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OBJECTIVE: To detect the expression of PD-L1 and K-ras gene status in colorectal cancer tissues and analyze the relationship between PD-L1 expression and the clinicopathological features and K-ras gene status in colorectal cancer. METHODS: Two hundred fifty colorectal cancer tissues were collected from the First Affiliated Hospital of Nanchang University. The normal intestinal mucosal tissues of 20 patients were randomly selected for inclusion in the control group. PD-L1 expression was detected by immunohistochemistry. K-ras gene mutation in colorectal cancer tissues was detected by sequencing. The clinical significance of PD-L1 expression and relationship between PD-L1 expression and K-ras gene mutation were analyzed. RESULTS: The immunohistochemistry assay showed that PD-L1 was highly expressed in colorectal cancer. The positive expression of PD-L1 was increased with lymph node metastasis and high TNM stage. The 5-year survival rate of PD-L1-positive patients was significantly lower than that of PD-L1-negative patients. The K-ras gene mutation rate was 35.6%, and the main mutation site was in codon 12. The positive PD-L1 expression rate in patients with K-ras gene mutations was significantly higher than that in patients with wild-type K-ras gene mutations. CONCLUSION: PD-L1 is highly expressed in colorectal cancer, and its expression is related to metastasis and tumor stage. PD-L1 expression is closely related to K-ras gene mutation, and the K-ras gene status may affect PD-L1 expression. TRIAL REGISTRATION: retrospectively registered.
RESUMO
OBJECTIVE: To investigate the effects of lanthanum chloride on proliferation and migration activity of human cervical cancer cells in vitro which may be a new anti-cervical cancer drug and provide experimental data for cervical cancer treatment. METHODS: HeLa cells cultured in vitro were divided into two groups: experimental group and control group. In experimental group, the cells were respectively treated with lanthanum chloride at different concentrations, 5, 50 and 100 µmol/L, while the cells in the control group were not treated with lanthanum chloride. The cell growth was observed by inverted microscope and the morphology changes of the cells were observed by the laser scanning confocal microscope (LSCM). Proliferation of HeLa cells in the two groups was detected by methyl thiazolyl tetrazolium (MTT) test; apoptosis rate was analyzed by flow cytometry (FCM). Cell migration test was applied to observe the effect of lanthanum chloride on migration. Reverse transcription (RT)-PCR was employed to evaluate the effects of lanthanum chloride on proliferation gene (cyclinD1), anti-apoptosis gene (zinc finger protein A20) and migration-related gene (matrix metalloproteinase 9, MMP-9). RESULTS: The status of cell growth was observed under the inverted microscope: with the increased of the lanthanum chloride concentrations, the cell density of reduced, the granule in cytoplasm increased, color intensifying and intercellular space enlarged; some cells became rounding and dead, floating in the culture media; the exfoliated cells increased gradually in the experimental groups. While In the control group, the cells grew adherently, with clear morphology and plump cytoplasm, and adjacent cell grew in lamellar. Observed with LSCM: the nuclear chromatin condensated and marginated with the volume of nuclear decreased in experimental groups. With the increase of the lanthanum chloride concentrations, nuclei in the experimental groups became pyknotic and then underwent karyorrhexis. However, the nuclear of the cells in control group were inact. The growth inhibition rates of lanthanum chloride groups (5, 50, 100 µmol/L) were 24%, 51% and 78%, respectively, in which each was significantly higher than that of the control group (P < 0.05); the apoptosis rates of lanthanum chloride group were (4.91 ± 0.39)%, (7.30 ± 0.71)% and (13.48 ± 0.92)%, respectively, which were all significantly higher than that of the control group [(0.89 ± 0.11)%, P < 0.01]. The migration ability of the cells was also decreased by the treatment of lanthanum chloride, the number of migrated cells in lanthanum chloride groups were 22.2 ± 4.3, 12.0 ± 3.2 and 7.8 ± 2.6 respectively, which were all significantly lower than that of the control group (41.2 ± 5.4, P < 0.01). The expression of genes of cyclinD1, A20 and MMP-9, were all decreased by the treatment of lanthanum chloride in a dose-dependent manner. CONCLUSION: Lanthanum chloride can inhibit the proliferation and migration of cervical cancer cells, and induce apoptosis by down-regulating cyclinD1, A20, and MMP-9 expressions in vitro.