While some members of the ubiquitous DExD/H box family of proteins have RNA helicase activity in vitro, their roles in vivo remain virtually unknown. Here, we show that the function of an otherwise essential DEAD box protein, Prp28p, can be bypassed by mutations that alter either the protein U1-C or the U1 small nuclear RNA. Further analysis suggests that the conserved L13 residue in the U1-C protein makes specific contact to stabilize the U1 snRNA/5' splice site duplex in the prespliceosome, and that Prp28p functions to counteract the stabilizing effect of the U1-C protein, thereby promoting the dissociation of the U1 small nuclear ribonucleoprotein particle from the 5' splice site. Thus, in addition to unwinding RNA, the DExD/H box proteins may affect RNA-RNA rearrangements by antagonizing specific RNA-stabilizing proteins.

Protoapigenone, isolated from the native fern plant Thelypteris torresiana, has anticancer activity against some cancer cells. However, the toxicological mechanism for protoapigenone is still unknown. Here, we investigated the anticancer effect of protoapigenone on human lung cancer cell lines. The comet assay showed that DNA damage induced by protoapigenone is dose-dependent. Trypan blue exclusion showed that the cell killing by protoapigenone is both time and dose dependent. The IC(50) of protoapigenone for 12, 24, and 48 h in H1299 cells is 6.11, 2.74, and 1.49 microM, respectively. Flow cytometry showed cell cycle perturbation such as sub-G(1) accumulation (at 1.57 microM for 48 h and at 3.57 microM for 12 and 24 h) and G(2)/M arrest (at 3.57 microM for 12 and 24 h) for protoapigenone. The sub-G(1) accumulation phenomena in the 3.57 microM for 24 h sample were shown to be apoptosis using Annexin V-immunofluorescence/propidium iodide staining. These results suggest protoapigenone is a potential chemotherapeutic agent for lung cancers.

GRP78 protein is a possible biomarker of oral cancer in Taiwan.

No abstract

Caffeic acid (CA), a natural phenolic compound, is abundant in medicinal plants. CA possesses multiple biological effects such as anti-bacterial and anti-cancer growth. CA was also reported to induce fore stomach and kidney tumors in a mouse model. Here we used two human lung cancer cell lines, A549 and H1299, to clarify the role of CA in cancer cell proliferation. The growth assay showed that CA moderately promoted the proliferation of the lung cancer cells. Furthermore, pre-treatment of CA rescues the proliferation inhibition induced by a sub-IC50 dose of paclitaxel (PTX), an anticancer drug. Western blot showed that CA up-regulated the pro-survival proteins survivin and Bcl-2, the down-stream targets of NF-κB. This is consistent with the observation that CA induced nuclear translocation of NF-κB p65. Our study suggested that the pro-survival effect of CA on PTX-treated lung cancer cells is mediated through a NF-κB signaling pathway. This may provide mechanistic insights into the chemoresistance of cancer calls.