Rosavin exerts an antitumor role and inactivates the MAPK/ERK pathway in small-cell lung carcinoma in vitro.

This study attempts to explore the function and mechanism of action of rosavin in small-cell lung cancer (SCLC) in vitro. The viability and clone formation of SCLC cells were assessed using cell counting kit-8 and colony formation assays, respectively. Apoptosis and cell cycle were detected using flow cytometry and cell cycle analysis, respectively. Wound healing and transwell assays were performed to evaluate the migration and invasion of SCLC cells. Besides, protein levels of p-ERK, ERK, p-MEK and MEK were determined using Western blot analysis. Rosavin repressed the viability and clone formation of SCLC cells, and promoted apoptosis and G0/G1 arrest of SCLC cells. At the same time, rosavin suppressed migration and invasion of SCLC cells. Moreover, protein levels of p-ERK/ERK and p-MEK/MEK were decreased after rosavin addition in SCLC cells. Rosavin impaired malignant behaviors of SCLC cells, which may be associated with inhibition of the MAPK/ERK pathway in vitro.

Redox-Active Azulene-based 2D Conjugated Covalent Organic Framework for Organic Memristors.

As a conjugated and unsymmetric building block composed of an electron-poor seven-membered sp2 carbon ring and an electron-rich five-membered carbon ring, azulene and its derivatives have been recognized as one of the most promising building blocks for novel electronic devices due to its intrinsic redox activity. By using 1,3,5-tris(4-aminophenyl)-benzene and azulene-1,3-dicarbaldehyde as the starting materials, an azulene(Azu)-based 2D conjugated covalent organic framework, COF-Azu, is prepared through liquid-liquid interface polymerization strategy for the first time. The as-fabricated Al/COF-Azu/indium tin oxide (ITO) memristor shows typical non-volatile resistive switching performance due to the electric filed induced intramolecular charge transfer effect. Associated with the unique memristive performance, a simple convolutional neural network is built for image recognition. After 8 epochs of training, image recognition accuracy of 80 % for a neutral network trained on a larger data set is achieved.

Donor-acceptor-type poly[chalcogenoviologen-alt-triphenylamine] for synaptic biomimicking and neuromorphic computing.

Polymer memristors are preeminent candidates for low-power edge computing paradigms. Poly[chalcogenoviologen-alt-triphenylamine] (PCVTPA) has been synthesized by direct coupling of chalcogeno-viologen as electron acceptor and 4-(bromomethyl)-N-(4-(bromo-methyl)phenyl)-N-phenylaniline as electron donor. The introduction of chalcogen atoms (S, Se, Te) into viologen scaffolds can greatly improve electrical conductive, electrochemical, and electrochromic properties of the materials when compared with the conventional viologens. Taking PTeVTPA as an example, the as-fabricated electronic device with a configuration of Al/PTeVTPA/ITO exhibits excellent multilevel storage and history-dependent memristive switching performance. Associated with the unique memristive behavior, the PTeVTPA-based device can not only be used to emulate the synaptic potentiation/depression, the human's learning and memorizing functions, and the transition from short-term synaptic plasticity to long-term plasticity but also carry out decimal arithmetic operations as well. This work will be expected to offer a train of new thought for constructing high-performance synaptic biomimicking and neuromorphic computing system in the near future.

US National Cancer Institute-China Collaborative Studies on Chinese Medicine and Cancer.

Since 2007, the US National Cancer Institute (NCI) Office of Cancer Complementary and Alternative Medicine (OCCAM), together with the Cancer Institute of the China Academy of Chinese Medical Sciences (CICACMS), institutes at China Academy of Sciences and Chinese Academy of Medical Sciences, have engaged in collaborations on Chinese medicine (CM) and cancer research. Through these collaborations, CM drugs and compounds have been studied at NCI labs. This paper summarizes the discoveries and progress on these research projects, exploring the aspects of cancer prevention, botanical drug mechanisms of action and component analysis/quality control (QC), and anticancer activity screening. These and other related projects have been presented in various jointly convened workshops and have provided the backdrop for establishing a new organization, the International Consortium for CM and Cancer, to promote international collaborations in this field.

Fufang Kushen injection inhibits sarcoma growth and tumor-induced hyperalgesia via TRPV1 signaling pathways.

Cancer pain is a deleterious consequence of tumor growth and related inflammation. Opioids and anti-inflammatory drugs provide first line treatment for cancer pain, but both are limited by side effects. Fufang Kushen injection (FKI) is GMP produced, traditional Chinese medicine used alone or with chemotherapy to reduce cancer-associated pain. FKI limited mouse sarcoma growth both in vivo and in vitro, in part, by reducing the phosphorylation of ERK and AKT kinases and BAD. FKI inhibited TRPV1 mediated capsaicin-induced ERK phosphorylation and reduced tumor-induced proinflammatory cytokine production. Thus, FKI limited cancer pain both directly by blocking TRPV1 signaling and indirectly by reducing tumor growth.

Compound Kushen Injection suppresses human breast cancer stem-like cells by down-regulating the canonical Wnt/ß-catenin pathway.

BACKGROUND: Cancer stem cells (CSCs) play an important role in cancer initiation, relapse and metastasis. To date, no specific medicine has been found to target CSCs as they are resistant to most conventional therapies and proliferate indefinitely. Compound Kushen Injection (CKI) has been widely used for cancer patients with remarkable therapeutic effects in Chinese clinical settings for many years. This study focused on whether CKI could inhibit MCF-7 SP cells in vitro and in vivo. METHODS: The analysis of CKI on SP population and the main genes of Wnt signaling pathway were studied first. Then we studied the tumorigenicity of SP cells and the effects of CKI on SP cells in vivo. The mice inoculated with 10,000 SP cells were randomly divided into three groups (6 in each group) and treated with CKI, cisplatin and saline (as a control) respectively for 7 weeks. The tumor formation rates of each group were compared. The main genes and proteins of the Wnt signaling pathway were analyzed by RT-PCR and western blot. RESULTS: CKI suppressed the size of SP population (approximately 90%), and down-regulated the main genes of Wnt signaling pathway. We also determined that MCF-7 SP cells were more tumorigenic than non-SP and unsorted cells. The Wnt signaling pathway was up-regulated in tumors derived from SP cells compared with that in tumors from non-SP cells. The tumor formation rate of the CKI Group was 33% (2/6, P < 0.05), and that of Cisplatin Group was 50%(3/6, P < 0.05), whereas that of the Control Group was 100% (6/6).The RT-PCR and western blot results indicated that CKI suppressed tumor growth by down-regulating the Wnt/ß-catenin pathway, while cisplatin activated the Wnt/ß-catenin pathway and might spare SP cells. CONCLUSIONS: It suggested that CKI may serve as a novel drug targeting cancer stem-like cells, though further studies are recommended.