Find our monthly reviews of selected 3D-cell-culture publications
3D cell culture can be a key technology to improve the reliability and biological relevance of cell-based assays. The number of publications in the field grows quickly, and it is hard to stay on top of current research activities worldwide. Our applications team keeps a close eye on new and relevant publications to keep our customers informed. Find below our monthly reviews of a small selection of current 3D-cell-culture journal papers!
02/2016 - Human Dynactin-Associated Protein Transforms NIH3T3 Cells to Generate Highly Vascularized Tumors with Weak Cell-Cell Interaction
Tatsuki Kunoh1, Weixiang Wang1, Hiroaki Kobayashi1, Daisuke Matsuzaki1, Yuki Togo1,Masahiro Tokuyama1, Miho Hosoi1, Koichi Koseki1, Shu-ichi Wada1, Nobuo Nagai1, Toshinobu Nakamura1, Shintaro Nomura1, Makoto Hasegawa1, Ryuzo Sasaki1,2,Tamio Mizukami1,2*:
Human Dynactin-Associated Protein Transforms NIH3T3 Cells to Generate Highly Vascularized Tumors with Weak Cell-CellInteractionAbstract Human dynactin-associated protein (dynAP) is a transmembrane protein that promotes Akt-Ser473 phosphorylation. Here, we report the oncogenic properties of dynAP. In contrast to control NIH3T3 cells expressing LacZ (NIH3T3LacZ), NIH3T3dynAP cells vigorously formed foci in two-dimensional culture, colonies on soft agar, and spheroids in anchoragedeficient three-dimensional culture. NIH3T3dynAP cells injected into nude mice produced tumors with abundant blood vessels and weak cell—cell contacts. Expression of dynAP elevated the level of rictor (an essential subunit of mTORC2) and promoted phosphorylation of FOXO3aSer253. FOXO3a is a transcriptional factor that stimulates expression of pro-apoptotic genes and phosphorylation of FOXO3a abrogates its function, resulting in promoted cell survival. Knockdown of rictor in NIH3T3dynAP cells reduced AktSer473 phosphorylation and formation of foci, colony in soft agar and spheroid, indicating that dynAP-induced activation of the mTORC2/AktSer473 pathway for cell survival contributes to cell transformation. E-cadherin and its mRNA were markedly reduced upon expression of dynAP, giving rise to cells with higher motility, which may be responsible for the weak cell-cell adhesion in tumors. Thus, dynAP could be a new oncoprotein and a target for cancer therapy.