Targeting Epidermal Growth Factor Receptor in Non-Small-Cell-Lung Cancer: Current State and Future Perspective.

Background: Lung cancer is one of the leading cause of cancer death worldwide, the most common histological type of lung cancer is non-small cell lung cancer (NSCLC), whose occurrence and development is closely related to the mutation and amplification of epidermal growth factor receptors (EGFR). Currently , a series of targeted drugs were developed on the inhibition of EGFR such as epidermal growth factor receptortyrosine kinase inhibitor EGFR-TKI and monoclonal antibody (McAb).

Objective: We sought to summarizes the current drugs targeting Epidermal Growth Factor Receptor in nonsmall- cell-lung.

Corilagin induces apoptosis, autophagy and ROS generation in gastric cancer cells in vitro.

Corilagin, a unique component of the tannin family, has been identified in several medicinal plants. In previous literature, corilagin exhibited a marked anticancer property in a variety of human cancer cells. However, the biological effects of corilagin on gastric cancer and the mechanisms involved remain to be fully elucidated.

Corilagin inhibits breast cancer growth via reactive oxygen species-dependent apoptosis and autophagy.

Corilagin is a component of Phyllanthus urinaria extract and has been found of possessing anti-inflammatory, anti-oxidative, and anti-tumour properties in clinic treatments. However, the underlying mechanisms in anti-cancer particularly of its induction of cell death in human breast cancer remain undefined. Our research found that corilagin-induced apoptotic and autophagic cell death depending on reactive oxygen species (ROS) in human breast cancer cell, and it occurred in human breast cancer cell (MCF-7) only comparing with normal cells.

Mesenchymal stem cells in inflammatory microenvironment potently promote metastatic growth of cholangiocarcinoma activating Akt/NF-κB signaling by paracrine CCL5.

Our previous work has demonstrated that mesenchymal stem cells (MSCs) could induce metastatic growth of the inflammation-related cholangiocarcinoma (CCA). However, the functional mechanism of MSCs on CCA progression in the early inflammatory microenvironment remained undetermined. Here, we showed that TNF-α and IFN-γ-induced inflammatory microenvironment stimulated the expression of TNF-α, CCL5, IL-6, IDO, and activated the NF-κB signaling with p65 nuclear translocation in MSCs cells.

Involvement of Wnt/β-catenin signaling in the mesenchymal stem cells promote metastatic growth and chemoresistance of cholangiocarcinoma.

Mesenchymal stem cells (MSCs) are multi-potent progenitor cells with ability to differentiate into multiple lineages, including bone, cartilage, fat, and muscles. Recent research indicates that MSCs can be efficiently recruited to tumor sites, modulating tumor growth and metastasis. However, the underlying molecular mechanisms are not fully understood.