Current Challenges and Future Advances in Lung Cancer: Genetics, Instrumental Diagnosis and Treatment

Vicidomini, Giovanni

doi:10.3390/cancers15143710

Cited by 8 publications

(2 citation statements)

References 10 publications

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“…Lung cancer is the second most common cancer globally and the leading cause of cancer-related deaths [1]. It encompasses two histological subtypes: small cell lung cancer (SCLC) and non-small cell lung cancer (NSCLC) [2]. Among NSCLC, lung adenocarcinoma (LUAD) is the most prevalent subtype, accounting for 60% of all lung cancer cases [3].…”

Section: Introductionmentioning

confidence: 99%

Long noncoding RNA LINC01106 promotes lung adenocarcinoma progression via upregulation of autophagy

SUN,

ZHENG,

CAI

et al. 2024

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Long noncoding RNA, LINC01106 exhibits high expression in lung adenocarcinoma (LUAD) tumor tissues, but its functional role and regulatory mechanism in LUAD cells remain unclear. LINC01106 expression was analyzed in LUAD tissues and its functional impact on LUAD cells was assessed. LUAD cells were silenced with sh-LINC01106 and injected into nude mice to investigate tumor growth. The downstream transcription factors and molecular mechanism were determined using the Human transcription factor database (TFDB) database and Gene Expression Profiling Interactive Analysis (GEPIA) database. Additionally, the impact of linc01106 on autophagy was analyzed by determining the expression of autophagy-related genes (ATGs) in LUAD cells. Our results showed that LINC01106 exhibited upregulation in both LUAD tissues and cell lines. The silencing of LINC01106 demonstrated a suppressive effect on tumorigenesis in a xenograft mouse model of LUAD. Additionally, LINC01106 was found to recruit TATAbinding protein-associated factor 15 (TAF15), an RNA-binding protein, thereby enhancing the mRNA stability of TEA domain transcription factor 4 (TEAD4). In turn, TEAD4 served as a transcription factor that bound to the LINC01106 promoter and regulated its expression. Further assays indicated that LINC01106 promoted autophagy in LUAD cells by upregulating the expression of autophagy-related genes (ATGs). The silencing of LINC01106 in LUAD cells inhibited autophagy, and cell proliferation, and promoted apoptosis, which all were effectively reversed by ATG5 overexpression. Overall, LINC01106, transcriptionally activated by TEAD4, interacts with TAF15 to promote the stability of TEAD4 and upregulates the expression of ATGs, promoting malignancy of LUAD cells.

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Section: Introductionmentioning

confidence: 99%

Long noncoding RNA LINC01106 promotes lung adenocarcinoma progression via upregulation of autophagy

SUN,

ZHENG,

CAI

et al. 2024

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“…In recent decades, much progress has been made to further our knowledge of the diagnostic and therapeutic approach to cancer in general and lung cancer in particular [2]. In this regard, significant information has been gathered about predictive biomarkers in NSCLC [3].…”

Section: Introductionmentioning

confidence: 99%

Differentially Expressed Genes Involved in Primary Resistance to Immunotherapy in Patients with Advanced-Stage Pulmonary Cancer

