miR-650 Promotes the Metastasis and Epithelial-Mesenchymal Transition of Hepatocellular Carcinoma by Directly Inhibiting LATS2 Expression.

Background/aims: Previous studies have confirmed that microRNAs are involved in the metastasis and epithelial-mesenchymal transition (EMT) of malignancies. In this study, we examined whether miR-650 promotes the migration, invasion, and EMT of hepatocellular carcinoma (HCC) cells by targeting the large tumor suppressor kinase 2 gene (LATS2).

Methods: qRT-PCR was used to detect expression of miR-650 in HCC tissues and paired normal tissues.

miR-103 promotes the metastasis and EMT of hepatocellular carcinoma by directly inhibiting LATS2.

Improving the long‑term survival of patients with hepatocellular carcinoma (HCC) remains a challenge due to metastasis and recurrence. In this study, we demonstrate that the overexpression of miR‑103 in HCC cells promotes epithelial‑mesenchymal transition (EMT), and is associated with an enhanced metastasis and poor outcomes, as shown by western blot analysis and immunohistochemistry. Mechanistically, using reporter luciferase assay we reveal that the serine/threonine‑protein kinase, large tumor suppressor kinase 2 (LATS2), a key component of the Hippo signaling pathway, is a direct target of miR‑103 in HCC cells.

MiR-195 suppresses the metastasis and epithelial-mesenchymal transition of hepatocellular carcinoma by inhibiting YAP.

MiR-195, a novel cancer-related microRNA, was previously reported to play an important role in many malignancies. This study aimed to investigate the role of miR-195 mediated epithelial-mesenchymal transition (EMT) and the progression of hepatocellular carcinoma (HCC) as well as the underlying mechanisms. Our result demonstrated that miR-195 were significantly down regulated in HCC and its decreased expression is associated with poor clinical features of HCC patients.

Potential rat model of anxiety-like gastric hypersensitivity induced by sequential stress.

Aim: To establish a rat model of anxiety-like gastric hypersensitivity (GHS) of functional dyspepsia (FD) induced by novel sequential stress.

Methods: Animal pups were divided into two groups from postnatal day 2: controls and the sequential-stress-treated. The sequential-stress-treated group received maternal separation and acute gastric irritation early in life and restraint stress in adulthood; controls were reared undisturbed with their mothers.

Apoptotic pathway induced by diallyl trisulfide in pancreatic cancer cells.

Aim: To investigate the effects of diallyl trisulfide (DATS), a garlic-derived organosulfur compound, in pancreatic cancer cells.

Methods: Human pancreatic cancer cells with wild-type p53 gene (Capan-2) and normal pancreatic epithelial cells (H6C7) were cultured in RPMI1640. DATS was prepared at a concentration of 100 μmol/L.

[In vitro anti-myeloma effects induced by myeloma idiotype-protein pulsed dendritic cell vaccine].

Objective: To investigate the specific antitumor immune response induced by idiotype protein (Id)-pulsed dendritic cells (DC) in vitro.

Methods: DC was generated from peripheral blood monocytes of the multiple myeloma (MM) patients using GM-CSF, IL-4, and TNF-alpha. The DCs were pulsed with idiotypic fragment, the F(ab')2 fragment of M protein from MM patient at the immature stage.

[Induction of active antitumor immune response by myeloma idiotype protein-pulsed dendritic cells].

Background & Objective: Most multiple myeloma (MM) patients could not be cured by high-dose chemotherapy and bone marrow transplantation. This study was designed to investigate in vitro killing effect of tumor-specific cytotoxic T lymphocytes (CTLs) stimulated by idiotype protein (Id)-pulsed dendritic cells (DCs) on autologous MM cells.

Methods: DCs were generated from peripheral blood monocytes of 6 MM patients using interleukin-4 (IL-4) and granulocyte-macrophage colony-stimulating factor (GM-CSF).