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:

"Colorectal cancer is the second-leading cause of cancer-related deaths worldwide. Understanding tumor metastasis mechanisms and the interactions between cell types in the tumor microenvironment can help researchers identify treatment targets. Recently, a team of researchers examined the interaction between colorectal cancer cells and fibroblasts. IL-1α is a signaling protein that in other systems and cancers has both pro- and anti-metastasis effects. Here, the two highly metastatic colorectal cancer cell lines expressed IL-1α, while the less metastatic lines and fibroblasts did not. Increasing the abundance of IL-1α increased the expression of another signaling protein, CXCL12, in fibroblasts. This worked by either adding IL-1α directly or co-culturing fibroblasts with IL-1α-expressing cancer cells. Increasing the abundance of CXCL12, either directly or via co-culture, increased invasiveness of colorectal cancer cells and promoted angiogenesis..."

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:

"While best known for its role in the brain, serotonin does more in our body than influence mood. There is even growing evidence that it is involved in tumor development. However, little is known about its role in colorectal cancer. In a recent study, researchers found that serotonin promotes colon cancer cell growth in cell culture and animal models. Further tests revealed that serotonin is moved into colorectal cancer cells via its transporter SERT and that once the serotonin is inside the cancer cells, the enzyme TG2 links serotonin to the protein RhoA, activating it. Through down-stream signaling mediators, activated RhoA increases expression of the known cancer-promoting protein YAP. Blocking SERT from transporting serotonin with citalopram reversed the serotonin-induced YAP expression and cell proliferation increases and blocked serotonin’s effects on tumor formation in mice..."

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:

"Metastatic invasion is driven by the reorganization of the cytoskeleton and the formation of cell-membrane protrusions called ‘invadopodia’. Invadopodia assembly is regulated by protein tyrosine kinases, but little is known about the roles of tyrosine phosphatases. An improved understanding of the mechanisms that form invadopodia could be used to combat tumor spread. To reduce this gap, researchers recently examined the role that the tyrosine phosphatase Shp1 plays in this process. They found that Shp1 localized to invadopodia and that this localization was facilitated by a phosphoinositide metabolite, glycerophosphoinositol (GroPIns). Once there, Shp1 associated with and dephosphorylated cortactin, which reduced the formation and extracellular matrix degradation activity of invadopodia. Treatment with GroPIns inhibited tumor invasion in mice when Shp1 was present, but this effect was dependent on the presence of Shp1..."

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:

"Type 2 diabetes mellitus often leads to muscle atrophy driven by diminished differentiation capacity in myoblasts. Myogenesis is complex, and while many involved pathways have been described, there may still be yet undiscovered therapeutic targets. With this goal in mind, a recent study combined experiments in diabetic mice and cultured myoblasts to identify key proteins in diabetes-induced atrophy. The gene for the relatively undescribed solute carrier Slc2a6, also known as glut6, was up-regulated during myogenic differentiation and down-regulated during diabetes-induced myopathy. Silencing Slc2a6 with RNAi in cell culture impaired differentiation and myotube formation. Transcriptomics and metabolomics revealed that Slc2a6 silencing disproportionally impacted the glycolysis pathway . Further experiments and analysis determined that Slc2a6 regulates myogenic differentiation in cultured myoblasts and that this regulation was partly through the glycolysis pathway..."

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:

"In cancer cells, even seemingly small gene expression changes can have a devastating impact, but for some molecules, like the enzyme USP22, researchers don’t know how their expression is regulated. High expression of USP22 is associated with poor prognosis in many human cancers. But the gene for USP22 is rarely mutated, suggesting that the expression changes happen at the transcription step. So, researchers set out to find transcription factors, which are transcription-modulating proteins, that regulate USP22. After identifying several that modulate USP22 expression, they focused on two related factors that increased USP22 expression, AP2α, and AP2β. Overexpressing AP2α/β in cultured non-small cell lung cancer (NSCLC) cells increased the expression of USP22 and the protein it targets, Cyclin D1, while also increasing the cancer cell behaviors proliferation, migration, and invasion..."

