Feedstock chemical dichloromethane as the C1 source for the chemoselective multicomponent synthesis of valuable 1,4,2-dioxazoles.

The development of mild and practical strategies to produce value-added fine chemicals directly from inexpensive and readily available commodity chemicals is actively pursued by chemists. However, the application of feedstock chemical dichloromethane (DCM) as the C1 source in organic synthesis is still in its infancy. Herein, we describe a multicomponent strategy for the chemoselective synthesis of valuable 1,4,2-dioxazoles by using DCM as a C1 source.

Epoxidized Soybean-Oils-Based Pressure-Sensitive Adhesives with Di-Hydroxylated Soybean-Oils Copolymerizing and Antioxidant Grafting.

Vegetable-oils-based pressure-sensitive adhesives (PSAs) are being developed as a substitute for petrochemical-based PSAs for application in daily life. However, vegetable-oils-based PSAs face the problems of unsatisfactory binding strengths and easy aging. In this work, the grafting of antioxidants (tea polyphenol palmitates, caffeic acid, ferulic acid, gallic acid, butylated hydroxytoluene, tertiary butylhydroquinone, butylated hydroxyanisole, propyl gallate (PG), tea polyphenols) was introduced into an epoxidized soybean oils (ESO)/di-hydroxylated soybean oils (DSO)-based PSA system to improve the binding strengths and aging-resistant properties.

In Situ Hypoiodite-Catalyzed Oxidative Rearrangement of Chalcones: Scope and Mechanistic Investigation.

It is highly desirable to avoid using rare or toxic metals for oxidative reactions in the synthesis of pharmaceuticals and fine chemicals. Hypervalent iodine compounds are environmentally benign alternatives, but their catalytic use has been quite limited. Herein, the protocol for in situ hypoiodite-catalyzed oxidative rearrangement of chalcones is first realized under mild and metal-free conditions, which provided a nontoxic, environmental-benign, and catalytic alternative to the thallium-based protocol.

CD47 blockade alleviates acute rejection of allogeneic mouse liver transplantation by reducing ischemia/reperfusion injury.

Despite advances in immunosuppressive therapies, acute rejection response is still a serious concern especially in the early phase after liver transplantation. This study aimed to evaluate whether blocking the TSP1-CD47 signaling pathway could attenuate the acute rejection after liver transplantation. An allogeneic mouse orthotopic liver transplantation model (Balb/c→C3H) with prolonged cold ischemic phase was used to induce severe IRI and lethal acute rejection.

miR-302a inhibits human HepG2 and SMMC-7721 cells proliferation and promotes apoptosis by targeting MAP3K2 and PBX3.

Hepatocellular carcinoma (HCC) is the most common liver cancer and has a poor prognosis. miR-302a is an important regulator of tumor occurrence and deterioration, while MAP3K2 and PBX3 genes are involved in cancer cell proliferation and apoptosis. In this study, the expression of miR-302a and MAP3K2/PBX3 were evaluated by qPCR in liver cancer cell lines.

Role of microRNA-141-3p in the progression and metastasis of hepatocellular carcinoma cell.

Hepatocellular carcinoma (HCC) is a leading cause of cancer related death worldwide. However, the mechanisms underlying HCC progression and metastasis are still in obscure. Here, we used bioinformatic analysis to identify miRNAs that regulate GP73, a specific marker for HCC diagnosis and prognosis.

Lentivirus-mediated knockdown of P27RF-Rho inhibits hepatocellular carcinoma cell growth.

Aim Of The Study: To investigate the effects of P27RF-Rho on hepatocellular carcinoma (HCC) cell growth and explore the possibility of using it as a novel therapeutic target for liver cancer treatment.

Material And Methods: P27RF-Rho in HCC cells was silenced by lentivirus-mediated RNA interference, and the silencing effect was verified by RT-PCR. Cell proliferation was determined by MTT and clone formation assay.

Overexpression of Aquaporin 1 on cysts of patients with polycystic liver disease.

Background And Objective: Polycystic liver disease (PCLD) represents a group of genetic disorders that include autosomal dominant polycystic kidney disease (ADPKD) and isolated polycystic liver disease (iPCLD). There is currently no definitive treatment except for liver transplantation. The aim of this study was to assess the expression level of aquaporin 1 (AQP1) on the PCLD cysts with different sizes and provide the potential therapeutic target.

Effects of Ras homolog gene family, member C gene silencing combined with rapamycin on hepatocellular carcinoma cell growth.

