Objective To investigate the impact of YTH N6 methyladenosine RNA binding protein 3 (YTHDF3) on the proliferation, migration, and apoptosis of human colorectal cancer cell line HCT-116. Methods The cells were divided into a negative control group, interference groups 1, 2, and 3. Small interfering RNA targeting YTHDF3 was transfected into colorectal cancer cells HCT-116. The expression of YTHDF3 in each group was assessed using qRT-PCR and Western blot analysis. Cell proliferation was evaluated using CCK-8 assay and plate cloning assay, while cell migration was assessed using transwell assay and scratch assay. Flow cytometry was used to measure cell apoptosis. Results The silencing efficiency of HCT-116 cells was validated through qRT-PCR and Western blot analysis. Transfection of small interfering YTHDF3 effectively reduced the expression of YTHDF3 in HCT-116 cells compared to the negative control group. Silencing YTHDF3 can significantly inhibited cell proliferation and migration while promoting apoptosis in HCT-116 cells. Conclusion Silencing YTHDF3 can decelerates cell proliferation and migration while enhancing apoptosis in HCT-116 cells.

Objective To investigate the expression of IFITM1 in colon cancer and the mechanism of its promotion of colon cancer cell proliferation. Methods The expression and prognosis of IFITM1 in colorectal cancer were analyzed by bioinformatics, and the correlation between IFITM1 and β-catenin was researched. Immunohistochemical SP staining was examined to observe the expression of IFITM1 and β-catenin in colon cancer tissues. The overexpressed cell model of IFITM1 was constructed, the changes of cell proliferation capacity were detected by CCK-8 assay, and the changes of TCF/LEF transcription factor activity were tested by dual luciferase reporter gene. The results of dual luciferase reporter gene showed that the promoter activity of OE-IFITM1 group was higher than that of OE-NC group (P<0.05), and there was no difference between OE-NC group and MOCK group (P>0.05). The expressions of key proteins β-catenin, C-myc and CyclinD1 in the Wnt/β-catenin signaling pathway were detected by Western blot. Results The results of online database analysis showed that IFITM1 was highly expressed in colon cancer (P<0.05), and significantly correlated with poor prognosis. There was positive correlation between IFITM1 and β-catenin. Immunohistochemical results showed that the expression level of IFITM1 was correlated with tumor diameter and tissue invasion degree (P<0.05), ranther than others factors(P>0.05). The expression of β-catenin was only correlated with tumor diameter(P<0.05), instead of other factors(P>0.05), and there was a positive correlation between IFITM1 and β-catenin. After overexpression of IFITM1 in HCT-15 colon cancer cells, the proliferation capacity of OE-IFITM1 group was significantly higher than that of OE-NC group (P<0.05), but there was no difference between OE-NC group and MOCK group (P>0.05). Western blot results showed that the expression levels of β-catenin, CyclinD1 and C-myc in OE-IFITM1 group were higher than those in OE-NC group (P<0.05), but there was no difference in protein expression between OE-NC group and MOCK group (P>0.05). Conclusion The expression of IFITM1 in colon cancer tissues is significantly higher than that in para-cancer tissues, and IFITM1 may promote cell proliferation through Wnt/β-catenin signaling pathway.

Objective To investigate the differential expression of microRNAs (miRNAs) in multiple myeloma (MM) and analyze the expression of hsa-miR-3937 in patients' peripheral blood and its potential clinical utility. Methods In this study, differential miRNAs expression in MM patients' plasma was screened using an open dataset from the GEO database and validated by real-time fluorescence quantitative PCR for differences in miRNAs expression between MM patients' plasma and healthy controls. Sensitivity and specificity of hsa-miR-3937 in MM diagnosis were analyzed using the subjects' working characteristic curve (ROC) and the association of hsa-miR-3937 in MM patient plasma with various clinical indicators was analyzed by Spearman method to evaluate its potential clinical utility. Results Expression of hsa-miR-3937 significantly upregulated in MM patients compared to healthy controls (P<0.01). The area under the ROC curve of hsa-miR-3937 showed high sensitivity and specificity in the diagnosis of MM. We also found that the expression of hsa-miR-3937 was highly correlated with the expression of serum M protein and bone marrow plasma cell, which is expected to be a potential novel biomarker for the diagnosis of MM patients. Conclusion The experimental data show that hsa-miR-3937 is highly specific in the plasma of MM patients, which has high sensitivity and specificity as a new clinical diagnostic marker, and is expected to become a potential new clinical diagnostic molecular marker.

Objective To study the effect of lncRNA-AK093407 (AK093407 for short) on colorectal cancer HCT-15 cells and related mechanisms. Methods Lv5 lentivirus overexpressed AK093047, and transfected siRNA to silence AK093407; qRT-PCR was used to identify the expression of AK093407; MTT and plate colony formation assays were used to detect cell proliferation; flow cytometry was used to detect cell cycle and apoptosis; wound healing assay and transwell was used to detect cell invasion and migration; qRT-PCR and Western blot were used to detect the expression of EMT-related factors. Results The expression of AK093407 increased after Lv5 lentivirus infection. Overexpression of AK093407 in colorectal cancer cells increased proliferation activity, promoted cell cycle evolution, decreased apoptosis, and enhanced migration and invasion ability. The results of qRT-PCR and Western blotting showed that the transcription and translation levels of occludin and E-cadherin were decreased (P<0.05), while β-catenin, vimentin and fibronectin were increased (P<0.05). After the AK093407 gene was silenced, the above results were opposite. Conclusion AK093407 promotes colorectal cancer cell proliferation, cell cycle, invasion and migration and inhibits apoptosis via promoting EMT.

Objective To study the effects of PU-H71 on the proliferation, apoptosis, cycle and other biological behaviors of colorectal cancer HCT-15 cells, and to explore the mechanism of apoptosis and cycle at the molecular level. Methods HCT-15 cells were cultured in vitro. The effects of PU-H71 at different time and concentration on the proliferation of HCT-15 cells were examined by MTT assay. The apoptosis and cell cycle of HCT-15 cells were examined by flow cytometry assay, western blot was used to detect the expression of apoptosis and cycle-related factors. Results After 24h and 48h treatment, PU-H71 showed significant inhibitory effect on colorectal cancer HCT-15 cells in time and concentration dependent manner. After treatment with PU-H71 at two concentrations of 50μg/L and 75μg/L without drug for 24h, the apoptosis rate of HCT-15 cells increased and the proportion of G2 phase cells increased. The protein expression levels of STAT3 and JAK2 were significantly decreased, the protein expression levels of CyclinD1 and Bcl-2 were decreased, and the protein expression levels of Cytc, Caspase9, Caspase3, and Bax were up-regulated. Conclusion PU-H71 can significantly inhibit the proliferation of colorectal cancer HCT-15 cells, arrest the cell cycle in G2 phase and induce cell apoptosis. PU-H71 may regulate the mitochondrial signaling pathway by negatively regulating the JAK-STAT3 pathway, thus affecting the expression of apoptosis and cyclic-related factors.