Chinchilla-Tábora,

Montero,

Corchete

et al. 2024

IJMS

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In the last few years, nivolumab has become the standard of care for advanced-stage lung cancer patients. Unfortunately, up to 60% of patients do not respond to this treatment. In our study, we identified variations in gene expression related to primary resistance to immunotherapy. Bronchoscopy biopsies were obtained from advanced non-small cell lung cancer (NSCLC) patients previously characterized as responders or non-responders after nivolumab treatment. Ten tumor biopsies (from three responders and seven non-responders) were analyzed by the differential expression of 760 genes using the NanoString nCounter platform. These genes are known to be involved in the response to anti-PD1/PD-L1 therapy. All the patients were treated with nivolumab. Examining the dysregulated expression of 24 genes made it possible to predict the response to nivolumab treatment. Supervised analysis of the gene expression profile (GEP) revealed that responder patients had significantly higher levels of expression of CXCL11, NT5E, KLRK1, CD3G, GZMA, IDO1, LCK, CXCL9, GNLY, ITGAL, HLA-DRB1, CXCR6, IFNG, CD8A, ITK, B2M, HLA-B, and HLA-A than did non-responder patients. In contrast, PNOC, CD19, TP73, ARG1, FCRL2, and PTGER1 genes had significantly lower expression levels than non-responder patients. These findings were validated as predictive biomarkers in an independent series of 201 patients treated with nivolumab (22 hepatocellular carcinomas, 14 non-squamous cell lung carcinomas, 5 head and neck squamous cell carcinomas, 1 ureter/renal pelvis carcinoma, 120 melanomas, 4 bladder carcinomas, 31 renal cell carcinomas, and 4 squamous cell lung carcinomas). ROC curve analysis showed that the expression levels of ITK, NT5E, ITGAL, and CD8A were the best predictors of response to nivolumab. Further, 13/24 genes showed an adverse impact on overall survival (OS) in an independent, large series of patients with NSCLC (2166 cases). In summary, we found a strong association between the global GEP of advanced NSCLC and the response to nivolumab. The classification of NSCLC patients based on GEP enabled us to identify those patients who genuinely benefited from treatment with immune checkpoint inhibitors (ICIs). We also demonstrated that abnormal expression of most of the markers comprising the genomic signature has an adverse influence on OS, making them significant markers for therapeutic decision-making. Additional prospective studies in larger series of patients are required to confirm the clinical utility of these biomarkers.

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Empowering lung cancer treatment: Harnessing the potential of natural phytoconstituent‐loaded nanoparticles

Siddiquee,

Bhaskaran,

Nathani

et al. 2024

Phytotherapy Research

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Lung cancer, the second leading cause of cancer‐related deaths, accounts for a substantial portion, representing 18.4% of all cancer fatalities. Despite advances in treatment modalities such as chemotherapy, surgery, and immunotherapy, significant challenges persist, including chemoresistance, non‐specific targeting, and adverse effects. Consequently, there is an urgent need for innovative therapeutic approaches to overcome these limitations. Natural compounds, particularly phytoconstituents, have emerged as promising candidates due to their potent anticancer properties and relatively low incidence of adverse effects compared to conventional treatments. However, inherent challenges such as poor solubility, rapid metabolism, and enzymatic degradation hinder their clinical utility. To address these obstacles, researchers have increasingly turned to nanotechnology‐based drug delivery systems (DDS). Nanocarriers offer several advantages, including enhanced drug stability, prolonged circulation time, and targeted delivery to tumor sites, thereby minimizing off‐target effects. By encapsulating phytoconstituents within nanocarriers, researchers aim to optimize their bioavailability and therapeutic efficacy while reducing systemic toxicity. Moreover, the integration of nanotechnology with phytoconstituents allows for a nuanced understanding of the intricate molecular pathways involved in lung cancer pathogenesis. This integrated approach holds promise for modulating key cellular processes implicated in tumor growth and progression. Additionally, by leveraging the synergistic effects of phytoconstituents and nanocarriers, researchers seek to develop tailored therapeutic strategies that maximize efficacy while minimizing adverse effects. In conclusion, the integration of phytoconstituents with nanocarriers represents a promising avenue for advancing lung cancer treatment. This synergistic approach has the potential to revolutionize current therapeutic paradigms by offering targeted, efficient, and minimally toxic interventions. Continued research in this field holds the promise of improving patient outcomes and addressing unmet clinical needs in lung cancer management.

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Current Challenges and Future Advances in Lung Cancer: Genetics, Instrumental Diagnosis and Treatment

Cited by 8 publications

References 10 publications

Long noncoding RNA LINC01106 promotes lung adenocarcinoma progression via upregulation of autophagy

Long noncoding RNA LINC01106 promotes lung adenocarcinoma progression via upregulation of autophagy

Differentially Expressed Genes Involved in Primary Resistance to Immunotherapy in Patients with Advanced-Stage Pulmonary Cancer

Empowering lung cancer treatment: Harnessing the potential of natural phytoconstituent‐loaded nanoparticles

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