for approximately 2.2 million cases annually and causing an estimated 1.79 million fatalities [1][2][3]. Histologically, lung cancer is typically categorized as non-small cell lung cancer (NSCLC) or small cell lung cancer (SCLC).…”

Section: Introductionmentioning

confidence: 99%

NCAPD2 serves as a potential prognostic biomarker for lung adenocarcinoma and promotes cell proliferation, migration, invasion and cell cycle <i>in vitro</i>

WU,

ZHAO,

ZHANG

et al. 2024

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The pro-oncogenic effects of NCAPD2 have been extensively studied across various tumor types; however, its precise role within the context of lung adenocarcinoma (LUAD) remains elusive. This study aims to elucidate the biological functions of NCAPD2 in LUAD and unravel the underlying mechanistic pathways. Utilizing bioinformatics methodologies, we explored the differential expression of NCAPD2 between normal and tumor samples, along with its correlations with clinical-pathological characteristics, survival prognosis, and immune infiltration. In the TCGA-LUAD dataset, tumor samples demonstrated significantly elevated levels of NCAPD2 expression compared to normal samples (p < 0.001). Clinically, higher NCAPD2 expression was notably associated with advanced T, N, and M stages, pathologic stage, gender, smoking status, and diminished overall survival (OS). Moreover, differentially expressed genes (DEGs) associated with NCAPD2 were predominantly enriched in pathways related to cell division. Immune infiltration analysis revealed that NCAPD2 expression levels were linked to the infiltration of memory B cells, naïve CD4+ T cells, activated memory CD4+ T cells, and M1 macrophages. In vitro experiments demonstrated that silencing NCAPD2 suppressed LUAD cell proliferation, migration, invasion, epithelial-mesenchymal transition (EMT), and cell cycle progression. In summary, NCAPD2 may represent a promising prognostic biomarker and novel therapeutic target for LUAD.

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Section: Introductionmentioning

confidence: 99%

NCAPD2 serves as a potential prognostic biomarker for lung adenocarcinoma and promotes cell proliferation, migration, invasion and cell cycle <i>in vitro</i>

WU,

ZHAO,

ZHANG

et al. 2024

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“…Lung cancer is one of the most common malignant tumors with the highest incidence and mortality worldwide in 2020, of which non-small cell lung cancer (NSCLC) accounts for ~85% of all lung cancer cases ( 1 , 2 ). The main types of NSCLC are adenocarcinoma and squamous and large cell carcinoma ( 3 ).…”

Section: Introductionmentioning

confidence: 99%

Combination of the cuproptosis inducer disulfiram and anti‑PD‑L1 abolishes NSCLC resistance by ATP7B to regulate the HIF‑1 signaling pathway

Li,

Sun,

Bai

et al. 2023

Int J Mol Med

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Disulfiram (DSF) is used to treat non-small cell lung cancer (NSCLC). DSF significantly increases expression of programmed death-ligand 1 (PD-L1), which may enhance immunosuppression and immune escape of tumors. Therefore, the present study aimed to investigate the role of combined treatment of DSF and anti-PD-L1 in NSCLC resistance. The viability and apoptosis of A549 cells were detected by the Cell Counting Kit-8 assay and flow cytometry, respectively. The expression levels of ATPase copper-transporting β (ATP7B) and PD-L1 in A549 cells were detected by reverse transcription-quantitative PCR and western blot analysis. The levels of reactive oxygen species (ROS), malondialdehyde (MDA) and superoxide dismutase (SOD) in A549 cells were detected by respective assay kits. The expression levels of cuproptosis-associated proteins ferredoxin-1 (FDX1), ATP7B, solute carrier family 31 member 1 (SLC31A1), succinate dehydrogenase B (SDHB), PD-L1 and hypoxia inducible factor (HIF)-1A were analyzed by western blotting in A549 cells. DSF inhibited the viability of A549 cells and promoted expression levels of ATP7B and PD-L1 at both mRNA and protein levels in A549 cells. The viability of cisplatin (DPP)-treated A549 cells was increased following DSF treatment. JQ-1 (a PD-L1 inhibitor) suppressed the viability of DPP-treated A549 cells pretreated with DSF. DSF increased expression levels of ATP7B and PD-L1. The combination treatment of DSF and JQ-1 in A549 cells increased levels of ROS and MDA, as well as expression levels of FDX1 and SLC31A1; however, combination treatment decreased levels of SOD, as well as expression levels of ATP7B, SDHB, PD-L1, and HIF-1A. PX478 (an HIF-1 inhibitor) acted with DSF to enhance the inhibitory effects on the viability and on the induction of apoptosis of A549 cells. PX478 upregulated the levels of ROS and MDA, while it downregulated levels of SOD in DSF-treated A549 cells. PX478 promoted expression levels of FDX1 and SLC31A1, while it suppressed expression levels of ATP7B, PD-L1, and HIF-1A in DSF-treated A549 cells. In conclusion, the combined treatment of A549 cells with anti-PD-L1 and DSF enhanced the effect of cuproptosis on the inhibition of NSCLC cell viability.

