ABSTRACT
Small cell lung cancer (SCLC) is a neuroendocrine tumor with fast progression, high malignancy, easy recurrence, and extremely poor prognosis. In the past 30 years, the clinical treatment strategy of SCLC has been mainly chemotherapy and radiotherapy, but the curative effect is not significant; the current immunotherapy of SCLC has gradually entered the clinic and has made certain progress. Tumor immunotherapy includes immune checkpoint inhibitors, tumor vaccines, cytokines, chimeric antigen receptor T-cell immunotherapy (CAR-T) therapy, etc. Currently, immune checkpoint inhibitors are the most widely used. This article summarizes the principles of immune checkpoint inhibitors and related drugs, summarizes their domestic and foreign clinical trials progress in SCLC treatment, reviews the biomarkers used in the therapy, and discusses its future development direction. .
Subject(s)
Humans , Cancer Vaccines/therapeutic use , Clinical Trials as Topic , Immune Checkpoint Inhibitors , Immunotherapy , Lung Neoplasms/drug therapy , Small Cell Lung Carcinoma/drug therapyABSTRACT
<p><b>OBJECTIVE</b>To study the effect of the synthetic peptide RGDSY-CTTHWGFTLC on the biological behavior of breast cancer MCF-7 cells in vitro.</p><p><b>METHODS</b>MCF-7 cells were incubated with different concentrations of the synthesized peptide RGDSY-CTTHWGFTLC (RGDSY-CTT), the positive control peptide CTTHWGFTLC (CTT), or the negative control peptide STTHWGFTLS (STT) in fibronectin-coated 96-well plates for different time lengths, and the changes in cell adhesion, invasiveness, proliferation, apoptosis and cell cycle were detected using Transwell chamber assay, MTT assay, and flow cytometry.</p><p><b>RESULTS</b>Incubation of the cells with 50, 100 and 200 µg/ml of RGDSY-CTT caused a significant concentration- dependent inhibition of the cell adhesion (cell adhesion rates of 85.1%, 74.1% and 63.8%, respectively) with stronger effects than CTT (P<0.05). At 100 and 200 µg/ml, RGDSY-CTT significantly inhibited the invasion (with inhibition rate of 41.8% and 63.9%, respectively) of MCF-7 cells with an effect similar to that by CTT (P>0.05). At 50, 100 and 200 µg/ml, RGDSY-CTT concentration-dependently suppressed MCF-7 cell proliferation (with cell proliferation rates of 98.8%, 82.4% and 63.0%, respectively), and this inhibitory effect was stronger than that of CTT at 100 and 200 µg/ml (P<0.05). The results of flow cytometry also demonstrated a stronger apoptosis-inducing effect of RGDSY-CTT (76.7%) than that in CTT, STT and the blank control groups (P<0.05).</p><p><b>CONCLUSIONS</b>RGDSY-CTT can inhibit cell invasion, suppress adhesion and proliferation, and induce apoptosis in MCF-7 cells.</p>
Subject(s)
Female , Humans , Apoptosis , Cell Adhesion , Cell Proliferation , MCF-7 Cells , Peptides, Cyclic , PharmacologyABSTRACT
Purpose To investigate the relationship between the expression of Syk,VEGF-C and lymph node metastasis in breast carcinoma.Methods Immunohistochemical EnVision and SP methods were used to detect the expression of Syk,NFκB(p65)and VEGF-C in 55 cases of breast carcinoma.Results The positive rates of Syk, VEGF-C and NFκB(p65)in 55 cases of breast carcinoma were 50.9%,56.4% and 81.8%,respectively.Lower positive rate of Syk was obtained in the group of positive lymph-node metastasis than that in the group of non-lymph-node metastasis (P0.75).Higher positive rate of p65 nuclear expression was obtained in the group of positive lymph-node metastasis than that in the group of non-lymph-node metastasis (P＜0.025).The expression of Syk was negatively associated with VEGF-C (r=-0.620,P=0.000);the nuclear expression of p65 was associated with the low expression of Syk(r=0.448,P=0.002)and the high expression of VEGF-C (r=0.310,P=0.036).Conclusions In breast carcinoma, Syk may downregulate the expression of VEGF-C by inhibiting the activation of NFκB, which suppresses the lymph node metastasis of the cancer.