Inhibition of proteinase-activated receptor 2 (PAR2) decreased the malignant progression of lung cancer cells and increased the sensitivity to chemotherapy.

OBJECTIVES: This study aimed to study the effect of protease-activated receptor 2 (PAR2) on the proliferation, invasion, and clone formation of lung cancer cells. It also aimed to evaluate the inhibitory effect of melittin on PAR2 and the anti-lung cancer effect of melittin combined with gefitinib. METHODS: The correlation between the co-expression of PAR2 and epithelial-mesenchymal transition (EMT) markers was analyzed. PAR2 in A549 and NCI-H1299 cells was knocked down using siRNA. MTT assay, Transwell assay, and colony formation assay were used to detect the effects of PAR2 on cell proliferation, invasion, and clone formation. The anti-cancer effect of PAR2 knockdown on gefitinib treatment was analyzed. The synergistic effect of melittin on gefitinib treatment by inhibiting PAR2 and the underlying molecular mechanism were further analyzed and tested. RESULTS: The expression of PAR2 was upregulated in lung cancer, which was associated with the poor prognosis of lung cancer. PAR2 knockdown inhibited the stemness and EMT of lung cancer cells. It also inhibited the proliferation, invasion, and colony formation of A549 and NCI-H1299 cells. Moreover, PAR2 knockdown increased the chemotherapeutic sensitivity of gefitinib in lung cancer. Melittin inhibited PAR2 and the malignant progression of lung cancer cells. Melittin increased the chemotherapeutic sensitivity of gefitinib in lung cancer by inhibiting PAR2. CONCLUSION: PAR2 may promote the proliferation, invasion, and colony formation of lung cancer cells by promoting EMT. Patients with a high expression of PAR2 have a poor prognosis. Inhibition of PAR2 increased the chemotherapeutic sensitivity of gefitinib. PAR2 may be a potential therapeutic target and diagnostic marker for lung cancer.

Hesperidin Inhibits the p53-MDMXInteraction-Induced Apoptosis of Non-Small-Cell Lung Cancer and Enhances the Antitumor Effect of Carboplatin.

Objective: This study aimed to observe the effect of hesperidin on the apoptosis, proliferation, and invasion of non-small-cell lung cancer, as well as to explore the possible mechanism. The inhibitory effect of hesperidin combined with carboplatin on non-small-cell lung cancer was also investigated. Methods: A549 and NCI-H460 cells were treated with different concentrations of hesperidin (10, 50, and 100 µM). The effect of siRNA knockdown on MDMX on the antitumor effect of hesperidin was observed. CCK-8 was used to detect cell activity. The apoptosis rate was determined by TUNEL. The transwell assay detects the ability of cell migration and invasion. The expression levels of the apoptosis-related proteins p53, MDM2, MDMX, p21, PUMA, Bcl-2, and Bax were detected by qRT-PCR. Cell-proliferation and transwell assays were used to detect the effects of the combined use of hesperidin and carboplatin on lung cancer cells. Results: Hesperidin significantly inhibited the activity and invasion of A549 and NCI-H460 cells in a dose-dependent manner. Hesperidin also induced the apoptosis of A549 and NCI-H460 cells. Hesperidin further inhibited the interaction between p53 and MDMX, increased the expression of p53, and played an anticancer role. The combination of hesperidin and carboplatin showed the most obvious antitumor effect. Conclusion: Hesperidin can inhibit lung cancer by inhibiting the interaction between p53 and MDMX. Moreover, the combination of hesperidin and carboplatin can inhibit the migration and invasion of lung cancer cell lines through p53 upregulation, thereby increasing the antitumor effect of carboplatin.

[SUDHL-4 cell culture in vitro and establishment of mouse tumor model].

This study was designed to investigate the biological and immunological characteristics of a human diffuse large B-cell lymphoma (DLBCL) cell line SUDHL-4, and to establish a mouse model for human DLBCL. SUDHL-4 cells were cultured under different conditions. The morphology and in vitro expression of B-cell and tumor-related markers were detected by microscopy and flow cytometry respectively. To establish the transplanted tumor, the cells were injected subcutaneously into SCID mice. Tumor formation and its histomorphology were analyzed. The results showed that the expression of B cell/tumor-related markers was found on cultured SUDHL-4 cells. A stable mouse model of human DLBCL was successfully established in SCID mice by subcutaneous injection of 10(7) SUDHL-4 cells. Tumor tissue from mice exhibited similar histologic manifestation to those of human DLBCL. It is concluded that the SUDHL-4 cells represent a high consistency in immunological characteristics with human DLBCL. Transplantation of SUDHL-4 cells provides a syngeneic mouse model for the study of human DLBCL.

[Research progress on antimicrobial peptides against malaria parasite].

Antimicrobial peptides have broad-spectrum antibacterial activity and high thermal stability. Researches prove that they can inhibit the development of Plasmodium or kill them. The paper focuses on research advances in their biological characteristics, natural or synthetic peptides as potential anti-Plasmodium agents in malaria research.