This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Gastric cancer, one of the most common cancers worldwide, is highly fatal, largely because of metastasis, a migratory process that requires rearrangement of the cellular skeleton. The protein MICAL2 is known to regulate cytoskeletal rearrangement and is highly expressed in some aggressive cancers, but whether it participates in gastric cancer metastasis is unclear. To find out, researchers recently examined MICAL2 in human gastric cancer tissues and cell lines. MICAL2 was upregulated in gastric cancer tissues compared to healthy tissues, and high MICAL2 expression was associated with reduced survival. In vitro silencing experiments on human gastric cancer cells suggested that MICAL2 encourages cell migration through the β-catenin signaling pathway. Specifically, it promotes degradation of the protein E-cadherin in a manner dependent on the cell division regulator Cdc42..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Epithelial-mesenchymal transition (EMT) is a cellular process critical to the spread of breast cancer. EMT leads to stem-cell like behavior, or stemness, and is largely responsible for distal lung metastasis. Many oncogenic pathways, including Fzd/Wnt-mediated pathways, contribute to this process. A new study explored the role of Fzd7 in EMT, stemness, and metastasis. Database searches found that Fzd7 expression was correlated with mesenchymal phenotypes and mesenchymal-associated genes. Fzd7 knockdown in vitro reduced the expression of mesenchymal-associated genes induced epithelial-like morphology and inhibited cell motility, impaired mammosphere formation, and decreased the Lgr5+ subpopulation. In mice, Fzd7 knockdown reduced lung metastasis of xenograft tumors while also delaying their formation and suppressing growth. To explore the mechanisms behind this, the researchers identified correlations between expression levels of Fzd7, Wnt5a/b, and Col6a1 in expression databases..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.