BackgroundOral squamous cell carcinoma (OSCC) is becoming more common across the globe. The prognosis of OSCC is largely dependent on the early detection. But the routine oral cavity examination may delay the diagnosis because the early oral malignant lesions may be clinically indistinguishable from benign or inflammatory diseases. In this study, the new diagnostic method is developed by using the surface enhanced Raman spectroscopy (SERS) to detect the serum samples from the cancer patients.MethodThe blood serum samples were collected from the OSCC patients, MEC patients and the volunteers without OSCC or MEC. Gold nanoparticles(NPs) were then mixed in the serum samples to obtain the high quality SERS spectra. There were totally 135 spectra of OSCC, 90 spectra of mucoepidermoid carcinoma (MEC) and 145 spectra of normal control group, which were captured by SERS successfully. Compared with the normal control group, the Raman spectral differences exhibited in the spectra of OSCC and MEC groups, which were assigned to the nucleic acids, proteins and lipids. Based on these spectral differences and features, the algorithms of principal component analysis(PCA) and linear discriminant analysis (LDA) were employed to analyze and classify the Raman spectra of different groups.ResultsCompared with the normal groups, the major increased peaks in the OSCC and MEC groups were assigned to the molecular structures of the nucleic acids and proteins. And these different major peaks between the OSCC and MEC groups were assigned to the special molecular structures of the carotenoids and lipids. The PCA-LDA results demonstrated that OSCC could be discriminated successfully from the normal control groups with a sensitivity of 80.7% and a specificity of 84.1%. The process of the cross validation proved the results analyzed by PCA-LDA were reliable.ConclusionThe gold NPs were appropriate substances to capture the high-quality SERS spectra of the OSCC, MEC and normal serum samples. The results of this study confirm that SERS combined PCA-LDA had a giant capability to detect and diagnosis OSCC through the serum sample successfully.
BackgroundTumor stages detection and histologic grades classification are essential for the diagnosis and prognosis of oral squamous cell carcinoma (OSCC). In this research, we apply surface-enhanced Raman spectroscopy (SERS) of blood serum to detect the tumor stages and histologic classification of OSCC.MethodsAccording to TNM classification and World Health Organization histologic grading system, the blood serum samples were collected from a total of 135 OSCC patients in the different tumor stages and histologic grades. Then the SERS spectra of serum samples from OSCC patients were diagnosed and classified into different groups using principal component analysis (PCA) and linear discriminant analysis (LDA) based on the tumor sizes, lymph node metastasis and histologic grades.ResultsThe SERS spectra of blood serum samples have shown the distinct changes and differences compared with each other, which were assigned to the biomolecule alterations (nucleic acids, proteins, lipids, and so on) in blood serums. And all accuracies of detection and classification reached above 85%.ConclusionThis study demonstrated that the SERS based on blood serum test had an enormous potential to carry out the preoperative assessment and prediction of the OSCC patients in different tumor stages and histologic classification.
Oral squamous cell carcinoma (OSCC) is a prevalent cancer affecting the head and neck region (Bozec, Peyrade, Fischel, & Milano, 2009). It alarmingly represents approximately 3% of all malignant cases (Jin et al., 2016). OSCC is characterized by high morbidity and mortality, with more than 300,000 new OSCC cases and over 140,000 deaths of OSCC patients every year (Chi, Day, & Neville, 2015; Sasahira & Kirita, 2018). Although surgery combined with radiotherapy, neoadjuvant chemotherapy, and targeted therapy has greatly improved the treatment of OSCC, the overall 5-year survival rate of OSCC patients has remained to be around 50% (
Mesenchymal stem cells (MSCs) can attract host endothelial progenitor cells (EPCs) to promote vascularization in tissue-engineered constructs (TECs). Nevertheless, the underlying mechanism remains vague. This study is aimed at investigating the roles of CXCR2 and CXCR4 in the EPC migration towards MSCs. In vitro, Transwell assays were performed to evaluate the migration of EPCs towards MSCs. Antagonists and shRNAs targeting CXCR2, CXCR4, and JAK/STAT3 were applied for the signaling blockade. Western blot and RT-PCR were conducted to analyze the molecular events in EPCs. In vivo, TECs were constructed and subcutaneously implanted into GFP+ transgenic mice. Signaling inhibitors were injected in an orientated manner into TECs. Recruitment of host CD34+ cells was evaluated by immunofluorescence. Eventually, we demonstrated that CXCR2 and CXCR4 were both highly expressed in migrated EPCs and indispensable for MSC-induced EPC migration. CXCR2 and CXCR4 strongly correlated with each other in the way that the expression of CXCR2 and CXCR2-mediated migration depends on the activity of CXCR4 and vice versa. Further studies documented that both of CXCR2 and CXCR4 activated STAT3 signaling, which in turn regulated the expression of CXCR2 and CXCR4, as well as cell migration. In summary, we firstly introduced a reciprocal crosstalk between CXCR2 and CXCR4 in the context of EPC migration. This feedback loop plays critical roles in the migration of EPCs towards MSCs.
Severe preeclampsia is one of the most serious obstetric diseases. However, the pathogenesis of the disease is not fully understood. In the present study, placental artery and blood serum was collected from patients with severe preeclampsia, as well as from normal pregnant women. The results of reverse transcription-quantitative (q)PCR, western blotting, and immunohistochemical staining revealed markedly decreased transient receptor potential cation channel subfamily V member 1 (TRPV1), ATP-sensitive potassium channel (KATP) subtype Kir6.1/SUR2B and endothelial nitric oxide synthase (eNOS) expression in severe preeclampsia tissue specimens compared with those in samples from normal pregnant women. The nitrate reduction method indicated lower NO levels in the tissue specimens and serum of patients with severe preeclampsia. Moreover, hematoxylin-eosin staining showed that the endothelial cell layer in the placental artery of patients with severe preeclampsia was notably damaged. To investigate the potential role of TRPV1-KATP channels in severe preeclampsia, HUVECs were used for in vitro experiments. The samples were divided into a control group, a TRPV1 agonist group (capsaicin) and a TRPV1 inhibitor group (capsazepine). qPCR and western blotting revealed that the relative gene and protein expression levels of TRPV1, Kir6.1, SUR2B and eNOS in the control group were significantly lower than those in the capsaicin group and considerably higher than those in the capsazepine group. Based on previous studies and the results of the present study, we hypothesized that impairment of the endothelial TRPV1-KATP channels results in decreased eNOS/NO pathway activity, which may be one of the mechanisms involved in severe preeclampsia. The increase in NO generation mediated by TRPV1-KATP may be a suitable target for the management of severe preeclampsia.
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