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:

"The hormone and receptor pair IGF-1 and IGF-1R and the Hippo-YAP signaling pathway are critical to breast cancer stem cells, but if or how these pathways interact in these cells remained unclear. So, researchers recently examined YAP and IGF-1R in triple negative breast cancer cell lines and xenograft models. YAP knockdown reduced viability and stemness in cell culture and tumorigenicity in vivo, suggesting that YAP contributes to stemness in breast cancer cells. Further tests determined that IGF-1R regulated YAP expression, and in turn, YAP regulated IGF-1 expression but not IGF-1R. Specifically, depleting IGF-1R decreased YAP expression, while addition of IGF-1 upregulated YAP and increased its nuclear localization. YAP overexpression increased IGF-1 expression without impacting IGF-1R expression. In clinical data from basal-like breast cancer patients, higher levels of YAP and IGF-1 are correlated with shorter overall survival..."

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

This module introduces students to sterile culture techniques using Saccharomyces cerevisiae. Studentslearn the relationships between species and strainsisolate individual colonies from liquid cultures on streak platesprepare serial dilutions of liquid cultures for spot plates, which are used to estimate the concentration of viable cells in the culturesestimate cell densities in liquid cultures using the spectrophotometerThis module is part of a semester-long introductory lab course, Investigations in Molecular Cell Biology, at Boston College.

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:

"Colitis and other diarrheal diseases cause serious health problems in dairy calves and are often managed by antibiotics. But heavy agricultural antibiotic use is a major driver of the global antibiotic resistance crisis, meaning there is a need for non-antibiotic therapeutics. One such potential therapeutic is ursodeoxycholic acid (UDCA) or its common formulation, ursodiol. UDCA is a bile acid with previously demonstrated effectiveness treating colitis but an unclear mechanism of action. In a multipronged study, researchers examined the microbiome and metabolic profiles of healthy and diarrheic calves and tested the impacts of UDCA and ursodiol in cell culture and mouse models. A core set of gut bacterial groups distinguished healthy calves from diarrheic ones and those beneficial groups were associated with microbial UDCA production, short-chain fatty acids, and other prebiotics. Further, in several cell culture and mouse models, ursodiol administration blocked bacterial growth and invasion..."

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:

"Liver cancer is the third deadliest cancer worldwide, and effective treatments are limited. But inducing apoptosis, a type of programmed cell death, could aid or replace current treatments. Apoptin is a protein that triggers apoptosis specifically in tumor cells. Apoptin also activates autophagy, or the breakdown of unneeded or damaged cellular components, which can either inhibit or induce apoptosis. However, the cellular mechanisms linking these processes remain unclear. So, researchers recently used cultured liver cancer cells and a mouse model of liver cancer to elucidate those mechanisms. First, they confirmed that apoptin increased apoptosis and autophagy in both the cultured cells and the mice. But they also found that the autophagy it activated was protective, slowing the rate of apoptosis. Mechanistically, apoptin increased the levels of reactive oxygen species (ROS) and activated mitophagy, a mitochondria- specific type of autophagy..."

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:

"In nerve cells, the waxy molecule ceramide plays roles in both cellular differentiation and death, but a new study shows those roles could vary based on how ceramide is formed. Ceramide is generated via 3 pathways: newly from palmitoyl-CoA and serine, from the breakdown of sphingomyelin, and through the endosomal salvage pathway. Experiments showed that blocking ceramide synthesis did not alter ceramide levels in PC12 cells, which require nerve growth factor (NGF) to survive and differentiate, but blocking synthesis did decrease ceramide levels in TrkA cells, which differentiate spontaneously. Blocking sphingomyelin breakdown, however, inhibited differentiation and reduced ceramide in both cell lines. Without NGF, PC12 cells begin to atrophy and die, and preventing sphingomyelin breakdown did not protect them, but it did suppress rising ceramide levels to some degree versus controls..."

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