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Objective To investigate the effect of piR-9994 on the biological behavior of gastric cancer cells and its possible mechanism. Methods The expression of piR-9994 in gastric cancer cell lines (MGC803 and AGS) and normal gastric epithelial cells (GES-1) were detected by qRT-PCR. MGC803 cell line with piR-9994 overexpression and knockdown were constructed. The effects of piR-9994 expression changes on cell proliferation were detected by MTT and clone formation assay. The scratch wound healing assay and Transwell invasion assay were used to detect cell migration and invasion abilities. qRT-PCR and Western blot were used to detect cell proliferation and EMT-related genes expression. Results The expression level of piR-9994 in MGC803 cells was significantly higher than that in normal gastric epithelial cell line GES-1 (P < 0.05). The overexpression of piR-9994 promoted the proliferation, invasion and metastasis of gastric cancer cells, while piR-9994 knockdown had the opposite effect. piR-9994 expression was closely related to cell cycle, especially in S phase. The overexpression of piR-9994 promoted the expression of proliferation-related genes PCNA, CCND1 and Bcl-2, inhibited the expression of apoptosis gene C-PARP, and promoted the expression of EMT-related genes N-cadherin, MMP7, Twist and Vimentin; while piR-9994 knockdown had the opposite effect. Conclusion Abnormal expression of piR-9994 affects the proliferation, invasion, metastasis and EMT process of gastric cancer cells. piR-9994 may be a new biomarker and therapeutic target for gastric cancer.

Objective To explore the expression of circ_0006692 in NSCLC and its relation with clinicopathological characteristics and related mechanism. Methods We collected 50 pairs of NSCLC tissues and adjacent tissues. The expression of circ_0006692 was detected by qRT-PCR and its relation with clinicopathological features was analyzed. We constructed lung cancer A549 cell line with circ_0006692 overexpression and knockdown. Cell proliferation, migration and invasion were detected by MTS, colony forming, wound healing and Transwell invasion assays. qRT-PCR and Western blot were used to detect the effect of circ_0006692 expression change on EMT-related gene expression. Results The expression of circ_0006692 in NSCLC was significantly higher than that in adjacent tissues (P < 0.05). The expression level of circ_0006692 was closely related to tumor size, TNM stage and pulmonary membrane invasion (P < 0.05). circ_0006692 knockdown inhibited cell proliferation, invasion and metastasis, while its overexpression promoted cell proliferation, invasion and metastasis. circ_0006692 knockdown inhibited the expression of EMT-related genes CDH2 and MMP7 in A549 cells and promoted the expression of CDH1. Conclusion The upregulated expression of circ_0006692 in NSCLC is closely related to tumor size, TNM stage and pulmonary membrane invasion. circ_0006692 expression could regulate the proliferation, invasion, metastasis and EMT progression of lung cancer A549 cells.

Objective To investigate the expression of ARL4C in NSCLC and its correlation with clinicopathological features, as well as its role in EGFR-TKI resistance. Methods We collected the tumor and adjacent tissues of 63 NSCLC patients. The mRNA expression of ARL4C was detected by qRT-PCR and the relation between ARL4C and clinicopathological features was analyzed. The expressions of ARL4C in TKI-resistant cell line, control cell line and ARL4C overexpressing cell line were assessed by qRT-PCR and Western blot. The changes of cell activity and IC50 were detected by MTS. Transwell invasion assay was used to detect the effect of ARL4C expression on cell invasion. Results The expression level of ARL4C in NSCLC tissues was lower than that in adjacent tissues (P < 0.05). The expression of ARL4C in NSCLC was closely related to lymph node metastasis, TNM stage and pulmonary membrane invasion (P < 0.05). Compared with control cell line HCC827, the expression levels of ARL4C mRNA and protein in TKI-resistant cell line HCC827/ER and the IC50 of ARL4C overexpressing TKI-resistant cell line HCC827/ER/ARL4C-OE were significantly lower (P < 0.05). Transwell assay results showed that the overexpression of ARL4C inhibited the invasion of lung cancer cell line (P < 0.05). Conclusion The abnormal expression of ARL4C is closely related to lymph node metastasis, TNM stage and pulmonary membrane invasion of NSCLC. Overexpression of ARL4C may improve the sensitivity of NSCLC cells to EGFR-TKI and inhibit the invasion of NSCLC cells.