The aim of the present study was to investigate the combined effects of inhibiting the Ras homolog gene family, member C (RhoC)/Rho kinase and phosphoinositide 3 kinase/Akt/mammalian target of rapamycin (mTOR) pathways on hepatocellular carcinoma cell growth. The RhoC gene was silenced by RNA interference (RNAi) and mTOR was inhibited by rapamycin (RAPA). Subsequently, an MTT assay for cell growth detection, western blot analysis for gene expression analysis, silver nitrate staining for cell proliferation, Wright's staining for analysis of the apoptotic rate analysis, soft agar clonogenic assay for the determination of cell growth characteristics and a Transwell assay for cell migration were performed.

In vitro regulation of hepatocellular carcinoma cell viability, apoptosis, invasion, and AEG-1 expression by LY294002.

Background: Hepatocellular carcinoma (HCC) is one of the most common malignancies in the world, and is characterized by advanced clinical stages at diagnosis and very poor prognosis.

Subjects And Methods: This study investigated the effects of PI3K inhibitor, LY294002, on suppression of astrocyte elevated gene-1 (AEG-1) and regulation of HCC cell viability, apoptosis, and invasion in vitro. Cell lines derived from normal liver and HCC were treated with LY294002 and evaluated by RT-PCR, western blot, cell viability, migration, and invasion assays.

STAT1 negatively regulates hepatocellular carcinoma cell proliferation.

Signal transducer and activator of transcription 1 (STAT1) regulates cell proliferation and survival. The present study aimed to investigate the role of STAT1 in the development and progression of human hepatocellular carcinoma (HCC). The levels of STAT1 expression in 36 HCC and 12 non-HCC liver tissues were examined by immunohistochemistry.

miRNA-22 suppresses colon cancer cell migration and invasion by inhibiting the expression of T-cell lymphoma invasion and metastasis 1 and matrix metalloproteinases 2 and 9.

Emerging evidence has demonstrated the altered expression of mRNAs in cancer development and progression. In this study, the precise role of miRNA-22 (miR-22) in colon cancer cells was investigated. Upon transfection with a miR-22 expression vector, the viability of HCT-116 human colon cancer cells was significantly reduced and tumor cell migration and invasion capacity were also suppressed.

Overexpression of Ras homologous C (RhoC) induces malignant transformation of hepatocytes in vitro and in nude mouse xenografts.

Ras homologous C (RhoC) is expressed in various cancers, including hepatocellular carcinoma (HCC). In this study, we first analyzed RhoC expression in 46 HCC tissue specimens and found that RhoC expression was significantly increased in HCC tissues compared to the adjacent normal liver tissues. Next, we investigated the role of RhoC in malignant transformation of normal hepatocytes.

Recombinant VAA-I from Viscum album induces apoptotic cell death of hepatocellular carcinoma SMMC7721 cells.

Researchers have proposed that VAA-I, a specific plant lectin found in Viscum album, has therapeutic effects on cancer and autoimmune diseases. VAA-I has shown some promising treatment results in some types of tumor cell lines, especially SMMC-7721 cells (human hepatocellular carcinoma cells). However, few details are known about the mechanism and process of cell death induced by VAA-I in tumor cells.

Effects of STAT3 gene silencing and rapamycin on apoptosis in hepatocarcinoma cells.

The PI3K/Akt/mTOR and JAK/STAT3 signaling pathways are important for regulating apoptosis, and are frequently activated in cancers. In this study, we targeted STAT3 and mTOR in human hepatocellular carcinoma Bel-7402 cells and examined the subsequent alterations in cellular apoptosis. The expression of STAT3 was silenced with small interfering RNA (siRNA)-expressing plasmid.

The role of RhoC in the proliferation and apoptosis of hepatocellular carcinoma cells.

In this study, we examined the effects of RhoC expression on the growth and apoptosis of human hepatocellular carcinoma cells (HCCs) in vitro in order to gain more understanding of its potential as a therapeutic target gene. We knocked down the endogenous expression levels of RhoC in human HCCs, BEL-7402, using siRNA and ectopically expressed RhoC in untransformed hepatocytes, HL7702. Stable cell lines were established, and cell growth was examined by MTT and colony formation assays, cell proliferation examined by silver nitrate staining of AgNORs, and cell cycle distribution examined by flow cytometry.

[Effect of RhoC on hepatocellular carcinoma cell growth and related molecular mechanisms].

Objective: To clarify the role of RhoC in the growth of hepatocellular carcinoma cells and its molecular mechanism, so as to explore the molecular target of tumor cell growth.

Methods: siRNA-RhoC plasmid was constructed and RhoC gene silencing the cell-line of hepatocellular carcinoma was setup. Cell growth was assessed by MTT assay.