Background: Colorectal cancer (CRC) is a leading cause of cancer-related death worldwide. P21-activated kinase 4 (PAK4) and miR-9-5p have emerged as attractive therapeutic targets in several tumor types, but in CRC, the regulation of their biological function and their target association remain unclear. Methods: The expression of PAK4 in CRC tissues was determined using quantitative real-time PCR and immunohistochemistry analyses. The targeted regulation between miR-9-5p and PAK4 was predicted and confirmed with bioinformatics analysis and the dual-luciferase reporter assay. Functional experiments, including the MTT assay and flow cytometry, were performed to investigate the impact of PAK4 knockdown and miR-9-5p overexpression on cell proliferation and apoptosis in CRC cells. Results: We found that the expression of PAK4 was upregulated in CRC tissues. PAK4 knockdown significantly suppressed cell proliferation and promoted apoptosis in cells of the CRC cell lines HCT116 and SW1116. We also found that miR-9-5p directly targeted the 3′-UTR of PAK4 mRNA and negatively regulated its expression. The degree of downregulation of miR-9-5p inversely correlated with PAK4 expression. Intriguingly, enforced expression of miR-9-5p suppressed cell proliferation and promoted apoptosis. This could be partially reversed by PAK4 overexpression. Conclusion: These results suggest that miR-9-5p targeting of PAK4 could have therapeutic potential for CRC treatment.

AimIn the current work, we aimed to explore whether Cancer‐associated fibroblasts (CAF) exosomes played crucial roles in vulvar squamous cell carcinoma (VSCC) chemoresistance via mediating long noncoding RNAs (lncRNA).MethodsThe IC50 value and cell apoptosis were assessed by the Cell Counting‐8 Kit (CCK‐8) assay and flow cytometry, respectively. Western blot analysis was used for the measurement of protein levels. The levels of urothelial cancer‐associated 1 (UCA1), miR‐103a and WEE1 G2 checkpoint kinase (WEE1) mRNA were detected by quantitative real‐time polymerase chain reaction (qRT‐PCR). The target relationships among miR‐103a, UCA1 and WEE1 were confirmed by dual‐luciferase reporter assays. Xenograft model mice were established to observe the impact of exosomal UCA1 on cisplatin (CDDP) resistance in vivo.ResultsOur data indicated that CAF enhanced CDDP resistance of VSCC cells in vitro. Extracellular UCA1 was transferred by exosomes derived from CAF. Exosomal UCA1 derived from CAF conferred VSCC cell resistance to CDDP. Moreover, UCA1 functioned as a miR‐103a sponge in VSCC cells. The promotion of exosomal UCA1 on VSCC cell resistance to CDDP was mediated by miR‐103a. WEE1 was a direct target of miR‐103a, and exosomal miR‐103a from CAF weakened CDDP resistance of VSCC cells by WEE1. Furthermore, exosomal UCA1 regulated WEE1 expression through sponging miR‐103a. Additionally, exosomal UCA1 enhanced tumor growth and CDDP resistance in vivo.ConclusionOur findings suggested exosomal UCA1 derived from CAF conferred VSCC cell resistance to CDDP in vitro and in vivo at least partly through the miR‐103a/WEE1 axis, highlighting a novel therapeutic method for improving the clinical benefits of CDDP chemotherapy in VSCC patients.

The control of financial risk has always been one of the important topics in financial research. Based on the theory of finance, this paper proposes a kind of financial risk dynamic system. By analyzing some properties of the dynamic system, the system shows obvious coexisting chaotic oscillations. In order to control the financial risk dynamic system effectively, this paper proposes a finite-time impulse controller to control the financial risk dynamic system. Simulation results show that the finite-time impulse controller has faster convergence speed than the impulse controller.

Objective. Creatine kinase (CK), cathepsin D (CTSD), Ki67, and tumour protein 63 (p63) have been proven to participate in the growth of some cancers. However, available literature suggested paucity of data on their involvement in oesophageal squamous-cell carcinoma (ESCC) development. Methods. We ascertained the presence of CK, CTSD, Ki67, and p63 expressions in ESCC to demonstrate the association between differentiation of ESCC and expressions of the abovementioned proteins. We collected related information on 48 patients prior to their division into well and poor differentiation groups, which were analysed retrospectively. Positive rates of protein expression were evaluated via immunohistochemistry. The proteins that were expressed positively in all the cases were selected. Comparison of the proteins within two groups was done to analyse the correlation between tumour differentiation and their expression. Results. We observed that CTSD, p63, and Ki67 were significantly and highly expressed in poorly differentiated patients with ESCC. Conclusions. This finding may suggest that the proteins were involved in ESCC progression, which may evidentially serve as potential markers of early identification and risk assessment of ESCC.

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