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Background: Hepatic cancer is the most common primary liver malignancy, with high incidence and mortality worldwide. Atractylon is an active constituent isolated from Atractylodes lancea (Thunb.) DC. and Atractylodes chinensis (DC.) Koidz., which proved to have multiple activities. Methods: In this study, we evaluated the antihepatic cancer (HCC) effect of atractylon in vitro and in vivo and investigated its underlying mechanism. Cell proliferation, colony formation, cell apoptosis, migration and invaison and was identified by MTT, crystal violet staining, flow cytometry analysis, and Transwell assay. The ∆Ψm of HepG2 and MHCC97H cells were detected by Rhodamine 123. The ROS level was determined by 2,7-Dichlorodi-hydrofluorescein diacetate (DCFH-DA) method. Protein expression was identified by Western blot analysis. The anti-HCC effect of atractylon in vivo was evaluated by a subcutaneous tumor model. Results: The results suggested that atractylon significantly inhibits the proliferation and promotes apoptosis of hepatic cancer cell lines, including HepG2, SMCC7721, and MHCC97H. Moreover, the results showed that atractylon reduces the mitochondrial membrane potential (∆Ψm), increases ROS level, inhibits the expression of Bcl-2, and promotes the expression of Bax and cleaved caspase-3, indicating that atractylon induces HCC apoptosis through the mitochondrial apoptotic pathway. Our results also demonstrated that atractylon inhibits migration and invasion of hepatic cancer cells by inhibiting the epithelial-mesenchymal transition (EMT) process and downregulating MMP-2 and MMP-9 expression. In addition, atractylon inhibited the growth of hepatic cancer and showed an inhibition effect on EMT process in vivo. Conclusion: In all, this study suggested that atractylon showed a promising anti-HCC effect with inhibiting proliferation, inducing apoptosis, and blocking invasion in vitro and inhibiting growth in vivo.

Sepsis is considered to be a systemic inflammatory response, which results in organ dysfunction. LncRNA nuclear-enriched abundant transcript 1 (NEAT1) involved in sepsis progression has been reported. However, the underlying mechanism of NEAT1 in sepsis-induced inflammatory response remains to be revealed. In this study, NEAT1 and POU domain class 2 transcription factor 1 (POU2F1) were highly expressed in LPS-induced septic RAW264.7 cells, opposite to miR-31-5p expression. Furthermore, we found that NEAT1 silencing inhibited LPS-induced inflammatory response and cell proliferation, and promoted cell apoptosis. Subsequently, we found that miR-31-5p interacted with NEAT1 and targeted the 3′UTR of POU2F1, and in LPS-induced RAW264.7 cells, the inhibition of NEAT1 silencing was reversed by miR-31-5p knockdown, while POU2F1 downregulation could cover the functions of miR-31-5p knockdown. In a word, this study indicates that NEAT1 inhibits the LPS-induced progression of sepsis in RAW264.7 cells by modulating miR-31-5p/POU2F1 axis, suggesting that NEAT1 will be the potential therapeutic target for sepsis.

Background: Exosomes are well-known natural nanovesicles, that represent one of the recently discovered modes of intercellular communication due to their ability to transmit cellular components. Exosomes have been reported to have potential as natural vectors for carrying functional small RNAs and delivering chemotherapeutic agents to diseased cells. In this study, we aimed to investigate the role of exosomes in carrying miRNA for targeting tumor cells.Methods: We present a novel method for engineering exosomes with functional miR-317b-5b to target tumor cells. MiR-317b-5b exerts its anti-tumor function via its expression in tumors. RT-qPCR was performed to assess the levels of miR-371b-5p, FUT-4. Western blot was performed to measure the levels of CD9, CD81, and FUT-4 proteins. Confocal microscopy was used to observe the internalization of miR-317b-5b in tumor cells. CCK-8, EdU, flow cytometry, wound-healing migration and transwell assays were performed to evaluate cell viability, proliferation, migration, and invasion, respectively.Results: Our findings illustrated that miR-317b-5b-loaded engineered exosomes were internalized by tumor cells. MiR-317b-5b was overexpressed in tumor cells treated with miR-317b-5b-loaded engineered exosomes. The internalization of miR-317b-5b in tumor cells was accompanied by changes of cell viability, proliferation, apoptosis, and migratory and invasive capability. We found that miR-317b-5b-loaded engineered exosomes were presence in tumor tissue sections and miR-317b-5b was overexpressed in tumor tissues of osteosarcoma tumor-bearing mice infected with miR-317b-5b-loaded engineered exosomes. MiR-317b-5b-loaded engineered exosomes had the anti-tumor efficiency in vivo.Conclusion: Our findings show that miR-317b-5b-loaded engineered exosomes can be used as nanocarriers to deliver drug molecules such as miR-317b-5b both in vitro and in vivo to exert its anti-tumor functions.

Krüppel-like factor 8 (KLF8) plays a key role in cancer progression. However, its expression pattern and relationship with clinicopathological characteristics in non-small cell lung cancer (NSCLC) has not been completely elucidated. The study aimed to investigate the expression of KLF8 and its correlation with clinical pathologic features in NSCLC and to explore the potential mechanism. The expression of KLF8 in NSCLC was detected by RT-PCR, Western blot and immunohistochemistry. The expression of Vimentin and E-cadherin, epithelial-mesenchymal transition (EMT) markers, were detected by immunohistochemistry in the NSCLC. The relationship between KLF8 expression and various clinicopathological features or EMT markers was investigated. The results showed m-RNA and protein of KLF8 were overexpressed in NSCLC and the percent of KLF8 positive cells was positively correlated with TNM stage, lymph node metastasis and poor overall survive. Moreover, high expression of KLF8 correlated with E-cadherin low expression, and Vimentin overexpression. Additionally, COX multivariate regression analysis suggested that TNM stage, KLF8, E-cadherin and Vimentin were independent prognostic indicators for overall survival of patients with NSCLC. The data demonstrate that KLF8 is overexpressed in NSCLC. KLF8 overexpression promotes the malignancy of NSCLC, which mechanism may be involved in EMT. KLF8 maybe serve as a potential therapeutic target for NSCLC.