ABSTRACT
Prolyl 4-hydroxylases (P4Hs) are a family of key modifying enzymes in collagen synthesis. P4Hs have been confirmed to be closely associated with tumor occurrence and development. However, the expression of P4Hs in head and neck cancer (HNSC) as well as its relationship with prognosis and tumor immunity infiltration has not yet been analyzed. We investigated the transcriptional expression, survival data, and immune infiltration of P4Hs in patients with HNSC from multiple databases. P4H1-3 expression was significantly higher in HNSC tumor tissues than in normal tissues. Moreover, P4HA1 and P4HA2 were associated with tumor stage, patient prognosis, and immune cell infiltration. P4HA3 was related to patient prognosis and immune cell infiltration. Correlation experiments confirmed that P4HA1 may serve as a prognosis biomarker and plays a role in the progression of nasopharyngeal carcinoma. These findings suggest that P4HA1-3 may be a novel biomarker for the prognosis and treatment of HNSC, which is expected to support the development of new therapies for patients with head and neck tumors and improve patient outcomes.
Subject(s)
Biomarkers, Tumor , Head and Neck Neoplasms , Immunotherapy , Procollagen-Proline Dioxygenase , Humans , Biomarkers, Tumor/metabolism , Prognosis , Head and Neck Neoplasms/therapy , Head and Neck Neoplasms/metabolism , Head and Neck Neoplasms/immunology , Head and Neck Neoplasms/diagnosis , Immunotherapy/methods , Procollagen-Proline Dioxygenase/metabolism , Procollagen-Proline Dioxygenase/genetics , Gene Expression Regulation, Neoplastic , Female , Male , Nasopharyngeal Carcinoma/therapy , Nasopharyngeal Carcinoma/immunology , Nasopharyngeal Carcinoma/diagnosis , Nasopharyngeal Carcinoma/pathology , Nasopharyngeal Carcinoma/genetics , Nasopharyngeal Carcinoma/metabolism , Nasopharyngeal Carcinoma/mortalityABSTRACT
Our previous studies have confirmed that transforming growth factor-ß (TGF-ß) plays an important role in tumor metastasis, and the serum deprivation protein response (SDPR) is a potential downstream target of TGF-ß. However, the role and mechanism of SDPR in gastric cancer are still unclear. We performed gene microarray, bioinformation analysis, combined with in vivo and in vitro experimental verification, we identified that SDPR is significantly downregulated in gastric cancer, and participates in TGF-ß-mediated tumour metastasis. Mechanically, SDPR interacts with extracellular signal-regulated kinase (ERK) and inhibits fatty acid metabolism key gene Carnitine palmitoyl transferase 1A (CPT1A) at transcriptional level by supressing ERK/PPAR pathway. Our findings suggest that the TGF-ß/SDPR/CPT1A axis play an important role in the fatty acid oxidation of gastric cancer, and provides a new insight into the crosstalk of tumour microenvironments and metabolism reprogramming and suggest that strategies to intervene the fatty acid metabolism may therapy gastric cancer metastasis.
Subject(s)
Stomach Neoplasms , Humans , Stomach Neoplasms/metabolism , Transforming Growth Factor beta/genetics , Transforming Growth Factor beta/metabolism , Cell Line, Tumor , Lipid Metabolism , Extracellular Signal-Regulated MAP Kinases/metabolism , Fatty Acids/metabolism , Tumor MicroenvironmentABSTRACT
BACKGROUND: The risk factors for operation complications of high-dose-rate dimensional (3D) interstitial brachytherapy for lung malignant tumors are still unclear. We aimed to provide a reliable reference for the preoperative safety assessment of interstitial brachytherapy. PATIENTS AND METHODS: We analyzed the degree and incidence of operational complications in 120 eligible patients with lung carcinoma who underwent computed tomography (CT)-guided HDR interstitial brachytherapy. Univariate and multivariate analyses were used to study the relationships between patient-related factors, tumor-related factors, operation-related factors, and operational complications. RESULTS: The most frequent complications of CT-guided HDR interstitial brachytherapy were pneumothorax and hemorrhage. In univariate analysis, smoking, emphysema, distance of implanted needles through the normal lung tissue, number of implanted needle adjustments, and distance of the lesion from the pleura were the risk factors for pneumothorax; the tumor size, distance of the tumor from the pleura, number of implanted needle adjustments, and distance of the implanted needle through the normal lung tissue were risk factors for hemorrhage. In multivariate analysis, the depth of the implanted needle through the normal lung tissue and distance of the lesion from the pleura were independent risk factors for pneumothorax. Tumor size, number of implanted needle adjustments, and distance through normal lung tissue were independent risk factors for hemorrhage. CONCLUSION: This study provides a reference for the clinical treatment of lung cancer by analyzing the risk factors for complications of interstitial brachytherapy.
Subject(s)
Brachytherapy , Lung Neoplasms , Pneumothorax , Humans , Lung Neoplasms/radiotherapy , Lung Neoplasms/surgery , Lung Neoplasms/complications , Pneumothorax/epidemiology , Pneumothorax/etiology , Pneumothorax/pathology , Brachytherapy/adverse effects , Lung/pathology , Hemorrhage/complications , Hemorrhage/pathology , Risk FactorsABSTRACT
Stress granules (SGs) are non-enveloped structures formed primarily via protein and RNA aggregation under various stress conditions, including hypoxia and viral infection, as well as oxidative, osmotic, and heat-shock stress. SGs assembly is a highly conserved cellular strategy to reduce stress-related damage and promote cell survival. At present, the composition and dynamics of SGs are well understood; however, data on the functions and related mechanisms of SGs are limited. In recent years, SGs have continued to attract attention as emerging players in cancer research. Intriguingly, SGs regulate the biological behavior of tumors by participating in various tumor-associated signaling pathways, including cell proliferation, apoptosis, invasion and metastasis, chemotherapy resistance, radiotherapy resistance, and immune escape. This review discusses the roles and mechanisms of SGs in tumors and suggests novel directions for cancer treatment.
ABSTRACT
Symptomatic colon metastasis from primary lung cancer is rare in clinical practice. We report the case of a 58-year-old patient with advanced lung adenocarcinoma who developed abdominal symptoms, including abdominal distention and difficulty defecating, after immunotherapy and chemotherapy. The patient was diagnosed with lung adenocarcinoma, and systemic positron emission tomography-computed tomography confirmed multiple lymph node, pleural, and adrenal metastases. Molecular detection indicated BRAF V600E mutation and high programmed death-ligand 1 (PD-L1) expression. After first-line anti-programmed cell death protein 1 immunotherapy combined with chemotherapy, the nodes in the chest remarkably diminished. However, it was followed by colon obstruction, incomplete ileus, and bone metastasis. Endoscopic histological examination confirmed adenocarcinoma but could not identify primary or secondary tumors due to insufficient tissue. We performed colon resection to remove the obstruction, and postoperative tissue pathological microscopy confirmed metastasis from the lung adenocarcinoma. We corroborated the BRAF V600E mutation and high PD-L1 expression and supported the molecular features of lung adenocarcinoma. During hospitalization, the patient presented with unbearable pain in the bone metastases, and palliative radiotherapy was administered. Then, the patient received dabrafenib plus trametinib as the second-line therapy. This report discusses the clinical characteristics, pathology, imaging, molecular profile assessments, and treatment of primary lung adenocarcinoma with colon metastasis.