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“…Lung cancer is the leading cause of cancer-related deaths globally ( 1 , 2 ). Among them, non-small cell lung cancer (NSCLC) is the most common histological type, accounting for more than 85% of the total number of patients ( 3 , 4 ), among which adenocarcinoma (ADC) accounts for nearly 60% of all NSCLC, making it the most common subtype of NSCLC. The vast majority of lung cancer patients are already in a locally advanced stage or with concurrent metastatic lesions at the time of diagnosis ( 5 ), thus losing the best opportunity for surgical resection.…”

Section: Introductionmentioning

confidence: 99%

Clinicopathological characteristics correlated with programmed cell death-ligand 1 expression in advanced lung adenocarcinoma

Gao,

Zou,

Wang

et al. 2023

J Thorac Dis

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Background Recent studies have shown that immune checkpoint inhibitors (ICIs) targeting programmed cell death-ligand 1 (PD-L1) have potential benefits in patients with non-small cell lung cancer (NSCLC) subgroups, while the clinicopathological characteristics associated with PD-L1 expression have not been well established. The purpose of this study was to detect the expression level of PD-L1 in tumor tissues of patients with advanced lung adenocarcinoma (ADC) and analyze its possible relationship with clinicopathological characteristics, so as to identify the predictors of PD-L1 expression. Methods This retrospective study was conducted by analyzing the clinicopathological and imaging characteristics of hospitalized advanced lung ADC patients with PD-L1 available data and admitted to the respiratory department of our hospital. The expression level of PD-L1 in fresh-frozen tumor tissue samples of 136 advanced ADC patients was analyzed by immunohistochemistry. The patients were divided into positive and negative groups based on a cut-off of 1% PD-L1 expression level. Subsequently, the significant correlation between PD-L1 levels and clinicopathological features were evaluated. The predictive performance of clinicopathological characteristics on PD-L1 expression was evaluated and the optimal cut-off values were identified by plotting the receiver operating characteristic (ROC) curve. Results The expression level of PD-L1 was related to sex, clinical stage, serum carcinoembryonic antigen (CEA), neuron specific enolase (NSE), white blood cell (WBC), and tumor (T) and metastasis (M) stage. Multivariate logistic regression analysis showed the CEA, NSE, T stage, and WBC were independent predictors of PD-L1 positive expression in lung ADC patients. The ROC curve suggested the model combining CEA with NSE [area under the curve (AUC) =0.815] could better predict the expression levels of PD-L1. The optimal cut-off values for identifying advanced lung ADC patients with PD-L1 positive were CEA ≤13.38 ng/mL and NSE ≤42.35 ng/mL, with sensitivity and specificity of 85.4% and 55.6%, and 92.7% and 32.1%, respectively. Conclusions Some commonly used clinicopathological features are related to the histological expression of PD-L1. The serum CEA, NSE, T stage, and WBC values can be used as indicators to predict the expression level of PD-L1 in advanced lung ADC, and are used as predictors to evaluate the efficacy of ICIs before treatment.

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Opportunities and Challenges of Kava in Lung Cancer Prevention

Cited by 5 publications

References 152 publications

NCAPD2 serves as a potential prognostic biomarker for lung adenocarcinoma and promotes cell proliferation, migration, invasion and cell cycle <i>in vitro</i>

NCAPD2 serves as a potential prognostic biomarker for lung adenocarcinoma and promotes cell proliferation, migration, invasion and cell cycle <i>in vitro</i>

Combination of the cuproptosis inducer disulfiram and anti‑PD‑L1 abolishes NSCLC resistance by ATP7B to regulate the HIF‑1 signaling pathway

Clinicopathological characteristics correlated with programmed cell death-ligand 1 expression in advanced lung adenocarcinoma

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